A 20-year-old female, with no significant past medical history, presented to the emergency department with a myriad of complaints of abdominal pain, nausea, nonbloody, nonbilious vomiting, and fever for 5-day duration. The abdominal pain was diffuse, dull aching in nature, and associated with occasional burning. She denied any recent travel, sick contacts, or change in diet habits. Review of system was positive for poor appetite, dizziness while standing up, palpitations, myalgia, and excessive fatigue but negative for diarrhea, productive cough, dysuria, vaginal discharge, or neck stiffness. Her initial vital signs were pertinent for hypotension with a blood pressure of 73/33 mm Hg, and tachycardia with a heart rate of 118 per minute. She did not require supplemental oxygen and had a temperature of 37.8°C. Physical examination revealed dry oral mucosa and mild diffuse tenderness to abdominal palpation, with no rash, ulcer, or discoloration of skin. Other physical examination findings were unremarkable.
Her lab work was significant for a white blood cell count of 9.9 (3.9–10.0) thou/mm3, serum creatinine of 1.31 (0.51–0.95) mg/dL, mild hyponatremia with a sodium of 130 (136–146) mEq/L, potassium of 5.0 (3.5–5.1) mEq/L, and serum blood glucose of 63 (70–99) mg/dL. Lipase was normal and liver function test was unremarkable. She was started on aggressive fluid resuscitation, broad-spectrum intravenous (IV) antibiotics, and admitted to the medical intensive care unit for management of shock secondary to sepsis from infectious gastroenteritis and volume depletion.
Despite fluid resuscitation, the patient's mean arterial blood pressure continued to decline, hence she was started on a vasopressor medication. A computed tomography of the abdomen with IV contrast was unremarkable, and no source of infection was identified on workup. However, the patient continued to require increasing vasopressor support. On hospital day 2, the patient had no episodes of vomiting and remained afebrile, with no leukocytosis. Given profound shock despite intravascular volume resuscitation and no clear identifiable source for sepsis, a morning serum cortisol level was ordered for suspected AI.
Cortisol testing was significantly low at <0.5 (10–20) μg/dL, suggestive of AI. Further testing showed a subnormal response to low-dose adrenocorticotropic hormone (ACTH) stimulation, confirming primary AI (PAI). She was started on hydrocortisone and the patient was able to be weaned off vasoactive medication infusion along with clinical improvement in symptoms. For further evaluation of the etiology of the adrenal crisis, magnetic resonance imaging of the abdomen was ordered, which showed atrophic bilateral adrenal glands ().
On further evaluation, her 21-hydroxylase antibody (Ab) was significantly elevated at 78.1 (0.0–1.0) U/mL, suggestive of autoimmune adrenalitis. Subsequent workup for additional autoimmune conditions revealed profoundly elevated thyroglobulin Ab at 109.6 (0.0–60.0) IU/mL and thyroid peroxidase Ab at 528.7 (0.0–60.0) IU/mL, with normal islet cell Ab and glutamic acid decarboxylase Ab level. Taken together, it was concluded that the patient developed shock secondary to adrenal crisis, and she was diagnosed with AIPS-II. Despite the presence of antithyroid peroxidase autoantibodies, her thyroid function tests remained normal; therefore, no thyroid replacement therapy was started. She was discharged on day 7 on a daily glucocorticoid (hydrocortisone 20 mg with breakfast and 5 mg with dinner) and mineralocorticoid (fludrocortisone 0.5 mg once daily) replacement regimen, with education on sick-day steroid use rules. The patient has close follow-up with an endocrinologist and her disease is currently well controlled.


A previously healthy 21-year-old male was referred to our hospital with a high-grade fever, decreased oral intake, generalized abdominal discomfort, and altered sensorium for 3 days. He was a resident of the United States with parents of Indian descent and had come to India for the first time on a personal visit. 10 days prior to admission, the patient developed diarrhea and low-grade fever and he self-medicated with paracetamol tablet with initial improvement in symptoms. He was brought to the emergency department in view of persisting fever and altered sensorium. On evaluation, the patient was disoriented to time, place, and person. There was slurring of speech and ataxia. He was moving all four limbs equally and had bilateral extensor plantar reflexes, normally elicitable deep tendon reflexes, and no neck stiffness. His cranial nerve examination was normal. Systemic examination was unremarkable except for hepatosplenomegaly.
A diagnostic possibility of tropical infection or meningoencephalitis was considered. Laboratory investigations revealed normal total leukocyte count, thrombocytopenia (platelets 96 × 109/L), serum creatinine 1.70 mg/dL (normal range: 0.5–1.3 mg/dL), aspartate aminotransferase (AST) 286 units/L, and alanine aminotransferase (ALT) 106 units/L. Cerebrospinal fluid study found glucose 66 mg/dL (blood glucose 94 mg/dL), protein 17 mg/dL, and nil white blood cell. Brain MRI on admission revealed an abnormal T2 hyperintensity in the splenium of corpus callosum showing restricted diffusion. There were no hemorrhagic residues or abnormal postcontrast enhancement of the lesion ().
Leptospiral, malarial, scrub typhus, and HIV serology were negative. Widal test was strongly positive with a S. typhi flagellar (TH) agglutinin level of ≥960. On day 5, blood cultures isolated Salmonella enteric serotype typhi. A diagnosis of typhoid fever with encephalopathy was made in view of positive blood culture and clinical features. The patient was managed with intravenous ceftriaxone twice daily for 14 days. There was improvement in sensorium by day 6 of hospital admission. Repeat MRI performed on day 8 revealed complete resolution of changes in the splenium of corpus callosum (). He was discharged from hospital without any central nervous system impairment.


The study received ethical approval from the Kyung Hee University Korean Medicine Hospital Institutional Review Board (KOMCIRB 2019-04-005).
In 12th December, a 84.2-year-old male patient visited to the Department of Neuropsychiatry at Kyung Hee University Korean Medicine Hospital due to memory impairment. He complained that he had often forgotten where he put things and could not find them and that he had sometimes forgotten what he had planned to do. He got lost twice in recent four years. He did not have distinct psychiatric and behavioral disturbances such as agitation, anxiety, apathy, dysphoria, delusion etc on the first day of treatment. He had 16 years of education and graduated university. He had undergone cataract surgery in 1993 and had no other past history except taking the hypertensive drugs. He suffered from memory loss and numbness since 2014 and was diagnosed with mild cognitive impairment. In the first visit, symptoms were assessed with Mini-Mental State Examination-Dementia Screening (MMSE-DS), Korean Version of Montreal Cognitive Assessment (MoCA-K), and Korean-Dementia Rating Scale (K-DRS). On 12th December, the MMSE-DS score was 28 points and the MoCA-K score was 15 points. K-DRS score was 120 points (7.6% by percentile values according to age and educational years) whose subscale scores were 35 (37.1%) for attention, 21 (2.9%) for initiation/perseveration, 6 (100.0%) for construction, 36 for (80.0%) for conceptualization, and 22 (34.3%) for memory ().
Hominis placenta pharmacopuncture was administered once a week from December 12, 2018 to January 4, 2019. The treatment consisted of injections of 0.2ml dosage of Hominis placenta extract into each acupoints, which were GV20, CV12, and bilateral ST36.
In the third visit, he was able to recall, remembering all the acupoints where the extract had been injected. At the end of treatment which included four treatments, he reported reduced fatigue of the whole body and increased motivation. He visited all of the scheduled dates.
MMSE-DS score was 28 points, which was the same at the beginning and at the end. The other measures showed a change. MoCA-K score increased from 15 points to 21 points. K-DRS score was 120 (percentile 7.6%) at the first visit but 137 (100%) on the last visit. In subscales, initiation/perseveration score increased from 21 (2.9%) to 34 (88.6%) and memory score increased from 22 (34.3%) to 25 (100%). Conceptualization score slightly increased from 36 (80.0%) to 37 (94.3%), while attention and construction score remained unchanged at 36 (37.1%) and 6 (100.0%) respectively.
There was no adverse reaction during the skin test before the initial administration and no discomfort or other adverse effect was reported during the treatment period.


A 35-year-old male patient has been reported in our outdoor with a complaint of a hard lesion on the glans penis. The lesion started 4 years back when it was a small pea-sized nodule and increased progressively to the present size of around 4 cm × 3 cm obscuring almost whole of the glans penis. Physical examination revealed a hard, nontender, pointed growth on the glans penis without any surrounding induration []. There was no palpable inguinal lymphadenopathy. Systemic examination was unremarkable. The lesion was excised with adequate margin, and the wound was closed primarily. Histopathological examination of the excised specimen showed hyperkeratosis, acanthosis, and parakeratosis []. There was no evidence of malignancy. Postoperative recovery was uneventful, and the patient was discharged in a stable condition and was on regular follow-up for the past 1 year.


A 2-year-old girl presented to our emergency room in cyanotic spells. She was a known case of TOF and midline thoracic defect for 3 months of age. The child had to be intubated in the emergency room considering severe desaturation not responding to usual measures. There was a visible midline cardiac pulsation on the chest wall with an overlying central raphe [] without any palpable sternum.
Echocardiography showed large malaligned subaortic ventricular septal defect (VSD), severe infundibular and valvular pulmonary stenosis, confluent- and adequate-sized branch pulmonary arteries, right aortic arch, and bilateral superior vena cavae. A computed tomography scan of the thorax was done to rule out any other associated malformations. The scan confirmed a complete CS []. The child underwent cardiac catheterization study to confirm intracardiac anatomy and to rule out aortopulmonary collaterals.
A combined staged surgical procedure in the form of intracardiac repair followed by chest wall reconstruction was planned. Meanwhile, the child was kept ventilated.
The patient underwent Dacron patch closure of VSD, infundibular resection, pulmonary valvectomy, and transannular autologous pericardial patch augmentation of the right ventricular outflow tract. Branch pulmonary arteries were adequate and confluent. A conscious decision was taken by the team members to postpone the sternal reconstruction by 24 h in view of a major intracardiac procedure having been performed. Sternal reconstruction was done subsequent morning. We performed bilateral sliding chondrotomies of the first four ribs and local advancement of the pectoralis major muscle to close the defect primarily with No. 2 stainless steel wires [Figure and ]. The child was electively ventilated and extubated on the 4th postoperative day. Her hospital stay was prolonged (20 days) due to the need for intense chest physiotherapy and oxygen dependency. The patient was discharged with stable sternum without any deformity. She is doing well on the last follow-up as well, 1 year after the procedure.


This is the case of an otherwise healthy 47-year-old female with history of well-controlled allergic rhinitis, who was referred by Neurology to our Otolaryngology clinic due to an incidental left “maxillary sinusitis” found on magnetic resonance imaging (MRI) performed for a chief complaint of headaches. The patient was asymptomatic at the moment of presentation and denied history of facial trauma and surgery. Physical examination revealed a mild left enophthalmos and hypoglobus, and the diagnosis of left maxillary SSS was confirmed on a CT scan ().
Surgery was offered at the time of initial presentation, but the patient was lost to follow-up and returned 2 years 5 months later with a new CT scan that revealed bilateral maxillary SSS (). The patient continued to be asymptomatic at the time of her second presentation, and the diagnosis of metachronous bilateral SSS was made. and depict the temporal development of right-sided enophthalmos secondary to maxillary sinus atelectasis from SSS. The patient underwent bilateral endoscopic sinus surgery, and postoperative endoscopic examination revealed patent and clear maxillary sinuses with reestablishment of adequate ventilation. The patient had a prompt recovery after surgery and has remained asymptomatic, without surgical complications or clinical progression of disease.


A 56-year-old male was referred to our emergency room with sudden onset of intermittent abdominal pain in the left upper quadrant. The pain started 5 days prior with no obvious traumatic cause. The patient had no clinical history of hepatitis, hypertension, coronary heart disease, diabetes, or any type of surgery, but he had a long-term history of excessive alcohol consumption with an average of 100 g of ethanol per day. During physical examination upon admission, he presented no fever with a body temperature of 36.2°C, a pulse rate of 80/min, and blood pressure of 170/90 mmHg. Abdominal palpation revealed tenderness in the left upper quadrant but no rigidity or spasm. The spleen was palpable at 10 cm below the left coastal arch. The result of the abdominal shifting dullness exam was negative. Diagnostic paracentesis yielded nonclotting blood.
The patient’s laboratory tests showed a white blood cell (WBC) count of 2.03 × 109/L, red blood cell (RBC) count of 3.46 × 109/L, haemoglobin level (Hb) of 109 g/L, and platelet count of 71 × 109/L, which are indicative of hypersplenism. Enhanced computed tomography revealed splenic subcapsular attenuation of echogenicity connected to a hypoechoic cystic mass (~3 cm) located at the splenic hilum, as well as free fluid in the abdomen, which are suggestive of intra-cystic haemorrhage–induced splenic rupture and haemoperitoneum ().
An exploratory laparotomy was performed due to the suspicion of splenic rupture and haemoperitoneum. During the surgery, ~2300 mL of fluid mixed with blood clots was collected from the peritoneum. The liver exhibited an irregular or nodular surface, blunt edges, and medium hard texture, which are suggestive of liver cirrhosis. The enlarged spleen (35 cm × 28 cm) presented subcapsular haematoma (>40% of the surface area) and laceration (~4 cm in depth). The intraoperative portal venous pressure was measured as 35 cm H2O. The ruptured spleen was removed, and a liver biopsy (5 mm × 5 mm) was obtained for histopathological purposes. During the splenectomy, the patient received a blood transfusion containing 800 mL of packed RBCs, 300 mL of plasma, and 1 unit of platelets.
The patient had an uneventful recovery and was discharged at 10 days post-surgery. Upon discharge, his laboratory test exhibited favourable outcomes (WBC 7.11 × 109/L, RBC 4.87 × 109/L, Hb 148 g/L, and platelets 424 × 109/L). Post-surgery microscopy of the liver revealed macrovesicular steatosis, perivenular fibrosis, and fibrous bands subdividing the liver into regenerative nodules, which is indicative of cirrhosis ( and ()). The spleen presented intra-cystic haemorrhage and a cyst covered with an endothelial layer, but there was no calcification or fibrosis (). There was also congestion and dilation of the sinusoids, active germinal centres, and increased numbers of macrophages in the spleen pulp ().


A 58-year-old woman, who is fond of eating fish, accidentally got a bone of a fish she caught 90 days ago stuck in her throat. She swallowed steamed bread and leeks repeatedly, as she had pain on swallowing, with no immediate relief. Hence, she visited the local hospital where an examination was conducted of the pharynx, followed by electronic laryngoscopy, and nothing was found. Thereafter, she felt relief without any treatment. She began to feel discomfort in the right submandibular gland after 80 days and reported for treatment at our hospital. The computed tomography (CT) images showed a linear high-density image of the right submaxillary gland. A hyperechogenic line was shown on the ultrasonic image of the gland, of about 1.39 × 0.39 cm, and was diagnosed as a foreign body (Fig. ).
After admission, relevant examinations were conducted, and she underwent an exploration of the right neck root and removal of the foreign body under general anesthesia, with no surgical contraindications. Probing of the submaxillary gland revealed a sharp and hard foreign body about 1.5 cm long, which was a fish bone. During the smooth operation, a plier was used to completely remove the 1.5-cm-long fish bone, which was measured to be the same size as on the ultrasonic image (Fig. ). The incision healed by first intention, and the suture was removed after 1 week. During 2 months of follow-up the patient showed no symptoms of pain or foreign body sensation.


A 59-year-old female presented to the dermatology outpatient department (OPD) with erythematous patches across her whole body, without Nikolsky's sign. Symptom onset was one week prior to presentation. Oral mucosal erosion and conjunctival injection were observed. The patient reported itching without pain. For the past ten years, the patient had been taking hormone replacement therapy (tibolone) for postmenopausal symptoms and an antihypertensive drug (lercanidipine). Two weeks prior to symptom onset, the patient began taking the following new drugs twice daily for back pain: CBZ (100 mg), tramadol (37.5 mg) and acetaminophen (325 mg) in combination, aceclofenac (100 mg), cimetidine (200 mg), and piprinhydrinate (3 mg). On the day of presentation, routine hematological test (complete blood cell count, CBC), liver function, renal function, and radiology exam (simple chest X-ray) were normal. The patient was afebrile, and an electrocardiogram (ECG) showed normal sinus rhythm. Ophthalmologic examination revealed moderate follicular injection and discharge in both conjunctivas. Excision skin biopsy (from the leg) confirmed erythema multiforme (EM). The patient was diagnosed with SJS with mucosal involvement of the eye and oral cavity and CBZ was suspected to be the culprit drug. All newly started drugs were stopped. Systemic corticosteroid, oral methylprednisolone (24 mg/day) and topical corticosteroid, desonide (500 ug/g) were prescribed. Oral antihistamine was prescribed for itching, and fluorometholone eye drops were also prescribed. Oral corticosteroid was tapered off after one week. The patient recovered without complication.


A 62-year-old male hospitalized with bacterial meningitis and cerebral infarction was referred to the dermatology department with erythematous patches across his whole body. Symptom onset was one week prior to dermatology consultation. Oral mucosal erosion and conjunctival injection were observed, as well as some blistering on the body. Forty-five days prior to dermatologic symptom onset, meropenem was started as an antiinfective drug, and PHT was commenced as an AED. The patient was also intermittently administered aceclofenac for pain relief. Laboratory tests revealed moderate eosinophilia and mild elevation of hepatic enzymes (WBC-Hb-Plt 14.47×109/L−12.8 g/dL−419×109/L, neutrophil 77%, lymphocyte 8%, monocyte 5%, eosinophil 7%, basophil 2%, and AST/ALT/ALP 38/62/484 U/L). Renal function was within the normal range (BUN/Cr 20/0.37 mg/dL). Excision skin biopsy (from the leg) confirmed EM. The patient was diagnosed with SJS with mucosal involvement of the eye and oral cavity. While PHT was suspected to be the culprit drug, meropenem could not be excluded as the possible culprit drug. Thus, PHT and meropenem were changed to ceftriaxone and levetiracetam. Tramadol was used to treat pain instead of non-steroidal anti-inflammatory drugs. Cyclosporine (125 mg, twice daily), desonide (500 ug/g), and fluorometholone eye drops were prescribed. After two weeks' treatment, symptoms and laboratory abnormalities improved, and cyclosporine was stopped. The patient recovered without complication.


A 47-year old female presented to the emergency department (ED) with erythematous patches across her whole body. Symptom onset was one week prior to presentation. Oral mucosal erosion and conjunctiva injection were observed. The patient had taken CBZ 200 mg and acetaminophen (unknown dose) for carpal tunnel syndrome for two weeks prior to symptom onset and stopped taking the drugs one week ago. On the day of presentation, routine hematological test (CBC), liver function, renal function, and radiology exam (simple chest X-ray) were normal, and ECG showed normal sinus rhythm. Excision skin biopsy (from the leg) confirmed EM. The patient was diagnosed with SJS with mucosal involvement of the eye and oral cavity, and CBZ was suspected to be the culprit drug. Oral methylprednisolone (12 mg, twice a day), and desonide (500 ug/g) were prescribed. Oral antihistamine was prescribed for itching, and fluorometholone eye drops were also prescribed. Oral corticosteroids were tapered off after two weeks. The patient recovered without complications.


A 40-year old male presented to the ED with erythematous patches across his whole body. Symptom onset was four days prior to presentation. Oral mucosal erosion was observed. The patient took VPA 500 mg due to seizures following traffic accident induced brain trauma, but the dosage and duration of taking the VPA were not accurate. Eight months prior to the current presentation, levetiracetam was prescribed at our hospital, before the patient was transferred to another hospital for supportive care. The time of change from levetiracetam to VPA could not be verified. The prescription medication record confirmed that VPA was administered at least two weeks before symptom onset. On the day of presentation, laboratory tests showed leukopenia, thrombocytopenia, and elevation of total bilirubin and hepatic enzymes (WBC-Hb-Plt 3.02×109/L−15.5 g/dL−96×109/L, neutrophil 62.2%, lymphocyte 20.9%, monocyte 16.6%, eosinophil 0.0%, basophil 0.3%, total protein/albumin 4.7/2.6 g/dL, AST/ALT/ALP 211/438/662 U/L, total bilirubin 11.1 mg/dL, glucose 179 mg/mL, and BUN/Cr 10/0.44 mg/dL). Simple chest X-ray showed subsegmental atelectasis in the right lower lung field; abdominal CT showed fatty liver without other hepatic abnormality, and ECG showed sinus tachycardia. The patient was diagnosed with SJS with mucosal involvement of the oral cavity and VPA was suspected to be the culprit drug. Intravenous methylprednisolone (60 mg/day), and desonide (500 ug/g) were prescribed. Oral antihistamine was prescribed for itching. Corticosteroids were tapered off after two weeks. There was no further elevation of hepatic enzymes and total bilirubin.


A 66-year old male presented to the OPD with fever due to infection, complaining of a “cold sensation” and purpura on the lower extremities. For the past year, the patent had been taking aspirin (100 mg), clopidogrel (75 mg/day), valsartan (80 mg/day), pravastatin (20 mg/day), nicorandil (5 mg/day), and trimetazidine (20 mg/day) for unstable angina. Three weeks prior to symptom onset, the patient began taking CBZ (200 mg) and thioctacid (200 mg) for tingling sensation in his hands. On the day of presentation, laboratory tests showed neutropenia, eosinophilia, and elevation of hepatic enzymes (WBC-Hb-Plt 2.37×109/L−12.3 g/dL−198×109/L, neutrophil 14%, lymphocyte 36%, monocyte 14%, eosinophil 35%, basophil 0%, total protein/albumin 7.5/4.2 g/dL, AST/ALT/ALP 67/76/332 U/L, total bilirubin 0.7 mg/dL, glucose 128 mg/mL, and BUN/Cr 12/0.9 mg/dL). HBsAg and HCV antibodies were negative. CMV IgG antibody was positive but IgM antibody was negative. Titers of EBV VCA IgM/VCA IgG/EA IgG/EBNA IgG were 0.33/1.07/0.29/2.40 IU/mL. Peripheral blood cultures (two pairs of aerobe and non-aerobe bottles) were negative for bacterial growth. Bone marrow examination showed normocellular marrow with eosinophilic hyperplasia. Excision skin biopsy (from the leg) revealed spongiosis, extravasated red blood cells, and superficial perivascular lymphoplasmacytic infiltration. The patient was hospitalized. Lung infiltration was detected on the day of hospitalization. High-resolution chest CT showed ground-glass opacity in the right upper lobe, bilateral pleural effusion, and enlarged lymph nodes at the neck, mediastinum, and both axillae. The patient was diagnosed with CBZ-induced DRESS syndrome, but not an infection. Intravenous methylprednisolone, 60 mg/day, was started. Fever and eosinophilia did not improve over the following week. The dose of methylprednisolone was increased to 120 mg/day. Then the symptoms and abnormal laboratory findings were gradually resolved. The patient experienced flareup twice during management. Corticosteroids were slowly tapered off over nine months.


A 77-year-old white Spanish woman referred to our outpatient clinic with hypertension and albuminuria with a normal glomerular filtration rate (GFR). In addition, she had a history of PXE since 1997, progressive visual deficiency, chronic left lower extremity oedema and an ischaemic stroke 4 years previously. She had primary hyperparathyroidism as a recent diagnostic. None of the patient’s first-degree relatives had a history of PXE.
The physical examination showed a weight of 61 kg; a height of 1.71 m; BMI of 20.8 kg/m2; blood pressure at 160/90 mmHg. Multiple, discrete, symmetrical, small yellow plaques as leathery skin were present bilaterally in the axillae, inguinal region and the neck. Angioid streaks were seen in the fundus. Asymmetric left lower extremity oedema was observed.
Laboratory findings were significant for an elevated parathyroid hormone level (170 pg/ml, reference range: 10–65 pg/ml); low serum phosphorus (2.3 mg/dl, reference range: 2.7–4.5 mg/dl); hypercalcaemia (11.6 mg/dl, reference range: 8.5–10.5 mg/dl) with a calcium-phosphorous product of 26.6 mg/dl; calciuria 376 mg/24h and albuminuria 132 mg/g. The remainder of the blood test results were normal (Hb 13.7 g/dl; Hto 43%; fasting glucose 99 mg/dl; uric acid 4.0 mg/dl; total cholesterol 200 mg/dl; TG 100 mg/dl; creatinine 0.6 mg/dl; eGFR <90 ml/min; K 4.7 meq/l; Na 131 meq/l; Cl 107 meq/l; calcitriol 46 pg/ml.
Imaging tests showed kidney ultrasound imaging with a slight increase in the echogenicity of the renal parenchyma () and normal BMD ().
The patient was taking: losartan 50 mg BID, acetylsalicylic acid 100 mg OD, simvastatin 20 mg OD, omeprazole 20 mg OD, pregabalin 25 mg OD.


The present case report is about a 61-year-old male patient who presented with a growth on the palate, which was present since many years. It was slowly growing and intermittent in nature. Intra-oral physical examination revealed a non-tender, non-mobile, oval, nodular mass on the middle of the palate. The lesion measuring about 2 × 1.5 × 1.5 cm, was well circumscribed and pedunculated []. The lesion had a smooth intact surface and was firm to hard in consistency. No cervical lymph nodes were palpable. Medical history was unremarkable and hematologic as well as biochemical parameters were within the normal limits. Family history and personal history were not contributory.
Based on the above findings the lesion was provisionally diagnosed as fibroma and differential diagnosis of peripheral osteoma, fibrosed pyogenic granuloma, BPNST was given. The lesion was excised with the patient consent under local anesthesia and was fixed in 10% neutral buffered formalin. Grossly, the dome shaped specimen appeared tan and cut surface has yellowish hue [].
Microscopically, the lesion was well-circumscribed and revealed lobules of adipose tissue and calcified structures separated from the surface epithelium by fibro-cellular connective tissue stroma [Figures and ]. Mass of moderately cellular spindle cells, bound on the deeper aspect by fibrous tissue were evident []. Histopathologically, these calcified structures revealed the presence of mature bone with entrapped osteocytes in lacunae. Abundant myxoid tissue with a small collection of lipid laden macrophages were also seen []. Immunohistochemical analysis revealed S-100 and GFAP positivity of the spindle cells while actin was positive around the blood vessels but negative for spindle cells [Figures –]. The lesional tissue was also negative for desmin, CD-57, human melanoma black-45. Mitotic figures and necrosis were not present. Based on the histopathological and immunohistochemical findings final diagnosis of collision tumor of BPNST with osteoma was made. Treatment involved surgical excision of the lesion [Figures and ]. Patient was followed up for 2 years and showed no signs of recurrence.


The present case report is about a 19-year-old Indian male patient reported with chief complaint of disliking his maxillary anterior removable appliance. He requested a fixed prosthesis, preferably an implant-supported one. The medical/social and family history was noncontributory. Patient gave history of trauma and exfoliation associated with tooth no. 11 5 years back []. Extra- and intraoral examinations were within normal limits and his dentition was in a good state of repair.
The clinical examination of alveolar ridge and soft tissue revealed thick gingival bio-type. There was a buccal defect on alveolar ridge in relation tooth no. 11 due to trauma and probably by pressure exerted from the removable appliance []. Furthermore, slight mesial drifting of tooth no. 21 was noted.


The patient is a 68-year-old gentleman who was diagnosed in April 2011 with a high-grade lymphoma. In the month prior to diagnosis, he experienced 13 kg of weight loss; after diagnosis, he developed a severe depression with extreme loss of appetite and proceeded to lose a further 23 kg over the following four months (body mass index reduced to 14.5). He was treated with chemotherapy between April and August 2011 and showed a good partial response to treatment. In August, three weeks after his last chemotherapy, he was admitted with a three-day history of confusion. He was found to be severely hypoglycaemic (1.9 mmol/L) and was treated with infusions of 50 ml 10% glucose until normoglycaemic. There was no history of alcohol use and his blood results did not suggest chronic alcoholism. A septic screen showed a slight leucocytosis (11.9 × 109/L) with neutrophilia (10.9 × 109/L), but chest X-ray, mid-stream urine, blood cultures and stool cultures were all normal. A head computed tomography showed no acute changes and no cerebral lymphoma. Over the next four days, he received repeat intravenous infusions of 5% dextrose without thiamine, nutritional supplements were started and he was also given co-amoxiclav in case of undetected infection. During this time, he showed good improvement, maintaining normoglycaemia whilst his neutrophilia and confusion resolved. However, on day 6 of admission, he deteriorated again with a new onset of confusion, this time accompanied by ataxia, agitation and visual hallucinations. Over the next three days, he became increasingly withdrawn and progressively drowsy, with episodes of hypothermia. This time he remained normogyclaemic and a repeat septic screen was negative. The only blood results of significance were hypomagnesaemia (0.34 mmol/L), but intravenous replacement of magnesium did not improve his condition, and a slightly low folate (3.5 ng/mL) for which folic acid was commenced. At this time, consideration was given to the possibility of Wernicke’s encephalopathy and intravenous thiamine was prescribed, with an initial dose of 500 mg, then 250 mg twice daily for three days. Under dietetic guidance, nasogastric feeding was commenced at a slow initial rate and we prescribed 15 mg mirtazapine for depression. In the days that followed, his confusion improved, but he became apathetic and by day 21, there was evidence of short-term memory loss. Thiamine was re-started (300 mg/day, orally) and by discharge, over three weeks later, confusion, apathy and short-term memory deficits had all resolved. His depression also improved significantly, which we attribute to a combination of mirtazapine, improved nutrition and appropriate social support.


A 52-year-old man was referred to our institution for muscle weakness, joint pain, progressive fatigue and ingravescent dyspnoea. These symptoms had persisted for almost 1 year and the patient was confined to a wheelchair. We observed thoracic scoliosis, waist obesity and bilateral lower limb amyotrophy, as well as electromyographic evidence of chronic partial denervation. Brain magnetic resonance imaging showed multiple hyperintense lesions in the cortical region, cortico–subcortical junction and bilaterally in the semioval centre. Blood tests, including lymphocyte subpopulations and immunoglobulin concentrations, were in the normal range. Antinuclear antibodies, antismooth muscular antibodies and rheumatoid factor were undetectable.
His clinical history showed an acute episode of poliomyelitis. At 5 months of age, he had received the first dose of Salk polio vaccine. The second dose, administered one month later, caused fever, vomiting, diarrhoea and shock. In July 1960, at 12 months of age and a few days after the third dose, the patient showed severe diarrhoeal discharges, neck stiffness and flaccid paralysis of his left lower limb. He was diagnosed with acute poliomyelitis. In June 1961, he experienced paralysis of his right lower limb. He underwent frequent hospitalization and therapeutic rehabilitation treatments.


A 30-year-old female patient presented with the complaint of pain in the lower left jaw since last 4 months. Extra oral examination revealed no facial asymmetry. Intra-oral mild swelling was present extending from lower left lateral incisor to left first molar region. Expansion of buccal cortical plate was evident with crepitus at some area. All laboratory findings were within normal range. Orthopentogram showed a well-defined radiolucency with corticated border in the body of the mandible extending from 32 to 36 regions and extending up to the inferior border of the mandible with impacted canine. Over-retained deciduous canine was present in lower left mandible []. Computed tomography showed an expansile osteolytic lesion with buccal cortical plate perforation [Figures and ]. Provisional diagnosis of lateral dentigerous cyst with impacted canine was suggested with differential diagnosis of KCOT, unicystic ameloblastoma and orthokeratnized OKC. Surgical enucleation of the lesion was done along with surgical removal of the impacted teeth [Figures and ]. Gross examination of the excised specimen revealed a thin cystic sac with luminal surface. The lumen also contained white cheesy material. Microscopic examination [Figures and ] of the specimen revealed an orthokeratinized stratified squamous epithelium of varying thickness lining a thin fibrous wall.


A 12-year-old male patient sustained a closed midshaft both-bone forearm fracture of their non-dominant arm from a fall on a trampoline (Figs and ). Anatomical reduction was achieved with a manipulation under anaesthesia (MUA), but it was noticed that there was a mechanical block to extension of the ring finger. The radius and ulna were therefore approached through separate incisions and it was discovered that the FDP was entrapped at the ulna fracture at the level of the musculotendinous junction. Following release the fingers regained a full range of motion and the patient went on to heal without further complication (Figs and ).


A 46-year-old female patient presented with a history of one month's duration of vertigo, gait, nausea, vomiting and dysphagia, which developed progressively. Head computered tomography scan revealed a low density lesion at the brainstem. She was referred for a brain MRI study with a preliminary diagnosis of brainstem infarction in a local hospital. T2-weight MRI and FLAIR image showed high signal intensity swelling from pons to medulla oblongata (). Low signal intensity and partial enhancement in the same territory were detected on T1-weight and contrast enhanced imagings (). The patient was transfered to our hospital. Neurologic examination revealed attenuation of left-side gag reflex and right-side nasolabial groove. Tongue extension moved to the right and muscular strength of left limbs was IV in this case. Left-side finger-to-nose test was postive. Spinal MRI disclosed abnormal flow void at ventral surface from craniocervical junction to cervical cord, suggesting engorged vessels (). Cerebral angiography performed five days after admission revealed DAVF with a meningeal branch originated from the radicular artery of the right C2 segment of VA as a feeding vessel, draining via abnormally hypertrophic pontomesencephalic veins ascending into basal vein retrogradely and descending into the anterior spinal vein, anterior internal vertebral venous plexus and vertebral artery venous plexus (). Arterial feeder originated from external carotid artery (ECA) was not disclosed from bilateral ECA angiography. A diagnosis of DAVF at the craniocervical junction with venous congestion of brainstem was made.
The patient underwent a transarterial endovascular embolization with Onyx-18 (ev3, Irvine, CA, USA). All procedures were performed under general anesthesia. A six-French sheath was introduced in the right-side femoral artery. Intravenous heparin was given before the guiding catheter was advanced to keep activated clotting time from 200 to 300 seconds. A six-French Envoy guiding catheter (Cordis Endovascular, Miami Lakes, FL, USA) and a Marathon microcatheter (ev3, Irvine, CA, USA) were used. Marathon catheter was advanced to the feeding artery. Onyx-18 was injected using real-time digital subtraction fluoroscopic mapping after the microcatheter lumen was flushed with 0.3 mL dimethyl sulfoxide (DMSO, ev3, Irvine, CA, USA). The injection was terminated when the angiogram confirmed complete obliteration of the fistula (). Low-molecular-weight heparin (LMWH) injection, aspirin and clopidogrel were administrated after endovascular treatment. LMWH 4100 U, twice daily, was administrated for three days. Meanwhile, aspirin (100 mg) and clopidogrel (75 mg), once a day, were administrated for one month. There were not any therapy-related complications. Previous neurological deficits improved gradually after embolization. This patient has been followed-up for six months and recovered completely without any neurological deficits. Cerebral angiography performed at six months after embolization showed complete obliteration of the fistula and disappearance of abnormal venous drainage (). MRI did not demostrate any abnormalities in the brainstem ().


An 8-year-old boy was admitted with a history of abdominal bloating associated with rectal tenesmus and increased flatus. These symptoms recurred especially during the afternoon and evening. No associated gastrointestinal symptoms were reported. His clinical history was characterized by rumination in the first years of life with associated non-organic feeding disorders as a picky eater. Radioallergosorbent test for alimentary and inhalant allergens, skin prick tests and celiac screening was negative. Ultrasonography did not reveal any organomegaly or fluid presence in the abdomen. Abdominal radiographs showed a distended colon with increased gas in the rectum and coprostasis, without signs of obstruction. On physical examination, weight was 22 kg and height 129 cm, with a mild degree of malnutrition according to the Waterloo classification. Cardiorespiratory objectivity was normal. A significantly non-tender, hypertympanitic abdominal distension was present. No hepatomegaly nor splenomegaly were noted. Rectal examination revealed a sensation of hypertonic anus sphincter without perineal erythema and stool. Neurologic examination was normal. The following laboratory investigations were performed: complete blood count (red blood cell count 5.1 × 106/mm3, Hb 13.8 g/dl, HCT 43%, MCV 84 fl, white blood cell count 5 × 103/mm3, neutrophils 34%, lymphocytes 60%, monocytes 4%, eosinophils 2%, basophils 0%, platelets 297 × 103/mm3), C-reactive protein was 0.10 mg/dl (normal 0–0.50 mg/dl), erythrocyte sedimentation rate 5 mm within the first hour, glycemia 68 mg/dl, serum glutamic oxaloacetic transaminase 26 IU/l, serum glutamic pyruvate transaminase 14 IU/l, serum gamma-GT 7 IU/l, amylase 67 U/l, lipase 27 U/l, BUN 26 mg/dl, creatine 0.5 mg/dl, iron 54 μg/dl, sodium 140 mmol/l, potassium 4.3 mmol/l, calcium 9.78 mg/dl, total proteins 7.1 g/dl, and albumin 48 g/l; coagulation parameters and urinalysis were normal. Also, lactate dehydrogenase (395 U/l), muscle enzymes (creatine phosphate kinase 75 IU/l, CK-MB 10 IU/l), thyroid hormones (free thyroxine 10.98 pmol/l, thyroid-stimulating hormone 1.925 μIU/ml), celiac serology, cytomegalovirus, Epstein-Barr virus, herpesvirus serology and autoantibodies (ANA, nDNA, ANCA) were normal, and megacolon was excluded using barium enema. After ruling out primary pathologic causes, a neuropsychiatric consultation was requested with the disclosure of continuous aerophagia and anxiety disorder with obsessive compulsive notes and game-playing dependency. It was possible to reassure the family on the absence of an organic gastrointestinal disease with indications to neuropsychiatric and cognitive follow-up.


A 7-year-old girl, affected by autistic spectrum disorder, was admitted to our hospital for abdominal distension and constipation that had started at 2 years of age. A history of severe abdominal distension and bloating was present chronically, especially in the postprandial period until the evening. The chronic constipation was treated with macrogol. The patient's general condition at admission was good, weight was 23 kg and height 121 cm. Physical examination showed excessive air swallowing associated with visible abdominal distension, in the absence of organomegaly, and significant bloating. No abdominal pain or other gastrointestinal symptoms were present. A routine basic metabolic panel was performed with red blood cell count 4.3 × 106/mm3, Hb 11.8 g/dl, white blood cell count 6.5 × 103/mm3 (neutrophils 44%, lymphocytes 51%, monocytes 3%, eosinophils 2%, basophils 0%), platelets 278 × 103/mm3, C-reactive protein 0.10 mg/dl, erythrocyte sedimentation rate 7 mm within the first hour, lactate dehydrogenase 518 U/l, glycemia 79 mg/dl, serum glutamic oxaloacetic transaminase 34 IU/l, serum glutamic pyruvate transaminase 19 IU/l, serum gamma-GT 8 IU/l, total proteins 6.6 g/dl and serum iron 56 μg/dl; serum electrolytes, celiac serology, coproculture and a parasitologic examination of stools were negative. Abdominal ultrasound showed increased gas in the small and large bowel without signs of obstruction. Abdominal radiography confirmed distension of the large and small bowel and presence of coprostasis. Anorectal manometry showed a normal recto-anal reflex of 30 ml. Neuropsychiatric consultation pointed out a moderate retardation of psychomotor stages and considered aerophagia as a stereotype symptom. A diagnosis of FA was made with indication of a cognitive-behavioral approach and associated therapy with macrogol, simethicone and otilonium bromide.


A 42-year-old man visited our outpatient clinic presenting with both leg weakness. Eight months before the visit, he had been diagnosed with elevated intraocular pressure accompanied by continuous headache and eyeball pain. Despite treatment for the glaucoma, the symptoms persisted and became aggravated. A week before admission, he experienced a seizure attack for several seconds, and a computed tomography scan at another hospital revealed hydrocephalus without intracranial causes. He complained of progressive both leg weakness, and sensory change below the T2 dermatome was found. He was then transferred to our institute. He had no other medical history. He had lost weight of more than 10 kg for the last 7 months. He complained of difficulties in urination and defecation. The neurologic examination showed hypoesthesia below the T2 and hyperactive deep tendon reflexes of the lower extremities.
Spinal magnetic resonance image (MRI) was done with contrast dye enhancement (). An intradural extramedullary (IDEM) mass lesion was found at the T2 level, ventral side to the spinal cord. The mass demonstrated a lower signal intensity than the spinal cord, and well enhancement of gadolinium in the T1-weighted image. The dorsal portion of the dura mater was slightly enhanced. There was no other lesion on the whole spine image. A brain MRI was performed, which showed no definite identifiable lesions.
Surgery was performed with respect to the benign IDEM tumor. A posterior midline approach was performed followed by a T2 laminoplasty. The dura matter was dark gray in color and was opened (), which showed a dark gray-colored mass that was severely adhered to the spinal cord and roots. After dissection, normal spinal cord was identified and the mass was removed as much as possible grossly. The black colored arachnoid membrane was also removed, but total resection was impossible. After decompression of the spinal cord, the dura was closed and sealed. There was no adverse event during the operation.
Histopathologic examination revealed a black or dark gray colored fragile mass in the gross view. Hematoyxlin and eosin stain of the tumor showed melanin pigmentation of tumor cells (). Immunohistochemical stain for human melanoma black revealed positive results for malignant melanoma. The MIB-1 index of 2.6%, atypia, and mitosis (0/10 in high power field) indicated that the melanoma was of intermediate grade.
After surgery, positron emission tomography (PET) was performed for evaluation of the primary lesion but there were no demonstrable metastatic or other primary melanoma lesions beyond the spinal cord. There were no skin lesions on physical examination. During the hospitalization period after surgery, a seizure attack occurred which was a generalized tonic and clonic type. The cause for the seizure was suspected to be hydrocephalus, so a ventriculo-peritoneal (VP) shunt was planned. CSF study was done but no malignant cells were observed. However, the patient refused further treatment and was discharged. He also refused further adjuvant treatment. The patient revisited our hospital and was admitted again 22 months after the initial surgery with progressive both leg we-akness. During the period of follow-up loss, a VP shunt was performed in another hospital but the patient still had not received chemotherapy and radiotherapy for the melanoma. An MRI scan was done which showed that the spinal cord had swelled with dorsal side adhesion to the dorsal surface of the dura mater. The surface of the entire spinal cord was enhanced and this finding was regarded as leptomeningeal dissemination (). Revision surgery for decompression of the spinal cord was performed. There was more aggressive dissemination of the melanoma in the arachnoid and pia mater. There was severe adhesion between the melanin-pigmented tissue and neural tissues. Bleeding continued during removal of the melanoma and it was difficult to control. Total resection of the melanoma was impossible but decompression of the spinal cord was achieved. After the revision surgery, weakness of both legs had slightly improved but the patient refused additional treatment again and was discharged finally.


A 26-year-old woman presented with persistent moderate headache after sudden onset of severe headache and nausea 5 days ago. She had regular menstrual periods since menarche at the age 14. Endocrine evaluation revealed no pituitary hormonal abnormality. The patient showed neither recent vision impairment nor focal neurological symptoms or signs except headache.
Computed tomography (CT) revealed hyperdense shadow on sella turcica in which might suggest hemorrhage within pituitary gland. Magnetic resonance imaging (MRI) demonstrated 19×5×9 mm mass in the postero-inferior sella turcica. This lesion showed high signal on T1-weighted image and low signal on T2-weighted image (T2WI). There was no enhancement of the mass after intravenous gadolinium injection ().
Because of the persistent headache for several days and the suspicion of pituitary hemorrhage, trans-sphenoidal exploration was performed. Cystic mass was identified after opening the dura at the inferior aspect of the sella. Dissection around the cyst revealed a lesion with yellow-gray colored mucoid gelatinous content which looked like a Rathke's cleft cyst within the pituitary gland. There was no macroscopic hemorrhage within the cyst. Normal pituitary gland was well preserved during operation. Microscopic examination showed the cyst wall to consist of well-formed salivary acini with a low-columnar epithelium in a fibrovascular network. The eosinophilic secretions are consistent with the mucinous material found at surgery. There was no evidence of neoplasm. These findings consisted with ectopic salivary gland tissue within pituitary gland ().
Postoperative course was uneventful except transient mild diabetes insipidus for a few weeks. No hormonal deficiency was observed.


This 65-year-old woman had exhibited progressive gait disturbance over a one year period. For 15 years, her son had been in a vegetative state due to head trauma, and she had taken care of him. That had been a source of enormous stress for her. She was diagnosed with depression and had been taking antidepressants for five years. Last year, she felt that her legs dragged and were slow. These symptoms progressed slowly, despite intermittent fluctuation. When she presented in our clinic, she exhibited depressive mood; however, she denied any autonomic symptoms, including postural hypotension, urinary frequency, or constipation.
On neurological examination, she exhibited a mild masked face. Although the speed and amplitude of foot tapping were within normal limits, the amplitude of finger tapping decreased, additionally, speed slowed bilaterally. The motor power of her four extremities showed no weakness and there were no abnormalities on sensory examination. Deep tendon reflex was also normal. During walking, both of her feet dragged and were slowed with a bilateral decrease in arm swing. Sometimes, she hesitated to move exhibiting a glue feature while turning.
The findings of laboratory studies were unremarkable. A magnetic resonance imaging scan of her brain showed no abnormal findings. Interestingly, the patient reported that she could relieve her symptoms at will. When she concentrated hard on her gait or when she touched her hand to the posterior of her neck, her dragged and slow gait improved dramatically. Also, her abnormal gait improved when the examiner touched his hand to her neck (see ). Based on these curious conditions, we gave her placebo injections along with suggestion. However, there was no symptomatic change following this procedure. Subsequently, she was taken for an Fluoropropyl carbomethoxy-3b-(4-iodophenyltropane) ([18F]-FPCIT) positron emission tomography (PET) scan for evaluation of basal ganglia lesions. Results revealed a reduction in putaminal uptake bilaterally as compared to normal controls (). She was then diagnosed with PD, levodopa treatment was initiated. After two months of levodopa treatment, her bradykinesia on both fingers had improved; however, her abnormal gait had not improved markedly. Informed, written consent was obtained after the patient had been given a complete description of the study using a .


A 50-year-old woman was referred to our hospital because of persistent hypercalcemia after surgical removal of a parathyroid carcinoma. The patient had undergone an endoscopic parathyroidectomy using a bilateral axillo-breast approach for a right lower parathyroid adenoma 2 years earlier at a local hospital. The tumor was reported as having no histological features suggestive of malignancy. The serum calcium level was returned to normal after surgery. However, approximately 2 years after surgery, the patient's serum calcium level was found to be elevated again, and an enlargement of the left lower parathyroid gland was detected. The patient underwent conventional parathyroidectomy to remove a left lower parathyroid tumor, with a subsequent histological diagnosis consistent with parathyroid carcinoma. Despite the removal of the left lower parathyroid tumor, her serum calcium levels remained high for 2 months, prompting the referral.
Upon presentation, the patient complained of mild fatigue, anorexia, and constipation. Her family history was unremarkable for cancers or endocrine neoplasias. Physical examination revealed no significant abnormality except her previous surgical neck scar. The patient's weight was 46.1 kg, her height 154 cm, and her body mass index 19.4 kg/m2. On laboratory examination, her serum calcium level was 15.0 mg/dL (ionized calcium, 1.95 mmol/L) and serum phosphorus level 3.6 mg/dL. Serum alkaline phosphatase was elevated at 481 IU/L. Her serum parathyroid hormone (PTH) level was elevated markedly (540.2 pg/mL). Blood urea nitrogen on admission was 26.1 mg/dL with a serum creatinine of 1.7 mg/dL. Urine analysis showed low specific gravity, leukocyturia (24/HPF), and mild erythrocyturia (4 to 5/HPF).
A 99mTc-sestamibi scan was performed and demonstrated focal abnormal uptake in the upper mediastinal area in the 2-hour delayed image (). A subsequent 18F-fluorodeoxyglucose (FDG) positron-emission tomography (PET)/computed tomography (CT) imaging study revealed a mass in the soft tissue at the anterior border of the sternum, with focally increased FDG uptake (maxSUV, 2.6) that correlated with the initial 99mTc-sestamibi scan (). The patient displayed reduced bone mineral density at the lumbar spine (L1-4, 0.889 g/cm2; T-score, -1.9 SD) and at the proximal femur neck (0.695 g/cm2; T-score, -1.7 SD). There were no definite radiographic findings or signs of trabecular bone resorption in the skull or other bones, apart from mild subperiosteal bone resorption in the third metacarpal bone. A whole-body bone scan with 99mTc MDP showed diffuse, subtle uptake in the skull and long bones. An abdominal CT scan showed bilateral medullary nephrocalcinosis. Preoperatively, we marked the outline of the mass on the skin, based on the imaging and manual palpation ().
Based on the preoperative findings, the patient underwent an anterior chest wall mass resection. A frozen section revealed pathological parathyroid tissue, and a wide local resection of the tumor with surrounding structures was performed. A final pathological examination revealed a 2.3-cm parathyroid carcinoma with fibrous bands, numerous mitoses, nuclear pleomorphisms, and foci of capsular invasion (). An intraoperative PTH test showed an 82% decline from the pre-excision level (540.1 pg/mL) to the postexcision level (97.5 pg/mL). The postoperative serum PTH and calcium levels dropped significantly to 57.6 pg/mL and 9.3 mg/dL, respectively. Both levels remained stable and within the normal ranges with temporary oral calcium supplementation. Her hospital course was otherwise uncomplicated, and she was subsequently discharged.
During the patient's outpatient follow-up period, the serum PTH and calcium levels remained near the upper limits of normal. However, approximately 1 year later, her serum PTH level was elevated to 84.1 pg/mL, and a new mass was palpated in the upper portion of her left breast upon physical examination. A 99mTc-sestamibi scan and 18F-FDG PET/CT imaging were performed, revealing an abnormal lesion in the upper area of her left breast (). Subsequently, tumor resection was performed, and the pathological report demonstrated parathyroid carcinoma metastasis. Her postoperative serum PTH and calcium levels dropped significantly to 38.9 pg/mL and 9.5 mg/dL, respectively. We are currently watching her cautiously, conducting serial blood examinations and, more specifically, serum PTH and calcium measurements.


This is a case report of a 51-year-old white male patient who had a history of severe
alcoholism with a high daily consumption of alcohol over 30 years. His family reported
that he consumed rum, cognac and wines. He refused to treat his addiction. One year
prior to presentation, his family observed a decrease in his short-term memory, and he
complained of paresthesias of the lower and upper limbs. After an ingestion of large
amounts of alcohol, excessive drowsiness quickly evolved into torpor and then a coma. He
was taken to the Hospital Universitário of Universidade Estadual do Oeste do Paraná
(Unioeste). On admission, his Glasgow coma score was 7, and he showed no signs of
meningeal irritation, focal deficits or cranial nerve abnormalities. IV thiamine (500
mg/day) and high doses of parenteral B vitamins were administered.
Cranial computerized tomography scan (CT) revealed a hypodensity in the corpus callosum,
which was better characterized by MRI. MRI showed involvement of the cortical regions
and subcortical white matter of both frontal lobes as well as small areas of the
post-central and superior temporal gyri with no signs of disruption of the blood-brain
barrier (, and ). A mild improvement in his
level of consciousness was observed (Glasgow = 10) with mechanical ventilatory support,
but the patient developed multiple pulmonary infectious complications and remained in
the intensive care unit (ICU) with respiratory insufficiency dependent on mechanical
ventilation. He received a tracheostomy. After more than 10 weeks in the ICU, he became
septic, exhibiting a fever along with worsening of his respiratory status. Over the
course of 24 hours, his hemodynamic condition deteriorated, and both vasoactive drugs
and broad-spectrum IV antibiotics were started without success. Cultures of blood and
tracheal secretions revealed an uncommon fungus (Rhodotorula
mucilaginosa). Amphotericin B treatment was begun, but there was no
significant response, and he eventually succumbed to septic shock.


A 56-year-old man with hypertension, dyslipidemia and obesity presented with right hemiplegia, receptive dysphasia and confusion. Investigations demonstrated a left parietotemporal hemorrhage and a Cognard IV dAVF. Embolization was completed from the left middle meningeal artery (MMA) with no complications. After the procedure the patient recovered from his hemiplegia and confusion but dysphasia persisted and he was therefore discharged to a rehabilitation unit.


A 62-year-old man with hypertension and hypercholesterolemia was admitted for embolization of an incidentally discovered dAVF in 2006 but the patient was lost to follow-up. He was reinvestigated upon development of headaches after cardiac surgery 3 months previously which revealed a Cognard III fistula. During the procedure an attempt was made to wedge a Marathon microcatheter (ev3 Neurovascular) within the smaller accessory meningeal artery, but intractable arterial reflux occurred and hence the larger MMA was catheterized using the balloon catheter. Embolization was completed uneventfully and the patient was discharged the following day.


A 62-year-old woman presented with pulsatile tinnitus and was found to have a Cognard IIa+b dAVF. Onyx was injected from the right MMA with the venous balloon in the right transverse/sigmoid sinus and a diagnostic catheter was inserted in the left common carotid artery for angiography. The rationale for using venous protection in this case was the presence of an otherwise normal transverse sinus which did not require sacrifice per se, and the questionable presence of an antegradely draining vein of Labbé into the milieu of the fistulous network. During one of the arterial balloon re-inflations the balloon inflated beyond the margins of the MMA consistent with vessel rupture (). The embolization was completed with both balloons inflated and Onyx was injected via the balloon catheter as it was deflated and withdrawn. Successive angiography via the guide catheter as this was performed demonstrated immediate cessation of extravasation from the MMA. On-table flat panel CT was performed after withdrawal of the arterial balloon catheter, showing no evidence of an extradural hematoma. After the procedure the patient was asymptomatic and she was discharged the following day.


A 47-year-old male ex-smoker presented with acute onset of left-sided weakness and numbness and a history of two similar but self-limiting episodes. Investigations demonstrated a Cognard IV dAVF with no hemorrhage. In this case it was considered desirable to preserve the superior sagittal sinus (SSS) if possible in order to restore a more functionally normal pattern of cerebral venous drainage. A strategy deploying a venous side balloon was therefore employed. Successful embolization was performed from the left MMA with the venous balloon in the SSS. The SSS was preserved and reverted to normal cortical drainage at the end of the procedure. The patient made a gradual recovery and was discharged home 5 days after the procedure.


A 69-year-old man presented with a sudden onset severe headache and right homonymous hemianopia. Investigations revealed a left occipital hemorrhage and Cognard IV dAVF (). A venous balloon was placed in the SSS and successful embolization was completed sequentially from the right MMA and then the left MMA during the same procedure (). The SSS was preserved () and the patient was discharged the following day.


A 61-year-old man with hypertension presented with left hemiparesis and was found to have a Cognard III dAVF on angiography. This was successfully embolized from the anterior division of the right MMA with a venous balloon in the SSS. The procedure was uncomplicated and the patient was discharged home 2 days after the procedure.


A 45-year-old man was admitted to a hospital in central Italy in August 2000 for right pleural effusion. Three-months later, a diagnosis of malignant mesothelioma, epithelial type, was made on the basis of multiple pleural biopsies obtained at right thoracotomy. Hyaline pleural plaques were also visible. Partial right pleurectomy was performed on December 2000. In the following years, the patient was treated by chemotherapy. In May 2003, a progression of the disease was documented. Involvement of spinal cord and large subcutaneous neoplastic infiltration coexisted. The patient died in June 2003.
In the period 1974-1981, the patient had intermittently worked as an insulator at a sodium carbonate factory for a total of about 3 years. Moreover, in the period 1977-1986, he was intermittently employed in various sugar refineries for a total of nearly 3 years.


A 56-year-old man, the brother of the Case 1, was admitted to a hospital in northern Italy in March 2006. A thoracic computed tomography (CT) showed two nodules adjacent to pleura in the right lung. One year previously the patient had been treated with oral anticoagulants for pulmonary thromboembolism. At the right videothoracoscopy, multiple neoplastic pleural nodules were visible, associated with hyaline pleural plaques. At the histological examination, malignant mesothelioma, epithelial type, was diagnosed. Despite chemotherapy with cysplatin and alimta, thoracic CT showed severe progression of the neoplasia. In March 2007, the patient was treated with mediastinal radiotherapy for a mediastinal syndrome. He died in April 2007.
The patient had worked as an insulator for some 20 years (1967-1986). His work took place in thermoelectric plants and chemical industries in Italy as well as in foreign countries (Algeria, Libya, Saudi Arabia).
The two patients were born in central Italy. Their parents came from a town of Sicily; some degree of blood relationship existed between the parents, they being second cousins.


A 22-year-old nulliparous, woman from Mongolia visited a department of obstetrics and gynecology complaining of lower abdominal pain that had developed about 1 week previously. She had undergone a pelviscopic myomectomy for uterine myomas 2 years before this visit. On transvaginal ultrasonography, an 8cm sized uterine solid mass and other pelvic masses were found, but both ovaries seemed intact. Computed tomography (CT) scanning showed similar findings to the ultrasonography. With the diagnosis of a gynecologic malignancy, she was referred to our hospital.
At initial workup in our hospital, moderate anemia was found: the patient's hemoglobin concentration was 8.7 mg/dL and the hematocrit 28.8%. The tumor marker CA-125 level was elevated (226 U/mL). Re-evaluation of the CT scan showed multiple solid enhancing masses in the uterus, peritoneal cavity, and retroperitoneal cavity with moderate amount of ascites. No lymph node was significantly enlarged (). Intravenous leiomyomatosis with pseudo-Meig syndrome was suspected, but the possibility of a uterine sarcoma could not be excluded.
After treating the patient's anemia with a blood transfusion, explorative laparotomy was carried out. Multiple solid masses were found in the omentum, the mesocolon, the abdominal peritoneum, the right ovary, and as well as in the uterus. Some biopsies of the omental and uterine masses were sent for frozen sectioning. The histopathology diagnosis was of a malignant tumor such as an endometrial stromal sarcoma or a leiomyosarcoma. Then, we performed total abdominal hysterectomy, right salpingo-oophorectomy, left salpingectomy, omentectomy, appendectomy, colon mesentery, and peritoneal mass removal. Moderate amounts of ascites were also aspirated. Because the patient was young, and she and her husband strongly wanted to save her ovary, we preserved the left ovary after explaining the risk of this procedure given her medical condition.
Unlike the presumptive clinical impression or the frozen-section biopsy result, the final histopathology finding with immunochemistry was of a malignant melanoma. The mitotic count was 11 per 10 high power fields and tumor cell necrosis was seen. The tumor was immunopositive for S-100, and HMB-45, and focally positive for cyclin D1, but negative for CD10, smooth muscle actin, and desmin (). The tumor had infiltrated the uterus, right adnexa, omentum, colon mesentery, appendix, and peritoneal mass, but not he uterine cervix or vagina. Ascitic fluid histopathology results the were negative.
After postoperative care, the patent was transferred to the department of hemato-oncology for further evaluation and chemotherapy. Whole body 2-[fluorine-18]-fluoro-2-deoxy-D-glucose positive emission tomography-CT and brain magnetic resonance imaging scans were performed with the aim of determining the primary tumor site, but no abnormal enhancing lesion was found. Except for a small nevus-like lesion in her right lower extremity, there was no pigmented skin lesion including the vulvar area. Because the couple wanted to return to Mongolia, a skin biopsy was not performed, and she was discharged from our hospital.


A 9-month-old boy with right parietal bulging presented to the emergency department. Before neurosurgery consultation, the emergency physician suggested a leptomeningeal cyst due to head trauma. However, the boy had no previous definitive head trauma history but had an accompanying increased head circumference (47 cm, 90th percentile), motor delay within 1.5 months and rapid onset of epileptic seizures 2 weeks previously. Cranial computerized tomography (CT) scans showed a cranial bony defect in his right parietal bone []. Magnetic resonance imaging (MRI) showed that the tumor was characterized by a cystic mass with a central homogeneous solid component enhancing with gadolinium attached to the dura, leading to a large effect on the ventricles in the temporoparietal region []. Antiepileptic treatment was commenced for seizure prevention.
A frontotemporal craniotomy was performed. A mass was observed to be attached to the dura. The solid component of the tumor was solid, vascularized and barely distinguished from normal glial tissue. The cystic part of the tumor was aspirated. The postoperative period was uneventful. Total removal of the tumor was documented on a control MRI. Because there was subdural hygroma formation squeezing the brain tissue on CT scan on the third day of the postoperative period, a subdural-peritoneal shunt was inserted. His 6-month follow-up revealed no identifiable pathology.
The histological examination revealed a mixed glial-neuronal tumor presenting with a nodular pattern involving the cerebral cortex and subcortex. Astrocyte-like cells had large, round and vesicular nuclei with surrounding large amphiphilic cytoplasm. Neuronal cells had vesicular chromatin and polygonal nuclei with large perikarya. A few multinucleate cells were observed. The cells were surrounded by diffuse reticulin and collagen fibers. There was only atypia, with no mitotic figures, necrosis or vesicular euchromatic nuclei (VEP). Vasogenic edema was present around the neural tissue, with non-gemistocytic gliosis. The conventional histochemical stains Massontrichome (MTC) and Gomori’sreticulin stain were used to stain interstitial collagen fibers and reticulin fibers, respectively []. Tumor cells were immunohistochemically stained for glial fibrillary acidic protein (GFAP) [], synaptophysin [Figures and ], chromogranin, S-100 and epithelial membrane antigen (EMA), and they were negative for CD34, NFP and progesterone. Nearly 2% of tumor cells were labeled with Ki-67/MIB-1 [], and approximately 1/3-2/3 of cells showed moderate nuclear staining for p53. The diagnosis was desmoplastic infantile ganglioglioma grade I (WHO, 2007).


A 29-year-old man presented with eight-year history of vague pain in the right knee that aggravated when squatting. He was a sedentary worker. He stated that there had been no prior trauma to the knee. There was no catching, swelling or sense of giving way. On physical examination, there were negative findings on the Lachman and pivot-shift tests and no swelling or tenderness along the joint line. The range of motion was full, with no loss of extension, but painful in extreme range of flexion. Patellar movements were normal and negative on patellar compression test. The findings on radiographs of the knee were interpreted as normal. Magnetic resonance imaging revealed that meniscus and posterior cruciate ligament were normal. Coronal and sagittal T1-weighted images demonstrated that the soft tissue mass was isointense to muscle and obscured the ACL. T2-weighted sagittal magnetic resonance images showed heterogenous, intermediate to low signal intensity, which was slightly higher than that of skeletal muscle (). There were no palpable mass-like lesions on his whole body and no family history of hyperlipidemia or xanthomatosis. Laboratory examinations, including platelet count, prothrombin time, bleeding time and total cholesterol, were all within normal limits. Other blood parameters showed normal range. Arthroscopic examination showed normal findings of both meniscus, posterior cruciate ligament and articular cartilage.
The ACL appeared to be diffusely bulging, but maintained normal tension. Posteromedial and posterolateral portals were made to visualize the mass more clearly. We were able to access the lesions by switching the posterolateral and posteromedial portal alternatively. The mass was located behind the ACL, close to the femoral attachment site. It was round in shape, measuring about 20 mm × 11 mm in diameter with a reddish-brown color (). It was excised using a motorized instrument and basket forceps by piecemeal (). A repeat performance of the Lachman test and pivot-shift test showed a stable knee.
Microscopic features varied on different parts of the tumor. The basic cellular composition of the tumor was well-defined polygonal mononuclear cells with a scanty, faintly eosinophilic cytoplasm. In some areas, there were bands or sheets of amorphous collagen (). Foci of xanthoma cells with foamy cytoplasm and vacuoles were present, accompanied by branching capillaries. Multinucleated giant cells had abundant eosinophilic cytoplasm and contained eight or more nuclei (). The patient had no further complaints following the operation, and there was no recurrence on 55-months of follow-up.


A 45-year-old woman was admitted to our university hospital for polymenorrhea, weight gain and pain in the left iliac region. Before admission, a Pap smear and a diagnostic hysteroscopy were carried out; the former tested negative, while the latter showed simple endometrial hyperplasia. During the physical examination, the patient was in a good condition and without weight loss. An abdominal examination revealed a flat and painless abdomen, and no palpable mass was found. During the gynecological visit, the uterus was larger in size, while the right ovary and fallopian tube were within expected limits. On the left side, an orange-shaped mass was observed; it had irregular layers, was fixed and painless. An abdominal ultrasound revealed a hypoechoic, inhomogeneous, 9.5 × 5.2-cm mass on the left side of the pelvis and behind the ovary. Computed tomography (CT) was not performed due to the patient's allergy to the contact medium. An atypical ultrasound appearance addressed the probable malignancy of the mass.
The patient underwent surgery. After opening the abdominal cavity, a free-fluid sample was taken, and the cytological result tested positive for malignant cells. The pelvic mass was firmly anchored to the small intestine, colon, sigma and uterine body (fig. ). After removing the adhesions, double ureters were observed, which had been incorporated in the mass. The resection of the unilateral double ureters was necessary in order to remove the entire mass, after which the left ovary and tube were removed.
A histological examination showed a malignant retroperitoneal mass with clear nuclear polymorphism, whereas the right ovary and tube were unaffected. Anti-reflux termino-terminal ureteral anastomosis with two double-J stents was carried out (fig. ). Total hysterectomy with preservation of the right adenexum and regional lymphadenectomy was performed. The postoperative recovery was uneventful, and after 7 days, the patient was discharged. The final histological results led to the diagnosis of a moderately differentiated retroperitoneal leiomyosarcoma. Radiotherapy completed the therapeutic management. After 1 year, the patient is healthy, and instrumental investigations are negative for recurrence.


A 31-year-old woman presented with a 5-year history of a slowly enlarging left mid-cheek mass in the pre-parotid region. Upon examination, a mobile non-tender and smooth-surfaced mass measuring 20 mm in the greatest dimension was noted in the left pre-parotid region. Her facial nerve function was intact. The serum amylase level was within the normal range. An unenhanced CT of the neck confirmed a well-circumscribed and homogenous mass measuring 18 × 10 mm and located anterior to the left main parotid gland and on the surface of the masseter muscle. This lobulated mass demonstrated isointensity and hyperintensity relative to the muscle on T1- and T2-weighted MRI images (WIs), respectively, and homogeneous enhancement on contrast-enhanced T1-WIs (fig. ). A time-signal intensity curve (TIC) generated from a dynamic MRI study revealed a gradual enhancement pattern (fig. ). On T2-WIs, the mass periphery was surrounded by hypointensity that was suggestive of a fibrous capsule. The tumor was most likely considered a pleomorphic adenoma (PA), given the clinical presentation and MRI findings. No remarkable cervical lymphadenopathy was detected. The patient refused fine-needle aspiration cytology (FNAC). The mass was resected under general anesthesia via a standard parotidectomy incision. The mass and the surrounding salivary tissue were completely separated from the main parotid gland and connected to the parotid duct via a ductule. Myoepithelioma was suspected during an intraoperative pathological examination of a frozen specimen. All facial nerve branches and the parotid duct were successfully preserved, and postoperative complications such as facial paralysis and salivary fistula were not observed. Grossly, the tumor was well encapsulated, solid, and lobular (fig. ), with a yellowish-white cut surface. Microscopically, the tumor primarily comprised cells with round nuclei and a few cells with oval and slightly spindle-shaped nuclei. The neoplastic cells were arranged in an epithelial and mostly lattice-like structure with hyalinous and mucinous stroma. Neither cartilaginous myxoid stroma nor a glandular structure was observed (fig. ). Immunohistochemical staining indicated a positivity for calponin (fig. ), CAM5.2 (cytokeratin stain), S-100 protein, smooth muscle actin (SMA), cytokeratin14, and AE1/AE3 (pan-keratin stain), as well as negativity for carcinoembryonic antigen. Based on these results, the final histopathological diagnosis of the tumor was epithelioid myoepithelioma. There have been no signs of recurrence at 3.5 years after surgery.


A 64-year-old man presented with recurrent attacks of vertigo, one of which was provoked by head movement one day prior to presentation. The patient had a history of left vestibular neuritis 2 years prior. A caloric test was performed at that time, and the results showed a 64% left vestibular function deficit. There were no abnormal findings on the brain magnetic resonance imaging (MRI).
A caloric test was performed on the current presentation, and the results showed a 53% left vestibular function deficit. A physical examination was also performed, and spontaneous nystagmus was not observed with the patient in the sitting position. A Dix-Hallpike test revealed bilateral geotropic horizontal nystagmus, in which the nystagmus was direction-changing nystagmus depending on the head position and was more pronounced on the right. Subjective dizziness was also more severe on the right. However, a head roll test did not induce any nystagmus on either side (). A diagnosis of right horizontal canal BPPV (HC-BPPV) was made, and the patient was treated with the Lempert maneuver.
The next day, the patient still complained of dizziness, but the character of the dizziness was different. On video nystagmography, left-beating horizontal spontaneous nystagmus was observed with the patient in the sitting position (). The Dix-Hallpike test and the head roll test showed persistent left-beating nystagmus in either side (). Based on these findings, we diagnosed a canalith jam in the right horizontal semicircular canal that developed after the canalith repositioning maneuver in the setting of HC-BPPV. We instructed the patient to perform frequent head shaking and had him maintain a left decubitus position. After one day, the nystagmus was not observed on portable video nystagmography in any position and subjective dizziness was completely disappeared.


A 16 year old male patient presented with complaints of pain and clicking sounds in the right knee for the last 6-month. There was no history of trauma, fever or any previous surgery of the knee. There was no effusion or laxity of the joint. A click was felt at the terminal flexion of the knee. The range of motion was from 0° to 130° with painful terminal restriction of flexion. The differential diagnosis considered were meniscal tear, discoid meniscus, anterior cruciate ligament (ACL) ganglion cyst, and myxoid degeneration of ACL. Anteroposterior radiographs were normal []. The lateral radiograph of the right knee showed a radio opaque shadow at the posterior aspect of the distal end of femur []. Axial and sagittal T2 weighted MR images showed a lobulated heterogeneously hyper intense lesion arising from medial aspect of the lateral femoral condyle []. Medullary cavity of the lateral femoral condyle is continuous with the of the lesion []. Arthroscopy revealed a swelling in the intercondylar notch of the femur occupying most of the space in the flexed knee. On probing it was hard and attached to the roof and lateral wall of the intercondylar notch []. It was displacing the ACL anteriorly []. There was evidence of synovitis in the posterior aspect of the joint. Posterior cruciate ligament and menisci were normal in appearance. The lesion was excised with the help of a curved osteotome and removed with grasper []. The base was abraded with a motorized shaver. Excised tumor was sent for histologic examination which revealed cancellous bone covered with cartilage and was diagnosed as an osteochondroma []. Postoperatively, quadriceps and range of motion exercises were started and the patient was mobilized full weight bearing. At 1-year followup, clicking sounds had disappeared completely, range of motion improved to 0° to 140° and the knee was painless.


A 59-year-old female presented at the prosthodontic department as an emergency. Patient reported looseness of the maxillary implant-retained tissue-supported overdenture (IOD) from four weeks and increased mobility specifically on chewing at the left side from last 72 hours. The removable maxillary prosthesis and the bar retainer have been in function from the last 50 months; during this period, the patient was seen for review of prosthesis retainer at 1, 6, 12, and 18 months postoperative. During the service of prosthesis, patient has had complains of repeated screw loosening and soft tissue inflammation and growth around the distal left maxillary implant.
The patient was wearing a loose implant-retained maxillary overdenture on a gold bar retainer splinting four implants, the bar retainer had no cantilever extensions. The implants (Straumann®, 4.1Ø, RN Standard) were positioned at tooth number 15, 13, 21, 24 in the maxilla and connected by three gold U-shaped Dolder bars (H 3.0 mm, regular, Elitor® Straumann®) soldered to gold copings, made to fit passively. The framework-reinforced overdenture prosthesis incorporated three corresponding riders/clips (Straumann®, Dolder matrix, regular) acting as matrices on the intaglio surface providing attachments to the bar retainer []. It was clear that the gold bar fractured mesial to the gold coping at implant 24 but was not displaced []. The maxillary implant overdenture prosthesis was found to be satisfactory with regards to fit, occlusion, aesthetics, and phonetics, however, was unstable due to the fracture in the supporting gold bar. The treatment plan suggested to the patient included the fabrication of a new bar retainer and maxillary IOD prosthesis. However, due to the patient's time restraint and after discussion of benefits and risks, an informed consent was developed and the decision was taken to retain the prosthesis and repair the gold bar using gold solder.


A 45-year-old white female presented with a 1year history of papular lesions,
ulcerations, and scarring on the abdomen, back, and limbs. Six months after symptom
onset, she developed nausea, vomiting, and weight loss of 15 kg. The patient
reported she had been admitted to hospital for abdominal pain and ascites at some
time during the last 3 months. During this hospitalization, exploratory laparotomy
and peritoneal biopsy were performed, with noncontributory findings.
Physical examination revealed scarring and ulcerations on the chest, back, and
abdomen, as well as papules with a porcelain-white center, some with an erythematous
halo, on the extremities ( and ).
Laboratory tests, including antinuclear and antiphospholipid antibody titers, were
within normal limits. Histopathological examination of an upper extremity papula
showed thrombosed vascular structures and scant inflammatory cells around the
vessels (). The patient was prescribed
acetylsalicylic acid (300 mg/day), dipyridamole (150 mg/day), and enoxaparin (40
mg/day). Her condition improved during the first week of treatment, but she
developed abdominal pain caused by a bowel perforation, and died of sepsis.


A 55-year-old right handed male with a past medical history of diabetes, hypertension, and a greater than 10 pack-year history of cigarette smoking, presented with headache, nausea, vomiting, and worsening double vision. On physical examination, the patient was alert and oriented. His cranial nerves were intact. He was noted to have facial asymmetry and slight mass over the right forehead. Further on examination it was noted that he had a lesion on his right breast and nipple that he reported had been present for approximately one year, with occasional enlargement, bleeding, and purulent discharge. He had no lymphadenopathy on examination. Noncontrast computed tomography (CT) head indicated a 4.3 × 2.2 × 1.7 cm right frontal calvarial lesion, with internal trabeculated bone mixed with fatty components, and no associated involvement of overlying soft tissue or brain parenchyma []. Magnetic resonance imaging (MRI) of the brain confirmed the presence of a right sided heterogeneously enhancing calvarial lesion with mild mass effect on the adjacent frontal lobe []. A CT of the chest, abdomen, and pelvis showed a soft tissue density in the right retroareolar space, corresponding to the location of the painful breast lesion, and associated with enlarged right hilar and subcarinal lymph nodes.
The patient initially underwent a punch biopsy of the breast lesion and subsequent histopathologic analysis revealed the lesion to be invasive ductal carcinoma. In order to obtain a tissue diagnosis and relieve symptoms caused by the calvarial lesion, the patient underwent a right frontal image-guided craniectomy. A modified bicoronal incision was carried out with exposure of the mass. Using image guidance, a craniectomy was carried out with en-bloc calvarial tumor resection. There was no dural involvement. A titanium mesh cranioplasty was performed. Postoperative imaging showed no residual tumor and the patient was discharged on postoperative day 2 with improvement in his headaches. The patient later underwent a modified radical mastectomy and biopsy of an axillary sentinel node. Pathology and staging demonstrated a T4aN1aM0 Stage IIIB infiltrating ductal carcinoma.
The pathologic calvarial specimen consisted of a 5.5 × 5.5 × 0.8 cm portion of calvarium involved by an expansile lesion measuring 3.5 × 3.5 × 1.5 cm. The lesion was well-circumscribed and showed mixed areas of firm-to-soft tan and red lobulated tissue. Histopathologic analysis performed on the specimen proved the tumor to be an angiolipoma. Microscopically, the lesion consisted of mature trabecular bone intermixed with mature adipocytes and variably sized dilated vascular channels []. The adipose component was mature and composed of normal appearing lobules separated by thin, fibrous septa. No cytologicalatypia, hyperchromasia, mitoses, or lipoblasts were present. No increased cellularity or epithelioid cells were noted, and immunohistochemical stains for pankeratin were negative.


A 28-year-old man who was known to have FHI in the right eye was referred for secondary IOL implantation. Six years before referral, his right eye had undergone cataract surgery which was complicated by the capsular rupture and vitreous prolapse, for which the patient received complete anterior vitrectomy with removal of all capsular remnants. The patient was left aphakic and was prescribed with aphakic contact lens; however, he developed contact lens intolerance over time. On presentation, his uncorrected visual acuity was 20/20 in the left eye and counting finger in the right eye which could be corrected to 20/20 with aphakic correction. Intraocular pressure was normal in both eyes. Slit-lamp examination of the right eye revealed diffuse fine keratic precipitates over the entire corneal endothelium and mild iris stromal atrophy with notable heterochromia. There was aphakia with no capsular remnant. No cell was present in anterior chamber or vitreous. The left eye was normal. Advantages and unknown risks of the surgery were thoroughly explained for the patient and he consented to have secondary IOL implantation. Under general anesthesia, an iris-claw IOL (Artisan, Ophtec, Groningen, The Netherlands) was implanted in right eye through a limbal incision followed by a superior peripheral iridectomy. Enclavation of the IOL haptics was easily performed; no intraoperative complication including hyphema was noted. After surgery, the patient received a topical antibiotic and topical steroid eye drops. The latter was prescribed as 0.1% betamethasone every 2 hours while awake for 1 week and then four times a day which was tapered within 6 weeks. Postoperative follow-up examinations were performed at 1, 2, 3, 5, and 7 days, then weekly for 1 month, monthly for 3 months, and every 2–3 months thereafter until 1 year. Postoperative course was uneventful with no significant anterior chamber inflammation (more than 1+ cellular reaction) or fibrin formation. On the first postoperative day, the examination showed 1+ cellular reaction and pigments in the anterior chamber which disappeared within 2 weeks. No subsequent exacerbation of the intraocular inflammation was observed during 12 months of postoperative follow-up; therefore, no additional course of steroid was required. Occasional cells in the anterior chamber were seen at some visits which were left untreated. There were few visually insignificant deposits on the IOL surface []. One month after surgery, the patient achieved a best-corrected visual acuity of 20/20 in the right eye which was maintained for 12 months of follow-up. The IOL remained stable with no subsequent iris atrophy at the enclavation sites, subluxation, or pupil ovalization. Furthermore, the patient did not develop any anterior or posterior segment complication including glaucoma, vitreous inflammation, or clinical cystoid macular edema.


A 51-year-old male patient applied to our hospital with the complaint of rhinorrhea started three months ago after an upper respiratory infection. There were no any other symptoms present such as headache or fever and also there were no history of trauma or sinus operation. Biochemical analysis of the fluid was positive for beta-2-transferrin. Cranial MRI and CT cisternography images show a fluid collection in the right sphenoid sinus and confirm a lateral sphenoid sinus meningocele []. The patient was operated via endoscopic endonasal transsphenoidal approach. In the surgical procedure, a meningocele sac originating from the lateral wall of the right sphenoid sinus exposed subsequent to removal of the sphenoid sinus floor by the right mononostril approach. A CSF leakage was observed from the meningocele sac []. After resection of the meningocele by bipolar electrocoagulation, remnants of the sac were pushed through the bony defect in the lateral wall of the sphenoid sinus by using 30 degree optic endoscope. For a multilayer complete closure of the bony defect, we used fat and fascia lata grafts respectively, harvested from the right lateral thigh incision []. That followed with the application of fibrin sealent. We did not use a lumbar drainage cathether in this patient.
Postoperatively the patient was conscious, responsive and his general condition was good with normal vital functions. No postoperative complication occured and he was discharged at the fifth day of hospitalization. After six months of postoperative follow-up, there was no reccurrence or complication observed.


A 45-year-old man presented to our outpatient department with painless progressive diminution of vision both eyes for the past 10 days. Medical history included XDR-TB on treatment with linezolid (600 mg/day), ethambutol (800 mg/day), moxifloxacin (400 mg/day), cycloserine (500 mg/day), ethionamide (500 mg/day), and kanamycin (750 mg/day) for the past 6 months. He was a non-smoker and non-alcoholic.
On examination, his visual acuity was 20/200 (OU), not improving with pin hole. Color vision was defective in both eyes. Anterior segment examination was unremarkable and pupils were 3 mm, round, regular, and reacting to light in both eyes (Direct and Indirect). There was no relative afferent pupillary defect (RAPD).
Fundus examination revealed hyperemic disc with blurred margins (OU) [Figs. and ]. Visual field evaluation by Humphrey field analyzer showed peripheral constriction and quadrantanopia in the right eye [] and low reliable fields in the left eye []. Optical coherence tomography (OCT) revealed increased retinal nerve fiber layer (RNFL) thickness in both eyes [].
Ethambutol-induced toxic optic neuropathy was initially suspected and tablet ethambutol was discontinued after discussing with the treating physician. After two weeks, the patient's visual acuity had dropped to 20/400 in both eyes, and the fundus picture remained unchanged. Hence, the possibility of toxic optic neuropathy due to linezolid was considered as reported in the literature and linezolid was discontinued (A total cumulative dose of 126 g had been already consumed by the patient).
Rapid improvement in visual acuity was seen four days after discontinuation of linezolid. Color vision was restored to normal and patient's vision was restored to 20/20 after one month. Fundus examination revealed resolved optic disc edema with setting in of temporal pallor in both eyes [Figs. and ]. Follow-up of visual field showed partial improvement with residual quadrantanopia [Figs. and ] and OCT demonstrated normalization of RNFL []. Tablet ethambutol was restarted at the instance of the physician. The patient is under regular follow-up and no toxic effects have been noted at three months of follow-up.


A 59-year-old Caucasian male presented with asymptomatic black discoloration of his left big toe. At least 5 years earlier, he had originally noted some dark spots on the undersurface of his toe. Recently, in November 2013, he was prompted to seek medical attention since he thought new fainter spots had appeared which looked like a bruise, but were irregular in shape and colored.
As a teenager, he had acne. He had been treated with various topical preparations. In addition, during high school, he received oral tetracycline for at least 3 years.
His past medical history was also remarkable for adenocarcinoma of the prostate, diagnosed at age 51 years. He had mild lower urinary tract symptoms in late 2004; in April 2005 he had an abnormal digital rectal examination of his prostate and his prostate-specific antigen was elevated at 7.1 ng/ml. In May 2005, he underwent a trans-rectal biopsy of his prostate that showed a Gleason score of 4 + 3 with bilateral involvement.
Treatment was initiated with bicalutamide (Casodex®, Astrazeneca, Delaware, USA) 50 mg daily. His prostate-specific antigen dropped to 0.3 ng/ml by July 2005. Seven months later, in December 2005, leuprolide (Lupron Depot®, AbbVie Inc., Chicago, USA) injections, every 3 months, were added.
A magnetic resonance imaging (MRI) study in January 2006 showed extension of the tumor outside the prostate into the seminal vesicles and surrounding tissues (stage T3b radiographically). From March 2006 to May 2006, he was treated with external beam radiation. He continued to receive androgen deprivation therapy for approximately 2 years. The last leuprolide injection was in December 2006 and he stopped using bicalutamide in March 2007. His prostate-specific antigen continues to remain below 0.4 ng/ml.
Examination of the plantar surface of his left big toe showed three areas of black-brown hyperpigmentation (Fig. ). Each patch had fading, irregular-shaped borders. The proximal macule was 15 × 12 mm with a lighter proximal area and a darker distal area; both areas were biopsied and each showed melanoma in situ. In addition, the distal dark macule (5 × 5 mm and closer to the tip of the toe) and the lateral dark macule (6 × 4 mm and near the second toe) were also biopsied; microscopic examination showed melanocytic hyperplasia and atypical intraepidermal melanocytic proliferation, respectively. With regard to management, treatment of the latter diagnosis is similar to that of melanoma in situ.
Complete excision of all three black-brown patches, including an additional 5 mm margin of normal-appearing skin, was performed and the wound was covered with a full-thickness skin graft.


A 47-year-old female patient reported to the department of oral diagnostics with pain in the left lower back region and food lodgedment in the right lower back region of the jaw for 1 year.
The pain was severe throbbing type that aggravated on sleeping and consuming food. It was relieved on taking analgesics. Clinically, on examination there was decayed 38 that was of concern. On right lower jaw missing 46 and silver amalgam restored 47 was seen [].
An intraoral periapical radiograph (IOPA) was advised as a part of investigative procedure for 38 and 47. Tooth 38 showed periapical pathology suggesting abscess and tooth 47 showed an interesting finding in the periapical region. Crown showed radiopacity involving occlusal and mesial aspect with a distal radiolucency involving the crown suggestive of dentinal caries. Periapically, a small well-defined radiopacity was seen in relation to mesial root that was attached to the apex of the root measuring approximately 1 cm []. Surrounding the radiopacity a uniform radiolucent halo was seen. To enhance the view, digital volume tomography (DVT) was taken []. Coronal, axial and sagittal view of the concerned area showed a rounded well-defined radiopaque mass attached to the root of the respective tooth surrounded by a well-defined radiolucent halo. A differential diagnosis of condensing osteitis and benign cementoblastoma was considered. Other lesions considered were PCOD and osteoblastoma.
Further, vitality test of 47, 48, 37 and 38 was carried out. Tooth of concern 47 showed delayed response, indicating that the tooth was vital. Teeth 48 and 37 were vital, whereas 38 was nonresponsive.
Based on the findings of the vitality test, IOPA of 47 and DVT, a diagnosis of benign cementoblastoma was made. It was decided to extract 47 along with the periapical mass followed by a through curettage. The specimen was obtained as gritty fragments [ inset] and was sent for histopathologic examination.
The decalcified sections showed anastomosing curvilinear bony trabeculae (ginger root pattern) in a fibrous stroma with basophilic outlines, noted focally [Figure and ]. Areas of hemorrhage were appreciated close to the mineralized masses []. Section from other fragments revealed cellular mesenchymal tissue composed of spindle-shaped fibroblasts, collagen fibers and several engorged capillaries with mixture of short, irregular and thick trabeculae of immature bone/and irregular basophilic cementum-like masses []. Irregular thick trabeculae of immature bone with osteocytes and osteoblastic rimming [] and few osteoclasts on the edge of bony trabecule within a homogenous fibro-cellular background [] were also evident.
Based on the findings of the histopathology, a final diagnosis of FCOD was made. No postoperative complications were seen [] and patient was followed up for a period of 6 months with no signs of recurrence.