A 75-year-old woman visited our hospital presenting with temporary chest pain. She had hypertension and type 2 diabetes mellitus (T2DM) treated with calcium antagonist and metformin, respectively, by her family physician. Physical examination revealed that she had neither lymphadenopathy nor hepatosplenomegaly. Electrocardiogram revealed no signs of acute coronary syndrome (data not shown). Slight elevation of serum lactate dehydrogenase level as well as anemia was observed. Enlargement of the left adrenal gland was identified incidentally by abdominal computed tomography (CT), whereas her right adrenal gland was normal in size and shape. Her left adrenal gland was elliptically shaped, with the longest diameter being 35 mm. As shown in , the T1- and T2- weighted views in the magnetic resonance image (MRI) of her enlarged left adrenal gland showed a low- and isointensity signal, respectively. Because she has hypertension and T2DM, we first suspected a functioning adrenal tumor such as Cushing's syndrome, primary aldosteronism, or pheochromocytoma. However, endocrinological examinations revealed that her adrenal function was normal. Her serum ACTH and cortisol levels at that time were 34.3 pg/mL and 8.7 μg/dL, respectively. Administration of 1 mg dexamethasone at midnight suppressed her serum cortisol level up to 2.8 μg/dL in the next morning, indicating that there was no autonomous cortisol production from the adrenal tumor. Primary aldosteronism was unlikely because her serum renin activity (0.5 ng/mL/hr) and aldosterone levels (78.5 pg/mL) were both within normal limits. Her serum adrenaline, noradrenaline, and dopamin levels were 30 pg/mL, 306 pg/mL, and 11 pg/mL, respectively, indicating that adrenal tumor was not typical with pheochromocytoma. Six months later, the size of her adrenal glands was unchanged. However, the CT scan at the next 6 months revealed obvious enlargement of both adrenal glands (). Her serum ACTH and cortisol levels at that time were 96.6 pg/mL and 10.2 μg/dL, respectively, indicating that her adrenal function was still normal. Her serum level of soluble interleukin-2 receptor (sIL2R) was 5,930 U/mL, and the exclusive strong uptake in both adrenal glands in F-18 fluorodeoxy-glucose positron emission tomography (FDG-PET) () was observed. We suspected adrenal tuberculosis infection, adrenal metastasis from unknown primary cancer, or malignant lymphoma. To make a definite diagnosis, laparoscopic left adrenalectomy was performed. Histological examination demonstrated diffuse infiltration of atypical lymphocytes, with large nuclei not only replacing normal adrenal structure but also mainly proliferating into the lumina of small vessels. Immunohistochemical staining demonstrated that most tumor cells were positive for B- cell markers such as CD20 (), bcl-6, and multiple myeloma oncogene 1 (MUM1), whereas those same tumor cells were negative for CD3, CD5, CD10, or bcl-2 (data not shown). Taking the findings together, a final diagnosis of IVLBCL was concluded. Bone marrow examination revealed no lymphoma cells but a hemophagocytosis (data not shown).
As treatment, CHOP therapy at a reduced dose was started due to her advanced age. We used 600 mg/m2 of cyclophosphamide (80% of standard dose), 40 mg/m2 of adriamycin (80% of standard dose), 1.12 mg/m2 of vincristine (80% of standard dose), and 100 mg/body of prednisolone (standard full dose) for 5 days, combined with 375 mg/m2 of rituximab (standard full dose) on the first day (R-CHOP). After the 8th cycle of R-CHOP therapy, her right adrenal gland decreased in size () and her serum sIL2R levels were decreased from 5,930 U/mL to 734 U/mL. One year after R-CHOP therapy, FDG-PET scan revealed disappearance of radioactivity in her right adrenal gland (data not shown), indicating that chemotherapy led her to the condition of complete remission.


A 69-year-old woman with a history of early gastric cancer was admitted to our hospital with a 3-day history of general weakness, headache and nausea. On physical examination she was pale and appeared acutely ill, but was oriented to person, place and time. Her vital signs were as follows: blood pressure 130/75 mmHg, pulse rate 83 beats/min and respiratory rate 20 breaths/min. She exhibited no focal neurological signs, including abnormal reflexes, sensory deficits, nystagmus or neck stiffness. Her conjunctivae were pale and sclerae were anicteric. Breath sounds were clear and heart sounds were regular and without murmur.
The patient had been diagnosed with early gastric cancer 29 months prior to presentation, and had undergone a radical subtotal gastrectomy with Billroth I anastomosis and D1+ lymphadenectomy (Figure ). Histology performed at the time had shown diffuse-type gastric adenocarcinoma confined to the mucosa with the presence of signet ring cells. No metastases were found in the 34 dissected lymph nodes. Her postoperative course was uneventful. She visited the surgery outpatient clinic for follow-up 6 weeks, 3 months and 6 months after surgery, and at 6-month intervals thereafter. She also underwent gastric endoscopy and abdominal computed tomography (CT) every 6 months. There was no evidence of recurrence until 26 months after surgery, when the patient complained of palpable masses in her left neck and axilla. She subsequently underwent neck CT, fluorine-18-fluorodeoxyglucose positron emission tomography, and fine needle aspiration of the left supraclavicular lymph node. Neck CT showed enlargement of multiple nodes in the left neck and axilla, including the left supraclavicular lymph node, and fine needle aspirate histology showed metastatic adenocarcinoma. She was diagnosed with recurrence of early gastric cancer and scheduled to receive systemic chemotherapy with leucovorin, fluorouracil and oxaliplatin (FOLFOX-6). She received 100 mg/m2 oxaliplatin and 100 mg/m2 leucovorin on the first day of treatment, followed by 2,400 mg/m2 of 5-fluorouracil on the first and second days of treatment every 2 weeks. After four cycles of chemotherapy, tumor response evaluation showed that disease stability had been achieved, prompting a fifth cycle of the same chemotherapy regimen.
She presented as an outpatient 7 days after completing the fifth chemotherapy cycle, complaining of general weakness, headache and nausea. A lumbar puncture was performed, and analysis of the cerebrospinal fluid (CSF) showed malignant cells (Figure ), elevated protein, normal glucose, and the presence of tumor markers carcinoembryonic antigen and carbohydrate antigen19-9 She was diagnosed with metastatic leptomeningeal carcinomatosis of early gastric cancer and admitted to the hospital. On the seventh day of admission, she complained of dyspnea and her level of consciousness decreased, prompting intubation and admission to the intensive care unit. Symptomatic treatment was initiated with steroids and mannitol. Unfortunately, the patient died on the 20th day of admission.


A 50-year-old white man with a history of progressive vision loss and elevated intraocular pressure (IOP) in both eyes was referred to our hospital. He was previously diagnosed with angle-closure glaucoma in association with ocular cystinosis and was on three topical antiglaucoma therapy. Although the leukocyte cystine level was not measured at that time, conjunctival biopsy was reported to support the diagnosis of cystinosis. He underwent comprehensive systemic and ocular examination, and laboratory investigations. His family history was negative for cystinosis and nanophthalmos.
On examination, his visual acuity was 20/400 OU with hyperopic correction of +13.5 OD and +14 diopters OS. Despite three topical medications, his IOP measured 37 mmHg OD and 35 mm Hg OS and his cup-to-disc ratio was 0.85 OD and 0.8 OS. Slit-lamp biomicroscopy revealed bilateral refractile, polychromatic crystalline deposits in cornea and conjunctiva (Figure a and b). Gonioscopy revealed an extremely narrow angle with peripheral anterior synechiae (PAS) occupying approximately 50% of each angle (Figure c). Both anterior chambers were quite shallow. Anterior chamber depths measured by Allegro Oculyzer were 1.64 mm in the right eye and 1.55 mm in the left eye. Central corneal thickness was 509 μm OD and 506 μm OS. Corneal diameters were 9.5 mm in both eyes. Anterior chamber angle measured with Allegro Oculyzer were 22.2° on inferotemporal side of right eye and 19.1° on the inferotemporal side of left eye (Figure d). Ultrasound biomicroscopy (UBM) showed that the angle in both eyes was narrowed 360 degrees circumferentially without an evidence of plateau iris formation and uveal effusion. On A- Scan biometry, the axial lengths were 16.27 mm OD and 15.93 mm OS, with a lens thickness of 4.82 mm and 5.19 mm in the right and left eyes, respectively. Fundus examination revealed hyperopic disc with mild pallor, and areas of stippled and punctate hypopigmentation of the retinal pigment epithelium (RPE) at the midpheriphery and around the optic disc in both eyes (Figure a). Fluorescein angiography (FA) showed choroidal transmission hyperfluorescence corresponding to RPE atrophy (Figure b). Optical coherence tomography (OCT) imaging also revealed cystoid changes in a schisis-like pattern which was not detectable clinically (Figure c). The electroretinography showed that both rod and cone responses were affected and the b-waves were reduced in amplitude with mildly delayed implicit time. The serum creatinine was 0.7 mg/dL, with normal electrolytes and blood counts. The urinalysis was normal. Leukocyte cystine level determined using the cystine-binding protein method was 1.1 nmol half-cystine/mg protein. No medical evidence of renal tubular or glomerular damage was found. Bilateral Nd:YAG laser iridotomy was performed in both eyes, but the angle opened minimally and the IOP remained unchanged. Patient refused further operations despite recommendations.


A 3-year-old boy was referred to the Department of Pediatric Dentistry, Shiraz University of Medical Sciences, representing lack of teeth as the chief complaint. According to familial history, a brother of the patient also suffered from oligodonatia and heat intolerance. Extraoral examination revealed dry skin, hypoplastic midface, prominent lips, and sparse fine hair. These findings matched typical features of anhidrotic ectodermal dysplasia
(,). The intraoral examination revealed complete edentulism in the lower jaw, four peg shaped anterior teeth in the upper jaw, thin alveolar ridge, reduced vertical bone height and loss of vestibular depth in the lower jaw
(). The radiographic findings also confirmed the clinical diagnosis. Panoramic view revealed two unerupted molar teeth in the upper and two unerupted incisors in the lower jaw
().
Treatment plan included making complete overdentures for the upper and lower jaws to improve appearance, function and speech. Due to small arch size, preliminary impression was made by modeling plastic as custom tray and zinc oxide impression material. The lower anterior teeth were left unmodified because of short crowns. When properly fitting custom tray was ready, final impression was made by elastomeric materials. Jaw relationship was recorded using temporary base and wax rim. The arranged teeth were verified in the mouth during the try-in appointment. After laboratory processing, the overdentures were delivered to the patient
(). In the delivery appointment, instructions were given to maintain proper oral hygiene. Continuous follow-ups every six months were planned for adjustment or replacement of old denture.


A 10-year-old girl was referred to the Department of Pediatric Dentistry, Shiraz University of Medical Sciences, representing oligodontia. Familial history revealed that close relatives including grandmother on the mother’s side and cousins were afflicted with the same condition. In extraoral examination, sparse fine hair, dry skin, reduced vertical height of facial lower third and prominent chin and lips were observed
(). Intraoral examination revealed four primary molars, five permanent molars, three incisors, and unilateral maxillary contraction
(). One permanent semi-erupted molar tooth and three unerupted premolars were found in radiographic view
(). These findings matched typical features of anhidrotic ectodermal dysplasia.
In order to improve appearance and mastication, removable partial prosthesis was established as treatment plan. First, maxillary crossbite was corrected using Hawley appliance for six months. The two anterior peg-shaped teeth were restored by composite resin. In order to fabricate removable partial denture, two impressions were made with a hydrocolloidal material (alginate); first with stock tray and then with custom tray. Removable partial prostheses were fabricated in coordination with patient’s occlusion and wrought wire clasps were used as retainers
(). Recalls were scheduled every 6 months to evaluate developing jaws and teeth eruption.


In this study, we report a case of a 70 year-old female who was diagnosed with SMTC 15 years ago. A total resection of the thyroid gland and a resection of the right lymph nodes in the neck were performed at age 55. At the time of surgery, a unilateral tumor was detected in the right lobe of the thyroid. Histopathological findings confirmed a 7.5x3.5x2cm tumor (T2) with extraglandular extension, 8/17 positive lymph nodes metastases (N1b) and no distant metastases (M0) were found. According to TNM classification, this patient was diagnosed as MTC stage III. One year later, the patient presented with persistently high serum CT levels (2,400 pg/mL). During a second surgery, a left lymph nodes resection was performed and histopathological analysis confirmed the presence of several lymph node metastases (10/49). At present, the patient is alive and has persistent disease, confirmed by periodical elevated serum CT levels (3,193 pg/mL at the latest screening).
Molecular diagnostic testing confirmed the presence of the M918T RET mutation in the tumor and lymph node metastases previously. Interestingly, our case study demonstrate that despite the mutation and the presence of several lymph nodes metastases, the patient experienced a good survival rate (15 years after surgery) and still alive. Then, we focused in search of genetic DNA alterations by CGH that could be important in the favorable prognosis of this patient. The CGH procedure was performed using reagents and kits from Vysis Inc. (Downers Grove, IL), following the manufacturer’s instructions. Tumoral DNA was labeled using the CGH nick translation kit and the hybridization mixture was prepared according to the CGH reagent kit, consisting of 200 ng of spectrum-green labeled tumoral DNA, 200 ng of spectrum-red labeled normal male reference DNA and 20 μg of human Cot-1 DNA. Hybridization was performed over 3 days at 37 °C on normal male metaphase spreads (Vysis, Downers Grove, IL). Digital images were collected using the Smart Capture (Vysis) software with a charged coupled device camera mounted on an epifluorescence microscope. In the primary tumor, the chromosomal alterations detected were losses in 6p and 16p and gain in 18p, while 25 chromosomal alterations were detected in the lymph node metastasis with more losses than gains (Table ).


A 24-year-old male presented initially to the emergency room with complaints of red and swollen eyes after a period of about one week of (nonbloody) diarrhea that started approximately three weeks before. He was discharged initially with the diagnosis of conjunctivitis (not confirmed by a ophthalmologist). He returned two weeks later with a painful swollen right knee accompanied by fever, general malaise, and back pain. The patient had been in Egypt 6 weeks earlier for one week. In Egypt, he had only been to the sea for diving. There was no history of insect bites. He had only ridden a camel and there had been no contact with other animals. There was no history of (unsafe) sexual contact. The patient informs us that he had travelled back via Poland and that he had eaten a typical sausage. The patient's medical history was blank. He started taking medication against diarrhea (paromomycine) and some acetaminophen.
On physical examination, we saw a non-ill-appearing patient; blood pressure: 102/59 mm Hg; pulse: 82/min, regular temperature: 36.3°C. The skin showed no abnormalities. Ophthalmological examination revealed signs of bilateral conjunctivitis. No palpable lymph nodes were found in the cervical or inguinal region. Chest auscultation revealed normal heart and breath sounds. Examination of the abdomen revealed normal peristalsis and slight tenderness on palpation without guarding and hepatosplenomegaly. The right knee was red, swollen, and painful with mobilization.
Laboratory examination revealed an elevated and rapidly increasing CRP (C-reactive protein), ESR (Erythrocyte sedimentation rate), leukocytosis with elevated neutrophils (no eosinophilia) with a limited normocytic anemia. Furthermore, there were elevated liver enzymes (liver transaminases as well as alkaline phosphatase and gamma-glutamyltransferase). Antinuclear antibodies were negative. Serologic tests for Entamoeba histolytica, several helmintic infections, Yersinia, Campylobacter, and Borrelia burgdorferi remained negative.
Examination of the urine revealed no abnormalities. A chest X-ray was normal. A puncture of the right knee was performed and while awaiting the culture result the patient was treated with flucloxacillin with an initial poor clinical response. Therefore, arthroscopy and joint flushing was performed. The punctate revealed many leukocytes but no bacteria. Hemocultures remained negative.
A CT scan of the abdomen showed a liver cyst, a thickened wall of the colon descendens/ascendens indicating colitis, para-aortic lymphadenopathy, and free fluid in the Douglas Space. A subsequent left colonoscopy showed colitis with aphthoid ulcerations (). Biopsy showed aspecific colitis (no inflammatory bowel disease).
Finally, one feces culture revealed Shigella species and confirmed initial suspicion of reactive arthritis. After a week, the patient made a good recovery and was discharged with diclofenac 75 mg 2x/d as necessary.


Our patient is a previously asymptomatic 29-year-old Caucasian man who was diagnosed with isthmic aortic coarctation at the age of 28 years. At that time, he presented with progressive shortness of breath, significant chest pain and diminished exercise tolerance. His blood pressure was 150/90mmHg without treatment. Echocardiography showed dilatation of his ascending aorta (39×40mm) and a bicuspid aortic valve with mild insufficiency.
Our patient underwent surgery three months after his symptoms began. The surgical technique was resection of the long segment (4cm) of the coarcted aortic arch and a termino-terminal anastomosis of an intervascular number 16 polytetrafluoroethylene (PTFE) tube. Two thoracic collaterals were ligatured during the resection of the aortic segment. Surgery was performed without any immediate complication. The gradient of the coarctation was 60mmHg before surgery, and was normal after the procedure. After ten days of hospital stay, our patient was discharged. He was asymptomatic and his blood pressure under treatment with nifedipine (2×30mg/day) was 120/85mmHg.
During the eight months after his surgery, our patient presented the following new symptoms, which worsened very progressively until they impaired his normal daily functioning: shortness of breath on exertion, light-headedness and dizziness on standing, fatigue, excessive daytime sleepiness and hypersomnia (up to 16 hours a day). Sleep was not restorative and our patient described daytime somnolence. He could no longer attend his work. He also complained of abdominal cramps after meals and constipation.
An echocardiogram and thoracic computed tomography showed no relevant findings. Our patient developed depressive symptoms, which showed partial improvement after the introduction of venlafaxine (150mg/day). Other medications included amlodipine (5mg/day) and valsartan (80mg/day) for residual hypertension, and aspirin (100mg/day).
Eighteen months after his aortic surgery, our patient was finally admitted to our hospital because the same symptoms persisted and had worsened. A complete history revealed that he was not known for snoring, but his girlfriend reported leg jerks during sleep and sleep talking. He denied chronic nasal congestion or substance abuse. He drank two litres of cola-drink per day.
On physical examination, our patient could not stand for more than 10 minutes because of dizziness and a sense of weakness. His body mass index was 21kg/m2 and a small oral cavity with micrognathia was observed. He scored 19 out of 24 on the Epworth Sleepiness Scale, 6.6 out of 7 on the Fatigue Severity Scale and 14 out of 63 on the Beck Depression Inventory. Laboratory values were in the normal range, including thyroid-stimulating hormone and arterial blood gases. Adrenal insufficiency was excluded. Pulmonary function tests and cerebral magnetic resonance imaging were not contributory.
A polysomnography and a multiple sleep latency test detected breathing abnormalities, as detailed in Table . There were no periodic leg movements (index of periodic limb movements in sleep: 7) and narcolepsy was ruled out by the multiple sleep latency test (mean latency: 11min 33s). Thus, it was concluded that our patient had UARS together with micrognathia and excessive daytime sleepiness []. The UARS was severe enough to explain part of his symptoms, such as his extreme fatigue and functional impairment, but could not explain the orthostatic symptoms [].
An orthostatic measurement of his heart rate and blood pressure showed an important heart rate increment on standing (from 77 beats/min supine to 106 beats/min when getting up and 146 beats/min after 5min of standing). During the test, his blood pressure remained stable at a value of 115/83mmHg and our patient developed his usual symptoms of dizziness, shortness of breath, paresthesia and general weakness. After seven minutes, he could no longer tolerate the standing position. A head-up tilt test reproduced the same orthostatic symptoms, with an increased sinus rate and stable blood pressure (Table ). The increase in heart rate without orthostatic hypotension along with the accompanying symptoms confirmed the presence of POTS. A 24 hour Holter monitoring excluded any significant arrhythmia.
Amlodipine and valsartan were stopped and propranolol was introduced (3×10mg/day), with some improvement of the orthostatic symptoms. Our patient entered an exercise rehabilitation program. He was encouraged to maintain a high liquid and salt intake.
Two months later, our patient was able to perform 70% of his normal activities of daily living under this treatment. He described nearly complete disappearance of hypersomnia, excessive daytime sleepiness and fatigue. Despite this initial improvement, our patient experienced a recurrence of the same symptoms after the following six months, albeit of reduced severity.


A 32-year-old Caucasian male presented with a three-week history of fever, abdominal pain, cough and exertional breathlessness after a recent trip to Turkey. He had been previously entirely healthy with no significant family history of note and was taking neither regular nor recently prescribed medications. He had no history of hypertension and his haemodynamic parameters remained normal throughout his admission. Investigations revealed: a white cell count of 13.8 x109/L; C-reactive protein of 278 mg/L; alanine transaminase of 468 units/L; serum albumin of 30 g/L and a serum creatinine of 535 μmol/L. There was evidence of haematoproteinura on dipstick urinalysis with a protein to creatinine ratio of 285 (normal range <30). A chest x-ray showed no evidence of consolidation, but revealed significant cardiomegaly. A subsequent echocardiogram revealed a bright echotexture to the myocardium and confirmed the presence of a 4 cm global pericardial effusion causing right atrial collapse, the cardinal sign of cardiac tamponade (Figure ). An ultrasound scan of his abdomen demonstrated splenomegaly without hepatomegaly, and kidneys of normal echotexture, the right measuring 9 cm and the left 10.3 cm. A nephritis screen including serum ANA, ANCA, complement levels and immunoglobulins was unremarkable.
He was treated initially for an atypical infection with appropriate broad-spectrum antibiotic cover with a corresponding improvement in both white cell count and CRP levels. The day after admission he underwent a pericardiocentesis because of the risk of tamponade. Subsequent histological examination of the pericardial fluid showed evidence of acute on chronic pericarditis secondary to uraemia. All cultures of blood, urine and pericardial fluid (including mycobacterium, leptospirosis and mycoplasma) were negative. Despite these measures, his creatinine continued to rise and a renal biopsy was performed.
Light microscopy showed: very active tubulointerstitial inflammation with lymphocytic and plasma cell infiltrates as well as interstitial oedema related to his concurrent antibiotic treatment with intravenous co-amoxiclav nd; global sclerosis of all 22 sampled glomeruli. Toluidine blue staining revealed abundant deposition of glycolipid inclusions within the podocyte (Figure a). Immunofluorescence was negative. Electron microscopy demonstrated the characteristic enlarged secondary lysosomes (myeloid or ‘zebra’ bodies) packed with lamellated membrane structures that are associated with Fabry disease (Figure b). The diagnosis was later confirmed, initially by a blood spot α-galactosidase activity of 3.61 pmol/spot/h (5.51-58.1) and subsequently by a reduced plasma α-galactosidase A activity of 1.88 μmol/L/h (3-20) as well as elevated levels of globotriaosylceramide (Gb3) in the urine at 0.5 mg/mmol creatinine (0-0.03). Genetic sequence analysis revealed a missense point mutation causing the substitution of arginine with proline at amino acid residue 356, consistent with a diagnosis of Fabry disease.
On resolution of his sepsis, his C-reactive protein and alanine transaminase levels returned to normal and a repeat abdominal ultrasound confirmed that his splenomegaly had also resolved. Despite an initial improvement in serum creatinine to 250 μmol/L after commencement of steroid therapy for the underlying antibiotic-induced nephritis, he became dialysis dependent after six months, although subsequently received a living, non-related renal transplant from his wife. He is now receiving enzyme replacement therapy.
Interestingly, he had no symptoms suggestive of Fabry disease. In particular there were no acroparathesiae, gastrointestinal symptoms and no history of heat intolerance; he described sweating normally on exertion. He also denied any problems with his skin.


An 84-year-old woman was admitted to our hospital with complaints of left lower abdominal pain and nausea without fever. Her past surgical history included a hysterectomy and a femoral neck fracture repair. She also suffered from hypertension and hyperlipidemia. Her body mass index was 18.2kg/m2 and her vital signs were all within normal limits. Physical examination demonstrated tenderness in the left lower abdomen without Blumberg’s sign and with no demonstration of Murphy’s sign. Laboratory data were all within normal limits including inflammatory response, liver function tests, and biliary enzymes. A CT scan of her abdomen at admission demonstrated an enlarged and wall-thickened gallbladder without gallstone, prominent small bowel gas, and mild intestinal dilatation and wall thickening (Figure a). The findings of ultrasonography were the same as those of the CT scan. Therefore, we diagnosed her condition as acute enterocolitis or subileus and began a starvation and transfusion cure. After a half day, she suddenly presented with severe right upper abdominal pain and vomiting. Conservative treatment, including a painkiller and antiemetic, was not effective so another abdominal CT scan was carried out. The second CT scan of her abdomen demonstrated a more distended and wall-thickened gallbladder that had rotated approximately 180 degrees and deviated to the midline of her abdomen compared with the CT images at admission (Figure b). The cystic duct was located on the right side of the gallbladder. Taking these into account, we considered that her gallbladder was free hanging and a diagnosis of gallbladder torsion was clinically assumed. Therefore, the patient underwent an emergency laparotomy. During the operation we observed a gallbladder torsion (rotation more than 180 degrees) leading to necrosis and we performed detorsion and cholecystectomy. The gallbladder was free hanging and adhesion to adjacent organs was so mild that operative procedures were easy to perform. Pathological examination revealed necrotic change, compatible with an acute bleeding infarction of the gallbladder due to torsion (Figure ). There was no evidence of malignancy. The patient recovered without surgical complications but suffered from postoperative delirium. She was discharged about two weeks after surgery.


In September 2000, a 53-year-old Caucasian man who was a heavy smoker underwent a radical left nephrectomy for a grade 1, stage I, renal clear cell carcinoma revealed on a routine abdominal ultrasound exam. In July 2001, he presented with a dull pain in his right humerus which rapidly worsened. The pain caused the patient, a professional musician, such discomfort that he was forced to stop playing his instrument (the bouzouki, a stringed instrument from Greece), and strong opioids were required for pain control. The results of a computed tomography (CT) scan of his right humerus and a technetium bone scan showed a solitary bone metastasis. He was treated with closed nailing of his right humerus, but total resection of the metastasis was not achieved (Figure ). He was put on cytokine-based chemotherapy from May 2002 to February 2003. The chemotherapy consisted of IFN-α2α 6MU administered subcutaneously three times per week, recombinant human interleukin-2 at a dose of 9×106IU subcutaneously for 4 weeks followed by 1 week of rest, and vinorelbine 30mg/m2 and zolendronic acid 4mg every 21 days. Then he underwent a right humerus nail replacement with 10-fraction radiotherapy in order to render his extremity pain-free and capable of weight-bearing (Figure ). He was offered physiotherapy but declined. He received IFN-α treatment for a further 4 months and, notably, resumed playing the bouzouki, which requires significant upper-extremity dexterity, attesting to a dramatic improvement of his symptoms. His disease was stable and he led an active life from September 2003 to June 2008, when a chest CT scan revealed several enlarged subcarinal, left hilar, and axillary lymph nodes. He was treated with sunitinib at 50mg/day for 4 weeks with a 2-week washout phase along with vinorelbine 30mg/m2, bevacizumab 200mg, and zolendronic acid every 21 days. A partial response was observed until February 2009, when a chest CT scan revealed several pulmonary nodes consistent with metastases. Therapy was switched to temsirolimus at 25mg weekly until June 2009, when he experienced further deterioration with pleural effusions and a soft tissue metastasis of his thorax. He received sorafenib at 800mg/day along with bevacizumab at 200mg weekly and developed a grade III anemia that impacted negatively on his performance status and that was treated with erythropoiesis-stimulating agents and blood transfusions. The disease progressed until September 2009, when he died of allergic shock during a blood transfusion, 9 years after the initial diagnosis of RCC.


A 54-year-old Caucasian man, a civil engineer, presented with acute urinary retention in July 2002. An abdominal CT scan showed a mass in his left kidney, and he underwent an uneventful radical left nephrectomy for a pT2, grade IV renal clear cell carcinoma. On August 2003, a physical examination revealed an enlarged supraclavicular lymph node, which was histologically proven to be RCC. He was put on cytokine-based chemotherapy – IFN-α 6MU subcutaneously 3 days per week, and docetaxel 60mg and vinorelbine 50mg every 21 days – until November 2004, when a nodule at the upper lobe of his right lung was found on a chest CT scan. The biopsy of the solitary pulmonary nodule confirmed an RCC metastasis, and he underwent a metastasectomy. On September 2005, a magnetic resonance tomography scan of his brain revealed a focal lesion, 3cm in diameter, at the right occipitoparietal region. Two months later, the solitary brain metastasis was resected and was histologically proven to be RCC. In March 2007, a new solitary pulmonary nodule in his lower right lobe was found, and sunitinib at 50mg/day for 4 weeks with a 2-week washout phase was administered. The disease was stable until February 2008, when a chest CT scan revealed bilateral enlargement of axillary lymph nodes, a lesion with soft tissue density in the anterior aspect of the right pulmonary artery, and another one in the hilus of the left lung. Owing to his progressive disease, temsirolimus at 25mg weekly was initiated. Three months after temsirolimus initiation, intravenous zolendronic acid every 21 days was added because of the appearance of new bone metastases involving thoracic vertebrae. A partial response was observed until October 2008, when the soft tissue density lesions progressed and treatment with sorafenib 400mg/day was initiated. The disease was stable until June 2010, when a new pulmonary nodule appeared and the bone metastases became painful. Then the patient was treated with a second-generation mTOR inhibitor, everolimus 10mg by mouth every day, and 6-fraction palliative radiotherapy was applied to the painful spine bone metastases at a total dose of 24Gy. His disease was rendered stable for a year, when a new pulmonary metastasis appeared. The patient has since been receiving pazopanib at 800mg/day, resulting in stable disease to the present day. Ten years after the diagnosis of RCC, he leads an active life and only moderate bone pain prevents him from doing strenuous activity.


A 63-year-old Caucasian man presented to our hospital for chronic hepatitis C treatment. His initial physical examination results were unremarkable. An initial liver profile included aspartate aminotransferase (AST) 60IU/mL, alanine aminotransferase (ALT) 74IU/mL, total bilirubin 1mg/dL, alkaline phosphatase 81IU/mL, albumin 5.2g/dL, and a prothrombin time (PT) of 76%. Serum viral load was estimated to 3,545,770IU/mL (6.5log) with a genotype 2a2c. The assessment of liver fibrosis by FibroTest® and FibroScan® revealed a stage F2 of fibrosis. An abdominal ultrasound did not find any signs of portal hypertension or cirrhosis. Upper gastrointestinal endoscopy did not find any endoscopic signs of portal hypertension. He was started on a course of treatment comprising PEG-interferon α2a (PEGASYS®) 180μg subcutaneously per week and ribavirin 800mg/day in divided doses orally. A rapid virological response was obtained after four weeks.
In the fifth week of treatment, he reported painful paresthesia, tingling, numbness, and weakness of his lower extremities. His neurological symptoms progressed rapidly over the course of one week to the point of losing the ability to ambulate. In addition, our patient also complained of tingling and numbness in the upper extremities involving the fingers and wrists bilaterally. PEGASYS® was discontinued due to an acute onset of weakness of the upper and lower extremities. A neurological examination revealed normal cranial nerves with normal bulk of muscles and tone; but weak muscle strength in the upper extremities as well as in the hips, knees, ankles and toes bilaterally. His tendon reflexes were diminished significantly. A sensory examination revealed decreased light touch, pinprick, and temperature sensation from the feet to mid-calves as well as hands, except for vibratory sense. A clinical diagnosis of acquired acute inflammatory demyelinating sensorimotor polyneuropathy was made. Biochemical screening tests, complete blood count, erythrocyte sedimentation rate, anti-nuclear antibodies, serum cryoglobulin level, human immunodeficiency virus (HIV) test and cytomegalovirus (CMV) deoxyribonucleic acid (DNA) were all normal. The results of an electromyogram (EMG) revealed evidence of predominant motor polyneuropathy with prominent demyelinating features, including motor conduction block, low conduction velocity, and prolonged minimum F wave latency in the bilateral ulnar, median, peroneal, and tibial nerves (Table ). Our patient recovered completely after one month of stopping interferon (without stopping ribavirin) and symptomatic treatment. His muscle weakness and paresthesia were markedly improved, with normal strength in all muscle groups; eventually he could walk without difficulty. A further EMG showed a disappearance of neuropathy. Four weeks later, IFN was reintroduced with a gradually increasing dose (90μg for two months, then 120μg for one month followed by 180μg for the two remaining months) without reappearance of neurological symptoms. He has not experienced relapse and his neurological status remained stable. His viral load of hepatitis C was negative at week 24 and six months after stopping treatment. Currently our patient is well and his neurological symptoms have resolved completely with no residual neuromuscular deficits.


A previously well 37-year-old male patient presented with sore throat, odynophagia, high fever, and malaise for a period of one week. The patient reported that he had been using amoxicillin/clavulanic acid 1000-mg/62.5-mg tablet, twice daily, for a period of 5 days, but the clinical symptoms were deteriorating. An otorhinolaryngologic examination revealed hyperemic and congested oropharynx and tonsils with diffuse exudate predominantly on the left tonsil () and bilateral Level I-II cervical lymphadenopathies. The patient was immediately hospitalized, and penicillin G potassium was administered with a dose of 4 million-units q4 hrs. Throat culture for group A β-hemolytic streptococci showed normal flora. Monospot test for heterophile antibodies was negative. Chest X-ray and upper abdominal ultrasound examinations were within normal limits. A complete blood count showed leucocytosis (11.29 × 103/uL), with 73.2% neutrophilia and 12.4% lymphopenia. On the 4th day of the hospitalization, the patient gave a history of a sexual intercourse with a female sex worker (FSW), 9 days before hospitalization. The patient admitted that coitus did not take place, the sexual act was predominantly with cunnilingus and anilingus, and mutual masturbation with manual contact. On the 6th day, laboratory work-up for a STD (e.g., gonorrhea, syphilis, and chlamydia) declared a positivity for Chlamydial IgM with microimmunofluorescence. Total urine count showed rare leucocytes, and urine culture was negative. Medical therapy was changed to doxycycline 100 mg tablets, twice daily, on the 6th day of hospitalization. A pronounced symptomatic improvement was seen in the first 48 hours of the new drug regimen, the signs of tonsillopharyngitis settled down, and the patient was discharged on the 8th day. After completing a one-week course of doxycycline, the patient recovered completely.


A 72-year-old Caucasian male was admitted to the emergency department of the University Hospital of Ioannina due to diffuse abdominal pain, nausea and progressively increasing abdominal distension of ten-day duration. His medical history was free and no recent trauma was reported. Clinical examination revealed pyrexia of 38.5°C, tachycardia of 110 per minute, and normal blood pressure. Upon physical examination, a grossly distended and diffusely tender abdomen was revealed. On auscultation abdominal sounds were present. Rectal examination showed an empty rectum. The emergent laboratory tests revealed as follow: WBC 14700 mm3, haemoglobin at 10.5 g/dL, c-reactive protein was at 148 mg/l, creatinine, electrolytes, and liver function tests were normal. The examination of urine was also normal. The abdominal plan X-ray was normal and an urgent abdominal CT was arranged. The CT revealed a huge hepatic hydatid cyst (measuring 14.5 cm) with daughter cysts in the left lobe of the liver and multiple splenic hydatidosis. Additionally, a large echinococcal cyst was revealed at the left hypochondrium attached to the anterior wall of the stomach causing a huge pressure (Figures and ). Hydatid cysts were also revealed in the transverse mesocolon and in pelvis. Laparotomy was performed the day after the admission due to progressively increasing abdominal distension and to diffuse abdominal pain. Intraoperative findings confirmed the diagnosis of abdominal and splenic hydatidosis. The patient was treated with deroofing and omentoplasty for the large hepatic echinococcal cyst, splenectomy for the splenic cysts, and removal of the rest echinococcal cysts. The postoperative period was uneventful and the patient was discharged 15 days later, with the advice to receive albendazole for three months postoperatively.


In February 2010, a 55-year-old Japanese man was referred to our hospital due to a bleeding tendency. His blood cell count was hemoglobin (Hb) 10.0 g/dL, platelets 1.5 × 104/μL, white blood cells (WBC) 2.9 × 103/μL with 46% neutrophils and 49% lymphocytes, and absolute reticulocyte number 33,330/μL. Bone marrow examination revealed severe hypocellular marrow without any dysplasia. Chromosomal analysis showed a normal karyotype. A whole-body CT scan showed no abnormal findings. Thus, we diagnosed him with AA (stage 3). Serological studies for human immunodeficiency virus, hepatitis B and C virus, and cytomegalovirus (CMV) were all negative. Anti-EBV antibody titers at diagnosis were viral capsid antigen (VCA) IgG-positive, VCA IgM-negative, and EBV nuclear antigen- (EBNA-) positive. The quantities of EBV-DNA viral load in peripheral blood using the RT-PCR method were not measured at diagnosis. He depended on regulatory red blood cell and platelet transfusions.
Because he had no related HLA-identical donor, he was treated with immunosuppressive therapy consisted of methyl-predonisolone (125 mg/day days 1–5, then tapered), CSP (6 mg/kg/day, orally), and rabbit ATG (3.75 mg/kg/day, days 1–5) in May 2010. The dose of rabbit ATG was decided according to the guideline for the diagnosis and management of AA of the British Society of Haematology []. On day +9 after immunosuppressive therapy, his lymphocyte count decreased to 0/μL. Although, after day +13, his lymphocyte count increased gradually, it was maintained on the level below 100/μL. He developed no documented infection, and he was discharged with a regulatory blood transfusion dependency. In August 2010, he developed severe anemia and needed frequent red blood cell transfusions. Moreover, the serum LDH gradually increased to 358 IU/L from a normal range (119–229 IU/L). He developed general malaise and appetite loss. He was afebrile and did not develop superficial lymphadenopathy. Because occult blood tests in stools were positive, he underwent a colonoscopy, which revealed multiple tumors of the ascending, transverse, and descending colons (). All biopsy specimens from colonic tumors showed the proliferation of atypical lymphocytes (). Immunostaining revealed that the atypical lymphocytes were CD20+ (), CD79a+, CD3−, and CD5−. Immunocytochemistry studies for EBV encoded small RNAs (EBER) involving in situ hybridization were positive (). The PET/CT showed no lymphadenopathy other than the colonic tumors. On day +84 after immunosuppressive therapy, the EBV viral load was slightly increased to 140/106 WBC. He was diagnosed with EBV-LPD. He received only CSP as immunosuppressive therapy at day +84. The serum concentration of CSP was 333 ng/mL on day +90. We stopped the administration of CSP on day +97. After cessation, his symptoms gradually improved, and the serum LDH level decreased to the normal range. His lymphocyte counts gradually increased to 300/μL. One month after the cessation of CSP, he underwent colonoscopy again, which showed regression of the tumors (). Two months after the cessation of CSP, the EBV viral load was below the detectable level. In February 2011, he had achieved a partial hematological response and was independent of blood transfusion. At this moment, 2 years later, no EBV-LPD occurred.


A 4-year-old previously healthy girl was admitted to our hospital for severe anemia. Ten days before her admission, she had developed nonproductive cough and weakness and paleness. No family history of hemolytic attacks was noted. The patient had taken amoxicillin-clavulnate for seven days, but her complaints remained. On physical examination, the patient was very pale and tachycardic (140 beats/min). Blood pressure was 90/60 mmHg and body temperature was 36.8°C. Chest examination showed normal breath sounds. No rhoncus or whistling was heard. Respiratory rate was 20/minute. Systolic flow murmur was heard at every auscultation focus. The rest of the examination was unremarkable.
Admission blood count showed a haemoglobin level of 6.3 g/dl, a mean corpuscular volume of 83.1 fL, and white blood cell count of 11200/mm3, with 41% neutrophils, 51% lymphocytes, 8% monocytes, and a platelet count of 569000/mm3. The reticulocyte count was 6%. Lactate dehydrogenase (LDH) was 581 U/L (reference range: 100–250 U/L). Total bilirubin was 1.5 mg/dL (normal 0.1–1.0 mg/dL), of which 1.2 mg/dL was indirect (normal 0–0.8 mg/dL). Haptoglobin was 18 mg/dL (normal 30–200 mg/dL). The serum level of C-reactive protein was 0.81 mg/dL (reference range: 0–0.8 mg/dL), and the erythrocyte sedimentation rate exceeded 140 mm in 1 h. Other blood chemistry, liver profile, and coagulation studies were within normal limits. Blood, sputum and urine cultures were negative. The chest X-ray showed bilateral interstitial infiltration ().
A bone marrow aspiration was performed to rule out the possibility of an underlying hematological malignancy, and it revealed mildly increased erythropoiesis but no changes indicative of a hematological malignancy were observed. Direct Coombs test was positive. Mycoplasma pneumoniae IgM antibody was positive; M. pneumoniae IgG antibody titers determined by immunofluorescence test were 1/64. The patient was diagnosed with severe hemolytic anemia complicating M. pneumoniae infection. She was treated with clarithromycin (15 mg/kg/d, twice daily) and packed red cell transfusion (10 mL/kg). Then the symptoms were rapidly resolved and hemoglobin increased to 10.4 gr/dL. The antibiotic was continued for a total of 10 days. The patient was discharged in good health after an 8-day hospital stay. In discharge, thrombocyte count, blood chemistry and coagulations studies were normal. Erythrocyte sedimentation rate was 40 mm/hour.
Four months after the discharge, she remained clinically well, her physical examination was normal; her hemoglobin was 13.8 gr/dL; M. pneumoniae IgM antibody was negative and M. pneumoniae IgG antibody titer was 1/64. Coombs test was found negative.


We report the case of a 61-year-old Tunisian woman presented to the emergency unit with a 4-hour history of abdominal pain, diffused at both flanks without hematuria. Her medical history was significant for diabetes, hypertension and atrial fibrillation, besides her surgical history indicates left pneumectomy for pulmonary tuberculosis. Her medications consisted of aspirin, metformin, furosemide, and metoprolol. Physical examination showed vital signs as follows: body temperature of 37.2°C, blood pressure of 150/85 mmHg, heart rate of 133 beats per minute, respiratory rate of 20 breaths per minute; the abdomen was soft with slight tenderness in the renal angles. The remainder of the examination was normal.
An electrocardiogram showed atrial fibrillation. A biological analysis showed high serum creatinine levels (205μmol/L); her aminotransferases were twice normal the normal levels and her lactate dehydrogenase (LDH) level had increased to (8,636IU/L) with high leukocytosis at 15,000 cells/mm3. A urine analysis showed no hematuria or infection. A serum analysis done one month previously showed that her creatinine level was normal (93μmol/L). Nephrolithiasis and mesenteric ischemia were strongly suspected to be the causes for this acute pain.
Ultrasounds of the abdomen were performed and showed peri-renal fluid collection with heterogeneous parenchyma (Figure ). Contrast-enhanced helical computed tomography (CT) images showed: a thrombus in the left auricle, an increase in kidney’s size besides to perirenal edema and multiple parenchymal perfusion defects of both kidneys that are related to segmental distal arterial lesions which suggest arterial thromboembolic disease. Aorta and renal arteries were permeable with no atherosclerotic plaque; the renal vein and inferior vena cava were both less permeable. Figure .
Subsequent transesophageal echocardiography confirmed the presence of a thrombus in the left atrium without valvular vegetations Figure .
We concluded that it was a bilateral renal infarction of embolic origin caused by migration of an embolus from the left atrium. In addition to analgesic, continuous IV infusion of heparin was administered at the curative dose of 18 units/kg/hour and the outcome was favorable: the abdominal pain disappeared besides to a decrease of serum creatinine to (115 μmol/ l) after 3 days. One month later, the creatinine levels declined to 95 μmol/ l so we also concluded that acute renal failure was due to the infarction.


In December of 2006, a 57-year-old man presented with severe right upper posterior chest and back pain. A chest X-ray revealed a mass in the right upper chest. A subsequent CT scan confirmed an 8 cm mass in the posterolateral right upper lobe (RUL) with destruction of the adjacent ribs and invasion into the chest wall. Moreover, there was a separate spiculated mass in the contralateral left upper lobe (LUL) measuring 11 mm. A PET/CT showed the large RUL mass with a standardized uptake value (SUV) of 14, and the LUL lesion had an SUV of 3.4. There was no significant hypermetabolism in the mediastinum and there was no evidence of distant disease.
In January 2007, he underwent a cervical mediastinoscopy and left video-assisted thoracoscopy with wedge resection of the left upper lobe lesion. The LUL pathology showed a moderately to poorly differentiated adenocarcinoma measuring 1.0 cm. All of the mediastinal lymph nodes were negative. It was unclear whether or not the LUL nodule was a separate primary or a metastatic lesion from the RUL primary mass. A brain MRI showed a 6 × 6 mm lesion in the midline pons with minimal hemorrhage and mild surrounding edema that was strongly consistent with a single metastatic lesion (see ). Therefore staging was determined to be T3N0M1, Stage IV, and it was felt that his primary disease should be treated aggressively secondary to chest wall invasion and pain and limited metastatic disease. He was started on chemoradiotherapy to the RUL primary, and Gamma Knife radiosurgery was performed the next month to target the lesion in the pons. A prescription dose of 14 Gy to the 50% isodose line was used, which resulted in 100% of the tumor receiving 15.1 Gy (see for an example of the treatment planning process). The conformality index was excellent at 1.2.
He completed 60 Gy in 30 fractions via a 3D conformal radiotherapy course with concurrent carboplatin and Taxol to the RUL and chest wall mass. In April 2007, a follow-up brain MRI showed an excellent response to the GKSRS with no residual enhancement in the pontine metastasis and no new brain lesions (see ). In May of 2007, a restaging PET/CT showed 50% reduction in the size of the RUL tumor with reduced SUV of 8, but still with significant invasion of the chest wall, yet still no evidence of distant disease. Therefore, with excellent performance status, the patient elected to undergo a right thoracotomy, right upper lobectomy, and extensive chest wall resection. The primary tumor was excised, with good margins and without complication. The tumor-infiltrated region of the chest wall was resected along with large portions of the third and fourth ribs. Pathology revealed 99% necrotic poorly differentiated nonsmall cell carcinoma with few viable cells left in the specimen.
A follow-up MRI two months later illustrated that the lesion in the mid pons was no longer visible as an enhancing lesion and that the signal intensity of the lesion had decreased significantly. However, there were two new brain metastases. One 5 mm lesion in the right cerebellum was identified, and another 6 mm lesion was seen in the frontal corticomedullary junction.
The patient desired to avoid whole-brain radiation and elected to proceed with a second Gamma Knife treatment in July 2007. The two lesions were targeted with a prescription dose of 20 Gy to the 50% isodose line. It was noted that the lesions had grown in the interim with the right cerebellar lesion now 13 mm and the frontal lesion was 14.2 mm, respectively.
An interim MRI showed good response; however an MRI in January 2008 demonstrated that the right superior frontal metastasis had increased significantly in size to 27 × 27 mm and was accompanied with increased vasogenic edema. This was consistent with either progression or pseudoprogression (radiation change). The patient elected to proceed with a stealth stereotactic craniotomy with microsurgical tumor resection. A follow-up CT of the head showed that the craniotomy removed most of the enhancing large lesion; nevertheless, some residual enhancement along the posterior rim remained.
During a followup three months later, an MRI illustrated a new enhancing focus adjacent to the anterior margin of the resected lesion and the interval increase in the surrounding vasogenic edema compatible with disease progression. The patient underwent his third Gamma Knife radiosurgery in May 2008, with a prescription dose of 18 Gy to the 50% isodose line. The follow-up MRI showed a modest response in the treated right frontal lesion. An MRI two months later showed progression of the metastatic disease in the right frontal lobe with an increased interval of nodular peripheral margin enhancement to 2.7 × 2.2 × 2.7 cm, with surrounding reactive edema. He maintained good performance status and elected to proceed with a reoperative craniotomy later in Oct 2008. The tumor bed was excised successfully, and pathology confirmed 90% necrotic metastatic carcinoma consistent with a lung primary. There was no active disease at the margins. The follow-up MRI confirmed the absence of residual enhancement.
The patient was still adamantly against whole brain radiation or even a more limited fractionated radiotherapy course. Due to the extensively resilient nature of his local brain disease in the right frontal lobe, the patient opted to complete a final Gamma Knife radiosurgery to the resection margin in November 2008. The previously treated cerebellar tumor was seen as a tiny enhancing lesion on the planning MRI scan, which was not seen on previous scans. It was treated with 9 Gy to the 50% isodose line (16.8 Gy marginal dose). The right frontal resection bed was treated to 15 Gy to the 50% isodose line.
Subsequent MRIs have shown steady response and no definite evidence of disease. Currently he has no evidence of systemic or intracranial disease. He tolerated all the treatments remarkably well.
He denies any significant problems, although he states that he has some difficulty with memory problems. He has no neurologic problems and no headaches. The patient has made a remarkable recovery and has toiled his way through a potentially fatal prognosis to become a long-term survivor. He is leading a normal active life at this point; in fact, he recently completed construction on his own new home.


A 51-year-old-male with history of deceased donor renal transplant, who 2 weeks prior to presentation was treated for acute cellular and humoral rejection, presented with fever, polyarthralgia, and swelling. His past renal history included end-stage renal disease from unclear etiology, a living-related renal transplant that he rejected within a week, a deceased donor renal transplant a year later, and hypertension. His other medical issues included hyperlipidemia, gout, and hypothyroidism. His treatment two weeks prior for his cellular and humoral rejection consisted of Methylprednisone 500 mg intravenous (IV) × 3 doses, plasmapheresis × 4 treatments, intravenous immunoglobulin (IVIG) 1 gram per kilogram per day × 2 doses, Rituximab 375 mg/m2 × 1 dose, and Thymoglobulin 1.5 mg/kg × 5 doses.
On presentation, he reported arthralgias which started in the right knee and were subsequently followed by arthralgias in the left shoulder and left wrist. He had a fever of 101.1°F (38.4°C), his left wrist was swollen on exam, and his right knee was tender with an effusion. The rest of the vitals and physical exam were unremarkable. Laboratory studies showed white cell count (WBC) of 7.9 × 10 E3, hemoglobin 9.7 g/dl, hematocrit 29%, platelets 157 × 10 E3, sodium 136 meq/l, potassium 4.2 meq/l, chloride 105 meq/l, carbon dioxide 21 meq/l, blood urea nitrogen (BUN) 41 mg/dl, serum creatinine (Scr) 1.8 mg/dl (baseline 1.7 mg/dl), total protein 6.7 g/dl, albumin 2.2 g/dl, AST 27 Unit/L, ALT 71 Unit/L, creatinine kinase 119 Unit/L, and uric acid 5 mg/dl. His wrist X-rays did not show any abnormalities, whereas his knee X-rays indicated a mild joint effusion of the right knee. Joint aspiration of the right knee showed total nucleated cells of 830 with neutrophils 62%, lymphocytes 0%, monocytes 38%, and no crystals were seen by polarized microscopy.
Given his hemodynamic stability, he was not started on empiric antibiotics; however, extensive workup was sent to rule out bacterial and viral infections. All of the evaluated viral serologies were negative and included Epstein-Barr-Virus (EBV), Cytomegalovirus (CMV), BK Virus (BKV), and Parvovirus B19 (). Rheumatologic workup showed low complement C3 and C4, and elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), haptoglobin, and lactate dehydrogenase (LDH) ().
In light of his recent treatment with Thymoglobulin and Rituximab, presenting symptoms, and negative infectious workup (), a presumptive diagnosis of serum sickness was made. His serum sickness was thought most likely secondary to Thymoglobulin but Rituximab was also high on differential, as delineated further in this paper. Heterologous antibodies were noted to be positive against rabbit IgG and IgM, low positive against horse IgG, and negative for mouse IgG (). Therapeutic plasma exchange (TPE) and corticosteroids are treatment options for Thymoglobulin-associated serum sickness; however, serum sickness from Rituximab has only been shown to be treated with corticosteroids. Given uncertain cause of his serum sickness, we started our patient on high dose Methylprednisone 500 milligrams IV per day for three days. He had complete resolution of polyarthralgia and swelling after the third dose of Methylprednisone.
During his hospitalization and treatment for his serum sickness, he developed acute kidney injury (AKI). A day after his third dose of Methylprednisone, his Scr peaked at 2.8 mg/dl from an initial baseline of 1.7 mg /dl (). His urinalysis was negative for infection, and urine microscopy showed granular and muddy brown casts consistent with acute tubular necrosis (ATN). Thus, his dose of furosemide was decreased to 20 milligrams from 40 milligram by mouth twice a day, and he was encouraged to drink more fluids. His renal function began improving on day no. 2 after-treatment with Methylprednisone, and Scr retuned back to his baseline of 1.7 mg/dl on day no. 6 after-treatment with Methylprednisone.


A 29-year-old female patient with the chief complaint of intermittent dull pain in right maxillary central incisor was referred for RCT. Her medical history was non-contributory. She had undergone orthodontic treatment during last three years. On clinical examination, right maxillary central incisor did not exhibit any morphological variation. There was absence of dental caries, periodontal probing and mobility was within physiologic limits. Generalized spacing was present between the dentition and right maxillary incisor exhibited a mild distal rotation. The tooth did not respond to both electric (Parkell Electronics, Farmingdale, USA) and thermal pulp testing. Hence a provisional diagnosis of pulpal necrosis was made.
Preoperative radiograph revealed the presence of a single root with external apical root resorption in right maxillary central incisor with receded pulp chamber (). A faint radiolucent line was observed in both the right and left central incisors in addition to the main canal on the radiograph. Hence presence of an additional root canal in both the incisors was suspected. Multiple angulated radiographs were taken to confirm the presence of extra canals.
Access opening was performed under rubber dam isolation. The main canal was located and the access was further modified to locate the additional canal. Using a surgical operating microscope (Seiler Revelation, St. Louis, MO, USA) under ×3 magnification the additional canal was located distolabial to the main canal ().
Radiographic working length was determined using ISO 0.02 taper K-files (). The orifice was enlarged to #3 Gates Glidden drill (Dentsply, Ballaigues, Switzerland) in the main canal and with #2 in the additional canal. The canal was cleaned and shaped with K-files (Dentsply, Ballaigues, Switzerland) using step back technique. Canals were irrigated with 2.5% NaOCl, 17% EDTA (Prime Dental Products Pvt. Ltd, India) and saline. Calcium hydroxide (Vitapex, J. Morita, Tokyo, Japan) was placed as an intracanal medicament using lentulo spiral (Dentsply, Ballaigues, Switzerland) and the access was sealed with Cavit (ESPE America, Norristown, PA, USA).
The patient was recalled after three weeks and was found to be asymptomatic. The medicament was changed and the patient was kept under observation for three more weeks. In the subsequent visit, calcium hydroxide was retrieved using ultrasonics (Satelec, P5XS, Aceton euipments, NA, USA) and the canals were rinsed with saline and dried using absorbent paper points. Canals were Obturated with gutta- percha (Dentsply Ballaigues, Switzerland) using cold lateral compaction technique with AH plus resin sealer (Maillefer, Konstanz, Germany) and access cavity was restored with composite resin Filtek Z250 (3M Dental Products, St Paul, MN, USA). Patient was asymptomatic during the 1year follow-up period ().


We present the case of a 38-year-old man with end-stage renal disease secondary to diabetes mellitus type 1 on CAPD for 18 months and on APD for 40 months. The patient, who had no previously reported episode of PD-related bacterial peritonitis, was admitted to our department with a 2-day history of emesis, cloudy peritoneal dialysate, and abdominal pain in the upper abdomen as well as diarrhea. On admittance, he was afebrile and normotensive with a blood pressure of 125/85mmHg; his pulse was regular but tachycardic at 143 beats per minute. There was no abdominal tenderness. The PD catheter exit site was clean. An electrocardiogram (ECG) showed sinus tachycardia with a rate 143 beats per minute, but no signs of myocardial ischemia were seen. The complete blood count showed white blood cells of 14.6 cells/mm3 with 83% segmented neutrophils, 1% unsegmented neutrophils, 7% lymphocytes, 7% monocytes, and 2% eosinophils; hematocrit 33%; and platelets of 313 × 103/μL. C-reactive protein was 138mg/L and procalcitonin was 1.1ng/mL. The first dialysate leukocyte count was 1055/μL with 93% segmented neutrophils, 3% lymphocytes and 4% monocytes. The usual PD-related peritonitis was suspected and after sending the first PD effluent for culture to the laboratory, we started treatment with antibiotics according to hospital protocol: intra-peritoneal cefazoline and ceftazidime. The Gram stain of the first effluent was negative. The second Gram stain of the PD effluent 3 days after admittance was also negative. The exit site culture and coproculture were negative. The abdominal X-ray and abdominal ultrasound (US) were unrevealing. After 3 days of antibiotic therapy the clinical status of the patient did not improve. Furthermore, abdominal tenderness in the epigastrium and the upper right quadrant, inappetence and anuria, appeared. The patient was switched to hemodialysis using a central venous catheter in the vena jugularis interna. On the sixth day after admission the patient complained, for the first time, about pain in his left arm; his ECG was without signs of ischemia, and his troponin T was slightly elevated (0.19μg/L). On the seventh day after admission we decided to remove the peritoneal catheter in a surgical procedure under general anesthesia. The dialysate leukocyte count just before the operation was 4385/μL with 99% segmented neutrophils. After the surgical procedure the patient was treated with intravenous vancomycin and ceftazidime, but over the next few days his clinical situation was no better (severe abdominal pain with nausea and vomiting). On the 11th day the patient complained of pain in both arms; on the ECG signs of ischemia (T-wave inversion in inferior leads) were found. The troponin T on the same day was 1.13μg/L (Figure shows the enzymatic curve) and non-ST elevation myocardial infarction was suspected. Regarding this clinical condition a cardiologist was consulted about a coronarography and an abdominal surgeon about a relaparotomy. On the same day a decision was made for surgery to be carried out. Surgeons performed an explorative laparotomy and found diffuse peritonitis and gangrenous appendicitis. An appendectomy was performed. The patient was admitted to the intensive care unit. Mechanical ventilation support was needed. The next day on an ECG ST elevation in the anterior wall was present, and troponin T was 6.22μg/L; the echocardiography showed hypokinetic anteroapical wall of the left ventricle, the ejection fraction was 40%. The patient was treated with vasopressors, intravascular antibiotics and antimycotic therapy with vancomycin, imipenem-cilastatin and fluconazole. On the 15th day of admission paralytic ileus appeared. A relaparotomy and an ileostomy were performed. After this operation the patient improved. He was extubated, lucid and talking. On the 17th day of admission the patient became worse again, he was hypotensive, in shock, and between vomiting he aspirated. On the 19th day of hospitalization bradycardia developed and cardiopulmonary resuscitation was performed. On the 20th day of admission the patient died of septic-toxic shock and multisystem failure.


An obese (BMI 27), 24 y.o. female had a high tibial osteotomie (HTO) due to a varus deformity and medial knee chondromalacia. One year postoperatively, the patient elected to undergo implant removal as a result of discomfort over the medial knee joint line and anterior knee pain on extension. At arthroscopy a pathological plica in the knee was resected, before the plate was removed arthroscopic-assisted (Figures , and ). The Lysholm score improved from 62 preoperative to 78 postoperatively at the 1-year-follow-up visit.


A 29-year-old male patient with no significant medical or surgical past history presented to our emergency room (ER) with complaints of gradually progressive abdominal pain of two-week duration associated with recent development of nausea and vomiting. Abdominal pain was located in epigastrium, intermittent, 6/10 in severity, nonradiating, and was dull in nature. Patient also stated that he took some unknown over-the-counter antacid to relieve the pain but it did not help. Patient also complained of nausea and vomiting which started after his moderate alcohol intake 2 days ago. Patient denied taking any other medications. He also denied any history of trauma. Physical examination was negative except for presence of tenderness in epigastric area. Laboratory exam was completely normal including amylase and lipase levels (). A diagnosis of alcoholic gastritis was made and patient was discharged from ER with a proton pump inhibitor.
This patient again came to ER after about 72 hours with complaints of increased abdominal pain and intractable nausea and vomiting. On examination patient had generalized abdominal fullness and tenderness. Bowel sounds were sluggish on auscultation. Rectal examination was normal with stool negative for occult blood. Laboratory examination was abnormal with elevated levels of amylase and lipase. Laboratory examinations for day 1 and day 2 of presentation to ER are elaborated in .
Ultrasonogram of the abdomen demonstrated a 3.5 × 3 cm heterogenous, well-defined lesion anterior to the right kidney in the location of second part of duodenum (). This lesion failed to show any vascularity on Doppler sonogram. Computed tomography (CT) scan of abdomen without intravenous (IV) contrast showed a circumferential hyperdense lesion in the wall of the second part of duodenum with no definite mass with presence of minimal peripancreatic fat stranding. There was associated gastric outlet obstruction (). CT scan with IV contrast could not be performed as patient had acute renal failure at the time of presentation.
Patient was started on nil per oral and aggressive hydration therapy. Continuous gastric suction was performed by using a nasogastric tube. Laboratory blood tests were monitored at regular intervals and significant elevations in lipase, amylase, BUN, creatinine, and WBC were observed initially which started to trend down later. A graph depicting the levels of lipase is shown (). Serial abdominal CT scans without IV contrast were done (Total 3) and patient was managed symptomatically. Patient's hematoma slowly started to regress and pancreatic enzymes levels came down. Patient was admitted in the hospital for total of 12 days. His hematoma completely resolved at the time of discharge and he was completely asymptomatic.


A 30 year old female with a non-contributory medical history was referred to our private office with severe spontaneous pain and tenderness to percussion in the right mandibular region. The patient reported that the tooth #30 had been root treated one month ago. She had experienced localized swelling and pain since then.
Clinical examination revealed extensive amalgam restoration in the mandibular molar; however no swelling or sinus tract was present. Tooth #30 was sensitive to palpation and percussion. There was no mobility and probing did not reveal the presence of a periodontal pocket. The adjacent teeth responded normally to thermal and electrical pulp testing, and to palpation, and percussion.
Radiographic examination revealed a large radiolucency associated with the mesial root of tooth #30 (). A diagnosis of secondary or exacerbating apical periodontitis associated with incomplete root canal treatment was made. Therefore, endodontic re-treatment was indicated.
Local anesthesia with inferior alveolar nerve block using lidocaine (Daroupakhsh, Iran) was performed. After removing the coronal filling material and carious tooth structure, a prefabricated post was removed from the distal root. The tooth was isolated with a rubber dam and an adequately sized access cavity preparation was created. The floor of the pulp chamber was explored under magnification and illumination with the aid of a HEINE 2.5× HR Binocular Loupe and 3S LED HeadLight® (HEINE Optotechnik GmbH & Co. Herrsching, Germany). Two mesial and two distal root canal orifices had been inadequately treated during the first root canal treatment. Root filling materials were removed from the root canals with the aid of hand and rotary files. The unusually wide space between the two mesial orifices clinically and the radiographic appearance of the root canals indicated possible additional canal(s) in the mesial root. Moreover, during exploration of the groove with a sharp explorer and file, a sticky groove was felt. Two additional canals were located between the two previously discovered mesial orifices (). The working lengths of the root canals were determined using an electronic apex locator (ProPex™, Dentsply Maillefer, Montigny le Bretonneux, Switzerland) and were then confirmed with a digital radiography (Kodak RVG 5100 Digital Radiography System, Eastman Kodak Co., Trophy Radiology, Marne-la-Vallée, France). Root canal instrumentation was performed with ProTaper series Ni-Ti instruments (Dentsply Maillefer, Ballaigues, Switzerland) and EDTA gel (MD-ChelCream, Meta Biomed Co., Ltd., Cheongju City, Chungbuk, Korea). The root canals were irrigated with 2.5% sodium hypochlorite during instrumentation. Afterwards, the root canals were dressed with calcium hydroxide paste (Calcipex II, NISHIKA, Shimonoseki, Japan) and coronally sealed with a temporary filling material (Zonalin, Kemdent, UK).
At the next appointment (after 10 days), the tooth was asymptomatic. After completion of the chemomechanical preparation and radiographs with gutta-percha master cones (, ), the root canals were dried with paper points and obturated with laterally compacted gutta-percha (Meta Biomed Co., Ltd., Cheongju City, Chungbuk, Korea) and AH26 sealer (Dentsply, DeTrey, Konstanz, Germany) (, ). Coronal access was restored with a temporary filling material (Zonalin, Kemdent, UK) and the patient referred to another dentist for a coronal restoration and completion of the treatment.
At the 3-months follow up examination, tooth #30 was functional and asymptomatic, with no clinical signs. There was radiographic evidence of periapical osseous healing (). Further follow up examinations were recommended for evaluation of treatment outcome.


We report the case of a 49-year-old homosexual male being treated for AIDS who presented with worsening neck pain and left distal arm and hand weakness. MRI demonstrated an erosive mass within the C4 vertebral body extending through the pedicle on the left side and causing severe spinal stenosis (Figures and ). Additionally, multiple cervical spine vertebral bodies were involved in this pathological process with the fourth cervical body being the most remarkable. PET scan, CT scan of chest/abdomen/pelvis, prior recent colonoscopy, and upper endoscopy were all performed demonstrating no obvious source. No other lesions were noted elsewhere.
Patient underwent needle biopsy followed by anterior cervical corpectomy and fusion and finally posterior lateral mass instrumentation and fusion (). Pathological examination demonstrated metastatic adenocarcinoma composed of infiltrating glands and focal sheets of moderately differentiated tumor (). Immunohistochemical staining with appropriate controls shows that the tumor cells are positive for cytokeratin 7, cytokeratin 20, and CDX-2 and are negative for TTF-1 and napsin. The morphologic and immunohistochemical findings are most consistent with tumor origin from a gastrointestinal primary tumor, in particular from an upper gastrointestinal or pancreaticobiliary primary tumor.
The patient was successfully treated for post-operative cerebrospinal fluid collection in the neck with a lumbar drain. His neurological examination returned to its baseline. His CD4 counts remained stable preoperatively and postoperatively. He is currently undergoing palliative radiotherapy with 37.5 Gy over 15 fractions to his cervical spine.


A 39-year-old, G0, Hispanic woman presented with a mass in her right breast. The patient denied the use of hormone replacement therapy, birth control pills, or substance abuse in the past. She had never conceived naturally, had failed in vitro fertilization, and had never breast-fed. No family history of breast, ovarian, uterine, or colon carcinoma was present. An axillary ultrasound revealed an enlarged abnormal axillary lymph node. An ultrasound-guided core needle biopsy of the breast mass revealed a moderately differentiated infiltrating duct carcinoma.
The patient opted for a simple mastectomy of the right breast, and right axillary sentinel lymph node sampling was performed. The final pathology revealed a 2.2 cm, grade 2, hormone receptor positive, Her2/neu negative, infiltrating duct carcinoma (), with associated grade 2 in situ carcinoma and negative margins. One of 5 sentinel lymph nodes showed a 0.5 cm metastatic tumor deposit with extracapsular extension (). She received systemic chemotherapy after surgery.
In addition to invasive and in situ breast carcinoma, the breast tissue showed proliferative fibrocystic changes as well as lactational changes. In areas of lactational change, focal dilated glands contained intraluminal, acellular structures with equally spaced radial striations; these were identified as Liesegang rings ().


A 71-year-old Caucasian male presented with the New York Heart Association (NYHA) class III heart failure managed with HeartMate II LVAD as destination therapy and implantable cardioverter defibrillator (ICD). Following right renal colic, the patient underwent intravenous pyelogram at an outside institution which demonstrated right renal pelvic stones (). During ureteroscopic laser lithotripsy, multiple lesions were discovered in his right renal pelvis. Biopsy revealed high-grade urothelial carcinoma. The patient was then referred to our institution 9 months following his cancer diagnosis for further management. CT abdomen was performed and showed multiple filling defects in the right renal pelvis, enlarged retroperitoneal lymph nodes, incidental 4.9 cm abdominal aortic aneurysm, and no evidence of tumor metastases (). The aneurysm was asymptomatic and did not meet size criteria for a prophylactic repair.
Medical history includes atrial fibrillation, hypertension, hyperlipidemia, and diverticular disease. Surgical history includes bilateral open nephrolithotomy, repair of bilateral inguinal hernia, and cataract surgery.
The patient was counseled regarding management options for TCC. Being a high surgical risk, he was offered minimally invasive endoscopic laser resection; however he elected to undergo nephroureterectomy with bladder cuff excision. A conference was held with a team of cardiac anesthesiologist, cardiologist, perfusionist, and the managing urologist. Hemodynamic effects of pneumoperitoneum and risks of surgery were discussed. We detailed to the patient the risks of the periprocedural complications. After informed consent, RANU with bladder cuff excision and retroperitoneal lymph node dissection was planned. We thought the robotic approach may help minimize blood loss and expedite recovery.


A 53-years-old woman otherwise previously healthy and a non-smoker, was diagnosed with lung adenocarcinoma, stage IV T 3 Nx M1a (TNM classification 7th edition) on April 2009.
On March 2009, she presented with functional class III dyspnea. A Chest X-ray showed veiling in the left side of the thorax. CAT scans were performed, and a solid lung mass in the left lower lobe, associated with pleural effusion and moderate lung collapse was seen contralateral pleural effusion was also evidenced.
Bronchoscopy showed extrinsic compression of the left lower lobe bronchus. Pleural biopsy by thoracoscopy, and pleurodesis with sclerosing agents were performed (talc).
Histological examination of the pleura revealed a proliferation of epithelial-like atypical cells arranged in glands, nests, and cords with moderate anisocytosis, anisokaryosis, macronucleoli, and scattered mitoses. Pleural fluid was positive for neoplastic cells.
Immunostaining techniques were performed against the following antigens: cytokeratin 7, cytokeratin 20, calrretinina, chromogranin, and TTF, which were positive for cytokeratin 7 and TTF. These morphological findings are related to moderately differentiated adenocarcinoma of pulmonary etiology. Cobas EGFR test was non-mutated.
First line chemotherapy with carboplatin AUC 6 + paclitaxel 200 mg/m2 + bevacizumab 15 mg/kg every 21 days was started on May 2009. The patient received six cycles, and this regimen finished in September 2009. Tumor assessment showed partial response (RECIST). Maintenance therapy with bevacizumab 15 mg/kg + pemetrexed 500 mg/m2 every 21 days was administered no significant toxicity was associated with these regimens. Bevacizumab was discontinued in February 2010 and the patient was included in a compassionate program including Racotumomab. Pemetrexed was administered together with immunotherapy, and the patient is still on treatment. Partial response was maintained (Figure ). As for toxicity associated with the investigational regimen the patient exhibited a reaction at the site of injection of the vaccine grade 2. Adverse events related to pemetrexed were not different from expected, asthenia grade 2.


A 46-year-old Caucasian non-Jewish nonobese male was admitted to the hospital, because of a new onset headache, nausea, and vomiting. His past medical history is significant for the PC diagnosed 3 months ago after work up of vague abdominal discomfort. The upper gastrointestinal endoscopy was performed at that time and showed few small polyps (nonneoplastic polyps) and mild gastritis. Abdominal CT and ultrasound were done, which showed PC with metastases to the liver and omentum. A biopsy was done which showed pancreatic ductal adenocarcinoma.
The patient's prior hospital stay was complicated by the development of a pulmonary embolism and small bowel obstruction. It is relevant to note, that the patient never had any mucocutaneous hyperpigmentation, which could be suggestive of Peutz-Jeghers syndrome. The patient received treatment with oxaplatin, 5-fluorouracil, irinotecan, and leucovorin as a chemotherapy for his PC.
During this encounter, the patient described his headache as dull, intractable, and nonradiating. The patient denied fever, skin rash, any history of sick contacts, recent falls, but admitted that he hit his head in the bathroom 1 week prior. The patient denied any history of smoking, alcohol abuse, or use of recreational drugs. It is necessary to note that the patient was discharged from the hospital 8 days prior this admission.
Family history is significant for colon cancer in his father who was diagnosed at age of 80 and as well as other malignancies on his paternal side (the patient does not remember exactly the relatives affected or the types of cancer). The patient underwent genetic screening for the mutations associated with Lynch syndrome, which were negative (PMS2 sequencing rearrangement, EPCAM rearrangement, MLH1 rearrangement, MSH2 rearrangement, and MSH6 rearrangement analyses).
On a physical exam, the patient was in moderate to severe distress due to pain and malnourished. His eyes were icteric, equal, and reactive to light and accommodation, with intact extraocular muscles. Fundoscopic exam did not find any retinal abnormality or optic disc swelling. Neck was supple, without palpable thyromegaly and lymphadenopathy. Pulmonary exam was remarkable with decreased air entry at bases bilaterally and respiratory rate of 17 in a minute. Cardiovascular exam showed tachycardic rate with regular rhythm, normal S1/S2, and blood pressure of 116/76. Cranial nerves were grossly normal; muscle strength was decreased diffusely with intact sensation.
CBC, CMP, urinalysis, and head CT were ordered. His CBC and CMP were unremarkable from the last hospital stay (anemia of chronic disease, mild hyponatremia, and mild increase in alkaline phosphatase).
CT scan of the head was done which showed acute bihemispheric subdural hematomas with the maximum dimension of 2 centimeters () and neurosurgical consult was obtained, with no surgical intervention being recommended. The patient was started on ondansentron, metoclopramide, and dexamethasone. On the second hospital day, the patient developed syncope, with a generalized tonic-clonic seizure. A repeat CT scan of the head was done, which did not show any new or worsening hematoma. Brain MRI with and without contrast was done, which showed left hemispheric extra-axial heterogeneously enhancing lesions consisting with metastatic disease with the greatest lesion was 4 centimeters in dimension (). The patient was started on levetiracetam. The cranial irradiation was started on the third hospital day for 18 sessions with right and lateral fields were exposed to a dose of 37.5 gray in 15 fractions of 250 eGy utilizing 6 MV photons. The patient's headache and nausea significantly improved, and he did not experience any new seizures since then.
Important to note that patient tolerated radiotherapy well and did not require a treatment break.
The patient died 2.5 months later at home. No autopsy was performed as per family request.


A 70-year-old woman with degenerative lumbar scoliosis suffering severe low back pain and neurogenic claudication, aggravated during ambulation, underwent decompressive laminectomy at L4-L5 and posterolateral fusion with a reasonably good result. Four years later, her condition had worsened including neurogenic claudication and low back pain. Her primary care doctor referred her to our service as a new patient. At this point, the x-ray (Figure
) and MRI showed a left lumbar curve with a 34ª Cobb angle between T11 and L4, anterolateral lysthesis at L2-L3-L4-L5 and central and subarticular lateral recess stenosis. We used titanium 5.5 mm fenestrated pedicular screws (Expedium, DePuy Spine, Raynham, MA, USA) on both sides at each level from T10 to S1 and an iliac screw in the right side (Figure
), augmented with cement at T10, T11, L1, L5 and S1 (Confidence Spinal Cement System, DePuy Spine, Raynham, MA, USA) and prophylactic vertebroplasty at T9 to avoid the “topping-off syndrome”. There were no intraoperative pedicular fractures and special care was taken to preserve the structures of the tension band (posterior ligaments, facet joints, multifidi muscles) in the segment above the instrumentation.
The patient had a torpid postoperative recovery, complaining of pain in the thoracolumbar area, but her ability to perform different physical activities increased daily. The x-ray on day 3 post-surgery showed no abnormal finding. She was discharged walking 8 days after surgery.
One month after discharge, without recognizable inciting trauma, the patient complained of increasing spontaneous pain in the lower thoracic area and neurological impairment in the lower limbs. Physical examination revealed tenderness in the lower thoracic spine without a palpable defect between the posterior spinous processes. Neurological examination was abnormal without associated injuries. The motor exam revealed an overall decrease in lower limbs muscle strength (2/5 on the left leg, and 3/5 on the right leg) with inability to walk, and response in the patellar and Achilles reflexes was increased, Babinsky reflex was positive on both sides and abnormal bladder and bowel function were reported.
The initial supine radiographs showed a slight junctional kyphosis but no indications of vertebral fracture. CT scan (Figure
) and MRI (Figure
) demonstrated a collapse and wedging of the T10 vertebral body and a distraction pattern injury at the upper edge of the screw in the T10 pedicles, rupture of the posterior elements at T9-T10 with a high signal intensity consistent with hemorrhage and edema and subluxation at the cranial level. Abnormal intracanal tissue was noted compressing the spinal cord.
With the confirmation of a T10 vertebral compression fracture with subluxation of the adjacent level and neurological impairment, the authors performed posterior decompression at T9-T10 and extended posterolateral arthrodesis (Figure
) from T2 to T10 using bilateral pedicular screws augmented with cement at T2,T3,T4,T5 and T6, and non-cemented screws at T8 (Expedium-Confidence Spinal Cement System, DePuy Spine, Raynham, MA, USA). Samples of the intracanal tissue were obtained for histological study, which reported a ring of fibrous and vascular tissue compatible with soft fracture repairing callus.
The patient had prompt improvement in back pain and was mobilized routinely. At 3 months follow-up, she was able to walk without pain and the neurological exploration was normal.


A65-year-old otherwise healthy male patient presented to clinic with a sensation of discomfort in his left cheek. His past history is significant for left radical nephrectomyperformed 19 years earlier for clear cell renal cellcarcinomawithrenalveinthrombosis (pT3aN0M0), and there were no other sites of disease evident upon current presentation. Computed Tomography scan detected a 10 mm × 8 mm mass suggestive of malignant lesion in theleftbuccalmucosa () which was then surgically removed. Pathological examination showed metastaticclear cell renal cell carcinoma with clear excision margins. After 6 years of clinical followup and serial radiological controls, the patient showed no signs of local recurrence or new metastatic lesions.


A 26 year old Asian American man with no significant past medical history presented to his primary care provider for mid back pain of three months duration. The pain was sharp, 5/10 in intensity, intermittent, and left sided radicular in nature localizing to the T5 dermatome and partially-relieved by NSAIDs. The physical and neurological exams were unremarkable. The patient had no HIV, Lyme, or tuberculosis risk factors, and denies recent illnesses or infections. He was asked to continue to take NSAIDs for the pain and undergo MRI of the cervical, thoracic, and lumbar spine without contrast to rule out structural disease and look for evidence of radiculopathy.
The patient underwent 3T MRI at a tertiary medical center in a traditional closed scanner. The patient was provided with ear plugs. During the lumbar portion of the scan, the patient became acutely agitated, felt extremely hot, tachypneic, tachycardic with palpitations, intense anxiety and feeling of impending doom, and acute vertigo. He heard very loud noises and areas of intense heat over his external body. He thought he would sustain serious injury to his body by the MRI scanner. The scan was aborted and the patient was unsteady on his feet momentarily afterwards. He appeared frightened. As the patient had no history of claustrophobia or anxiety disorder, he was not premedicated with benzodiazepines. The cervical and thoracic spine MRI were unremarkable, and lumbar spine incomplete and no interpretation could be made.
Over the next two to four weeks, the mid back pain resolved. However, over the next three months, the patient developed increased arousal (difficulty sleeping and hypervigilance) and flashbacks of the MRI encounter with recurrence of symptoms (fear, tachypneic, tachycardia with palpitations, dizziness, and anxiety). He would feel as if the traumatic event was recurring. Moreover, he avoided further MRI scans, loud repetitive noises as experienced in the MR scanner, and reminders of the scan. He experienced difficulty falling asleep and concentrating.
He presented three months after the MRI. The structural clinical interview for DSM-IV (SCID) confirmed the diagnosis of PTSD. Specifically, the patient’s constellation of symptoms, duration (longer than one month), and impairment of psychosocial functioning met PTSD criteria. The top differential diagnoses were panic attack and panic disorder. Careful history taking did not reveal any past evidence of panic attack or other anxiety disorders. There were no other significant traumatic events or abuse. Although PTSD can result from panic, it is often less severe than prototypical external traumas such as rape or combat
[]. The temporal association of the external traumatic event with onset of hyperarousal, intrusions, and avoidance symptoms favors PTSD.
The patient refused pharmacological therapy and no further workup for his transient radicular pain was initiated.


The patient, a 48-year old man, was hospitalized for progressive left-sided hearing loss for 3 years. Upon examination, he had left-sided hearing loss. He also had an abnormal finger-nose pointing test, an abnormal rapid alternating movement, and a heel-knee-shin ataxia on the left side. He did not present with facial palsy and had normal muscle tone in the extremities. Magnetic resonance imaging (MRI) of the brain showed a round mass with a size of 5.42 × 4.27 × 5.35 cm in the left CPA region. The lesion was hypointense in the T1-weighted imaging (T1WI) and unevenly hyperintense in the T2-weighted imaging (T2WI). Heterogeneous enhancement in the tumor was observed in the contrast-enhanced MRI. The left cerebellum, the fourth ventricle, and the brain stem were compressed (Figure ). Computerized tomography angiography (CTA) of the head revealed a high-density, patchy calcification shadow on the left CPA region. The lesion had a clear boundary with the intracranial vessels, and no intracranial artery malformation was observed. The tumor was not stained on the CTA image (Figure ). Based on the clinical symptoms and signs, as well as the MRI and CTA findings, the patient was diagnosed with calcified VS.
The patient underwent a left retrosigmoid suboccipital craniotomy and total excision of the tumor with preservation of the facial nerve. The tumor, with a complete capsule originating from the internal auditory canal, was highly vascularized. It was yellow-grayish in color, and soft and brittle in texture. The tumor was cystic in the center and calcified in the periphery. After surgery, the patient had mild facial palsy and no improvement in left-sided hearing. At 1 week post surgery, the patient underwent a computerized tomography (CT) scan and MRI, which showed that the tumor was completely removed (Figure ). The histopathology of the tumor was suggestive of schwannoma. Hematoxylin and eosin (H & E) staining showed strongly stained nuclei and interstitial hyaline degeneration. In addition, a large patchy calcification was observed (Figure ). The patient had complete loss of left-sided hearing and an improvement in the facial palsy at the 6-month postoperative follow-up appointment.


A developmentally normal 6-year-old boy was admitted to our hospital for evaluation of lower abdominal pain on the right side. Physical examination revealed a hard and well-demarcated mass. Routine laboratory tests were normal. Subsequently, an abdominal CT was performed using a GE LightSpeed scanner (GE Medical Systems, Milwaukee, WI, USA), with parameters of 120 kV and 180 mA. This revealed a mildly lobulated, well-defined homogeneous soft-tissue mass, 5.0 × 5.7 × 6.7 cm in size, in the right lower abdominal cavity, and there was no evidence of pelvic lymphadenopathy (Figure
). The lesion had a density of 41 HU (Hounsfield units); it had no hemorrhagic, necrotic, or cystic components. Following infusion of a contrast agent, the tumor demonstrated marked homogeneous enhancement, and a density of 81 HU. Laparotomy revealed a tan-colored mass arising from the mesoappendix, without adhesions to the appendix or other organs and structures (Figure
). Macroscopically, the mass was well-circumscribed, with an incomplete capsule, and all margins were negative. Microscopically, the tumor consisted of proliferating spindle cells and epithelioid cells. Mitotic figures were noted in 12 of 50 high-power fields. Immunohistochemical staining revealed that the tumor was diffusely and strongly positive for c-Kit (CD117) (Figure
), myeloid stem cell antigen (CD34), DOG1, and Ki-67, slightly positive for vimentin, and negative for smooth muscle actin (SMA), neuron-specific enolase (NSE), S-100, and desmin. Based on these morphological and immunohistochemical findings, the final pathological diagnosis was that of a malignant gastrointestinal stromal tumor of the mesoappendix. The patient was treated by administration of Glevec as an adjuvant postoperative chemotherapy and has been living disease-free for 9 months of follow-up.


A 42-year-old man was referred due to a 1-month history of redness, ocular pain, and blurred vision in both eyes. His past medical history included acute otitis media complicated with bacterial pneumonia 1 year previous. He later presented with renal failure and arterial hypertension. He also had had diabetes for the past 10 years.
Ophthalmic examination revealed a visual acuity of 20/50 OD and 20/80 OS. There was an immovable, tender, inflamed scleral nodule on the temporal side of the sclera of the right eye associated with diffuse superior scleral inflammation and thinning of the cornea at IX meridian (Fig. ). In the left eye, there were two nodules in the temporal and superior sclera associated with diffuse scleral inflammation (Fig. ). The anterior chamber was deep with 0.5+ cells (Standardization of Uveitis Nomenclature Working Group []) in the OD and no cells in OS. The rest of the examination was normal. The diagnosis of bilateral nodular scleritis and sclerokeratitis in OD was made; because of the clinical and systemic findings, Wegener's granulomatosis was considered, and high-dose steroid treatment was begun after infectious causes were ruled out.
Laboratory tests included a complete blood count, an erythrocyte sedimentation rate, antinuclear antibodies, liver enzymes, c-ANCA and p-ANCA, CRP, urinalysis, chest x-ray, thoracic CT, VDRL, a fluorescent treponemal antibody absorption test, and a purified protein derivative skin test for tuberculosis. Serum urea nitrogen was 94 mg/dl and serum creatinine was 2.7 mg/dl; antinuclear antibodies were found to be 1:20 and were considered negative. The rest of the laboratory assessment was negative.
Kidney biopsy was performed because both antineutrophil cytoplasmic antibodies (c- and p-ANCA) and antibodies to proteinase-3 and myeloperoxidase were negative, and thoracic CT abnormalities were not found. Pathologic findings consisted of an adequate kidney biopsy (28 glomeruli) with 53 % global glomerulosclerosis, moderate tubular atrophy, and moderate interstitial fibrosis. The rest of the glomeruli showed diffuse proliferative mesangial hypercellularity with an increase of the mesangial matrix. The biopsy did not show endocapillary hypercellularity, crescents, segmental sclerosis, glomerulitis, vasculitis, or necrosis. Glomerular basal membrane thickness was normal. Immunofluorescence demonstrated granular deposits of IgA in a mesangial pattern with strong intensity (4 out of 4 points). Glomerular staining for IgG, IgM, lambda with less intensity (2 out of 4 points), and kappa predominance (3 out of 4 points) were also found. Others markers such as C1q, C3c, C4c, fibrin, and albumin were negative (Fig. ).
After one monthly pulse of IV cyclophosphamide therapy, the scleral nodules resolved completely, and there was development of mild scleral thinning. At 2 years of follow-up with azathioprine, there are no recurrences, and mild renal failure is stable.