A 39-year-old male construction worker was admitted to the emergency department of West China Hospital of Sichuan University 3 hours after falling from a second floor and landing ventrally on a clump of iron rods. Four metallic bars (1.5 cm in diameter) jabbed into his body at right anterior chest wall, left supraclavicular region, right temporoparietal region, and left temporal site, respectively. In addition to the impalement injuries, the patient also suffered from a left-hand dyskinesia, which was proved to be a distal radius comminuted fracture by X-rays. Bystanders cut the iron rods from the ground as gently as possible to prevent movement of the metallic bars within his body as instructed by a local health worker on scene.
On admission to the emergency department, the patient was fully conscious, oriented, and stable hemodynamically. His pulse rate was 157 bpm, regular, full volume with a blood pressure (BP) of 150/95 mm Hg. Routine blood test showed increased white blood cell count and no excessive loss of blood. Clinical examination found 2 metallic bars with entry sites at bilateral anterior upper chest wall and no exit site on backside. One iron rod penetrated the patient's right temporoparietal scalp through and through. Another iron rod was found traversing from the patient's left cheek to the region above the tragus with nearly 15 cm of the metallic bar under skin (Fig. ). No active bleeding was found at anyone of the entry or exit sites.
A chest computed tomography (CT) (Figs. and ) showed parenchymal lesions in both bilateral apical segments of lung and the presence of 2 foreign bodies with high density, 1.5 cm in diameter, extending in a ventridorsal direction from the bilateral anterior upper chest wall deepest to the left-side posterior paravertebral muscle. Fracture of several ribs and transverse process of vertebrae was also detected in chest CT. Thanks to the protection of the skull, no intracranial injury was found except for penetrating wounds of the scalp.
In order to inspect suspicious vascular lesions, CT angiography (computed tomography angiography [CTA]) was also performed, which found a blurring boundary between the left-side subclavian vessels and the foreign body.
The patient was immediately transferred to the emergency operating room for removal of the impaled objects and injury control. Bilateral closed chest tube drainage was promptly performed as soon as the patient was inside. In cases of severe acute respiratory distress syndrome (ARDS), extracorporeal membrane oxygenation (ECMO) was used as a temporary substitute for the injured lung to increase lung rest time, giving it time to recover from trauma.[
Head injury was first managed. Two iron rods were removed by a neurosurgeon and scalp lacerations were sutured after debridement. An orthopedist handled the left upper limb fracture by manipulative reduction maneuver and plaster external fixation.
During the surgical removal of the foreign body, plugging effect of the foreign body on the injured blood vessels wall might be relieved; anticipation of sudden gushing out of blood from an injured major vessel was essential.[ Therefore, as instructed by the CTA done before the operation, 2 vascular surgeons were summoned to explore the adjacent relationship between the foreign body and the left-side subclavian vessels.
Video-assisted thoracic surgery (VATS) was performed to take a thorough exploration of the thoracic cavities and to remove the foreign bodies under direct vision. Surprisingly, except for some avulsion injuries of the arteriovenous adventitia, our patient did not subject to any fatal injury to the major vessels, as the iron rod had just passed through the narrow rift between the left side subclavian artery and vein. Bilateral apical segments of lung were transfixed by the iron bars and the pleural cavity was found to be filled with 200 mL of blood and clots. No active bleeding point was found. Two iron bars were removed under direct vision by using VATS and a bilateral upper lobectomy was also performed by 3 thoracic surgeons (Fig. ). A conversion to thoracotomy was taken due to hemostasis of an intercostal artery. Inflated lung promotes effect of compression on the bleeding vessels and reduces dead space, which is a good protection against empyema.[ After extensive rinsing of the bilateral thoracic cavities, lung was fully insufflated to prevent atelectasis. Bilateral pleural drainage was a must, considering residual clotted blood as the major risk factor for the development of fibrothorax and empyema.
Total operative time was 12 hours. Surgeons involved in the operation include 3 senior thoracic surgeons, a neurosurgeon, 2 vascular surgeons, an orthopedist, and 5 surgery residents. Two thousand milliliter of blood was lost during the operation time associated with transfusion of 4 packed red blood cells and 600 mL fresh frozen plasma.
The patient was treated by broad-spectrum antibiotics and weaned from mechanical ventilation after 2 days stay in intensive care unit (ICU). He was then discharged from the ICU and admitted to an ordinary ward to receive a left upper limb fracture repair surgery, after which he had an uneventful recovery and was discharged from the hospital with a good general condition.


A male patient aged 38 years reported to the department with complaint of pain and purulent discharge from lower right first molar and wanted to save the tooth. The tooth was treated endodontically few years back. Clinical examination revealed broken lingual half of the crown of 46 and presence of buccal draining sinus. Tooth was firm and tender to percussion. Intra-oral Peri-apical radiograph (IOPA) showed periradicular radiolucency around a resorbed mesial root and presence of a periapical broken instrument. Under-obturated root canals of both the roots were evident.
Treatment plan included root canal re-treatment, surgical removal of instrument and bone graft followed by Porcelain fused to metal (PFM) crown. Patient consent was obtained. Gutta-percha (GP) was removed using H files. Canals were instrumented using rotary K3 files and obturated by lateral compaction. After reflection of full-thickness mucoperiosteal flap, mesial root apical curettage was done. Broken instrument was removed with a mosquito forcep. Demineralized freeze-dried bone allograft was used to graft the surgical defect. Flap was re-approximated and sutured. Patient was prescribed amoxicillin 500 mg/8 h for 7 days, ibuprofen 600 mg/8 h for 3 days, and 0.12% chlorhexidine gluconate mouthwash thrice a day for 7 days. Sutures were removed after 7 days and the access-cavity was restored with composite resin. Temporary crown was placed and later replaced with PFM crown. One-year recall radiograph demonstrates uneventful healing ().


An 18-year-old, healthy girl presented with the complaints of gradually progressive backache along with weakness of both lower limbs of 3 weeks duration. The progression of paraparesis to paraplegia was agile, over about a day. At the time of presentation, she was paraplegic, had absent sensation below D11 level bilaterally, bilateral plantar extensor, and bladder catheterized. Her magnetic resonance imaging (Siemens, Magnetom Essenza, Erlangen, Germany) thoracic spine showed lesion in anterior epidural space at the level of T9, 10 and 11 vertebral bodies, causing spinal canal stenosis, and compression of adjacent spinal cord [Figure and ]. The lesion was extending into left T9–10 neural foramina [] and adjacent left prevertebral space. The lesion appeared heterogeneously hypointense on T2-weighted (T2W) fast spin echo (SE) [] and isointense on T1W SE images [] to normal lumbar spinal cord with minimal heterogeneous contrast enhancement on contrast T1 image [].
She underwent D9, D10, and D11 left-sided hemilaminectomy and gross total excision of the lesion. Intraoperatively, a whitish, soft elastic, moderately vascular with necrotic areas in between extradural tumor compressing the spinal cord on the left side found. Tumor was found to be involving both D9, and D10 left intervertebral foramina. Tumor was dumbbell-shaped.
Tumor was removed completely in a piecemeal fashion, and there was multiple gray-brown soft tissue within on the left side of thecal sac which was extending along the T9-T10 foramen paraspinally. There was a severe mass effect on the cord. The lesion was dissected meticulously from the dura and nerve roots to achieve a gross total resection.
Histopathological examination showed cellular small round cell tumor arranged in sheets, rosettes and focally in the perivascular pattern. Cells had high nuclear-cytoplasmic ratio (N/C), round and hyperchromatic nuclei and exhibited brisk mitosis with large areas of necrosis. IHC was negative for myeloperoxidase and synaptophysin and positive for CD (Cluster of differentiation) 99. MIB-1 (cell proliferation marker) labeling indices were high. Findings were suggestive of PNET.
She was then referred to a radiation oncologist for further management. After 1 month of the review, she had only marginal improvement in symptoms.


An 8-year-old boy presented with insidious headache, vomiting, and difficulty in walking and diminution of the vision for the past 6 months. Previous important history included medium pressure ventriculoperitoneal (VP) shunt surgery as he was diagnosed as congenital hydrocephalus, for which he underwent right parietal burr hole and shunt insertion at the age of 1 year. Examination at current admission revealed vital stable; neurological examination revealed mild impairment of recent memory, left-sided upper motor neuron seventh nerve paresis, and left-sided hemiparesis of grade 4/5. Noncontrast computed tomography (CT) scan revealed asymmetrical bilateral frontoparietal calcified CCSDH with relatively larger sizes on the right side [Figure –]. The tip of VP shunt was lying in the lateral ventricle and presents in situ with well-decompressed ventricles []. Three-dimensional reconstruction of the skull revealed the presence of craniostenosis []. Although cerebral decongestant was prescribed, it did not respond. VP shunt chamber was well compressible and refilling suggesting well functioning VP shunt. Hence, plan was made to carry our burr-hole craniostomy and drainage of subdural collection under general anesthesia.
He underwent right frontal burr hole and evacuation of subdural collection. He tolerated surgical procedure well. His headache completely subsided but had only partial improvement of the visual acuity in the postoperative period. He was doing well at the last follow-up 1 year following drainage of chronic subdural hematoma. However, parents were not willing for any kind of surgical intervention for management for craniostenosis.


A 65-year-old man presented with a history of mild low back ache pain 1-month duration, radiating to flanks and anterior aspect of abdominal wall. He also had burning sensation and paresthesia in both lower limbs (below groin) of 1-month duration. He had dull abdominal pain for the last 3 weeks, which was associated with loss of appetite. There was no history of fever, trauma, or any focal weakness. There was no history of bowel and bladder disturbances. There was no history of diabetes, hypertension, or tuberculosis. There was no history suggestive of contact with tuberculosis. He was not a smoker or alcoholic. His nutritional status and general and systemic examination were normal. His abdominal examination was unremarkable, and there was no tenderness or hepatosplenomegaly. On spine examination, there was tenderness over L3–L4 region. There was no gibbous or deformity. Higher mental functions and cranial nerves were normal. Motor and sensory examination was normal. Deep tendon reflexes in the upper and lower limbs were normal. Planters were bilateral flexors. X-ray of the chest and lumbar spine was normal. His blood investigations except erythrocyte sedimentation rate (40 mm in 1 h) were within normal range. Ultrasound abdomen showed a lobulated measuring 5.8 cm × 4 cm × 7.3 cm in the left retroperitoneal paraspinal region lateral to the aorta at L3 level. The patient was further investigated with magnetic resonance imaging (MRI) of the lumbar spine which showed a heterogeneous mass at L3 level, mainly located in the left paraspinal area and involving the left psoas muscle. The lesion was extending into the neural foramina with signal changes in vertebral bodies; there was compression of the thecal sac and obliteration of the subarachnoid space [Figures –]. The mass was heterogeneously enhancing after contrast administration. Based on imaging findings and short clinical history, a diagnosis of the left paraspinal malignant tumor was suspected. The patient underwent L3–L4 unilateral partial laminotomy, there was grayish, relatively avascular lesion in the left paraspinal region, involving the left psoas muscle and going into the neural foramina, and a subtotal resection of the lesion could be performed. There was no pus in the lesion. Bony elements were relatively healthy on inspection. The patient recovered well after surgery. Histopathological examination of the excised tissue showed caseous necrosis with adjacent granulomas containing epithelioid cell, Langhans giant cells, and lymphocytes suggestive of tuberculosis []. The patient was advised to bear thoracic corset and started on antitubercular treatment (rifampicin, isoniazid [INH], pyrazinamide, and ethambutol for 3 months followed by rifampicin and INH for further 9 months) and doing well at 9-month follow-up.


Six-month follow-up cerebral angiography was performed in a 54-year-old woman having large vertebrobasilar artery-dissecting aneurysm for which endovascular coiling was done [Figure and ]. During cerebral angiography under local anesthesia, while taking vertebral artery injection, she suddenly became unresponsive. On examination, she had sustained gaze deviation toward the left with tonic posturing of limbs lasting for 1 min followed by postictal phase. Differential etiologies such as dye-induced seizure, iatrogenic embolic phenomenon, or contrast anaphylaxis were considered at first. Immediately, selective cerebral vessel injection was taken which ruled out intraprocedural vessel dissection or clot occlusion. After 10 min, she started responding to commands, but had bilateral visual obscuration with normal papillary light reaction, indicative of cortical blindness. A clinical possibility of Anton syndrome was also considered. Urgent noncontrast computed tomography head was done which revealed no evidence of bleeding or ischemic changes. Continuous electroencephalography monitoring revealed intermittent epileptiform discharges in bilateral temporal fields with episodes of transient background slowing. Magnetic resonance imaging (MRI) of brain showed bilateral occipital subcortical white matter T2 and fluid-attenuated inversion recovery hyperintensities [Figure and ], suggestive of PRES. Diffuse cortical hyperintensities [Figure and ] were noted in occipital, parietal, and temporal regions (postictal changes). The temporal sequence of events and clinicoradiological finding in our index patient was suggestive that PRES was induced by intravascular nonionic contrast (iohexol). Her symptoms improved completely with intravenous methylprednisolone and antiepileptic drugs.


The patient was a 1-year-old boy with no history of allergy to any food or drugs. He was prescribed by his family doctor tipepidine hibenzate, pranlukast, carbocistein, amoxicillin/clavulanate, and tulobuterol for acute upper respiratory inflammation. Tipepidine hibenzate, pranlukast, and carbocistein had been taken before without any side effects, while amoxicillin/clavulanate and tulobuterol had never been taken until that moment. Thirty minutes after taking these 5 medications, the patient began to show whole-body itching and developed generalized erythema and urticaria, swollen face, coughing and wheezing, followed by a single instance of vomiting. He was brought to our hospital for the treatment of an allergic reaction.
At presentation in the emergency room, his vital signs were as follows: body temperature, 38.7°C; blood pressure, unmeasurable; pulse rate, 170 beats/min; respiratory rate, 48 breaths/min; and oxygen saturation 85%–89% on room air. In addition, he had a decreased level of consciousness (Glasgow Coma Scale 7). He was diagnosed with anaphylactic shock, and immediate treatment with an intramuscular injection of adrenaline (0.01 mg/kg) and intravenous d-chlorpheniramine (0.1 mg/kg) and hydrocortisone (10 mg/kg) was given. Because of insufficient improvement of his anaphylactic symptoms, he received an additional intramuscular injection of adrenaline (0.01 mg/kg), followed by a bolus injection of normal saline (10 mL/kg). His symptoms gradually disappeared after the treatment.
One or more of the above 5 drugs was strongly suspected of being the causative agent of his anaphylactic shock. An allergology workup was performed to clarify the identity of the culprit drug. First, skin prick tests (SPTs) with tipepidine hibenzate, pranlukast, carbocistein, amoxicillin/clavulanate, and tulobuterol were performed 3 weeks after the anaphylaxis event. A full therapeutic dose of these drugs was dissolved or suspended with 1.0 mL normal saline. A saline solution or the suspension of each drug and its 1:10 dilution were used for SPT. Histamine dihydrochloride (10 mg/mL) and normal saline were used as positive and negative controls, respectively. The SPT was considered positive if a wheal had a maximum diameter at least 3 mm greater than the negative control at 15 minutes []. As shown in , the results were negative for all drugs. We then performed an oral drug provocation test (DPT) 6 months after the anaphylaxis event. Each drug was administered in a 3-dose graded challenge according to a previously described method with minor modifications []. This was conducted initially with 1/100th of the therapeutic dose, 1/10th of the therapeutic dose, and a full therapeutic dose, every hour. One hour after ingesting a full therapeutic dose of tipepidine hibenzate, the patient began to show overall itchiness. Subsequently, he developed erythema throughout the body and urticaria on his trunk (). These symptoms promptly disappeared after treatment with oral ketotifen fumarate and betamethasone. In contrast, the provocation tests with the other drugs at all doses were negative (). Based on the above results, we concluded that his previous episode of anaphylactic shock was attributable to tipepidine hibenzate. The patient was informed of an allergy to tipepidine hibenzate and advised not to take tipepidine hibenzate or any therapies including it again.


A 63-year-old male presented with a 6-month history of chronic cough and progressive dyspnea. He denied smoking and alcoholism. No other abnormal symptoms or medical history were recorded, such as chest pain, hemoptysis, or infection history. His cough and shortness of breath were aggravated by exertion. Physical examination found no abnormalities. Chest x-rays demonstrated a large mass occupying the left hemithorax (Fig. A). Contrast-enhanced CT revealed a large mass in the anterior mediastinum measuring 20 × 13 × 18 cm (Fig. B). This giant space-occupying lesion caused the extrinsic compression of the main and left pulmonary artery and the right shift of mediastinum. The mass was heterogeneous in density (−100–13 HU), with variable proportions of fat (50%), soft tissue (40%), and myxoid (10%). There was no calcification or postcontrast enhancement within this lesion. No percutaneous needle biopsy was performed.
The patient underwent a thoracotomy for resection of the mediastinal lesion via left thoracic approach. The mass was successfully resected from the anterior mediastinum with an intact capsule (Fig. A). The smooth lobulated yellow-red mass weighed 1575 g and measured 22.0 × 16.0 × 11.0 cm. Microscopically, the tumor was composed of spindle cells organized in a fascicular pattern and fat cells (Fig. B). Immunohistochemically, the spindle cells were positive for vimentin, CD 34, and negative for desmin, SMA, WT-1, S-100, SY, and WT-1. Thus, the tumor was diagnosed as a well-differentiated liposarcoma with regional dedifferentiated area. The patient was discharged without any complications and has been continuing to follow up in clinic without any complaints for 2 years.


A 78-year-old man was admitted to our hospital with 3 months history of continuous dizziness and gait disturbance. The patient underwent gastrectomy for gastric cancer 15 years ago. A contrast-enhanced CT (WCT-1000-140 Brilliance iCT, Philips, USA) scan showed huge densely enhancing solid mass with peripheral cystic component in the left posterior fossa, attached the left tentorium, with surrounding brain edema. A gadolinium-enhanced MRI (3.0T Archieva, Philips, Best, the Netherlands) demonstrated 5.6×4.8×3.2 cm sized mass lesion in left posterior cranial fossa, heterogeneously enhanced. Diffusion-weighted imaging showed high signal intensity for solid mass surrounded by low signal intensity of cystic component (). Dural tail sign was noted, but it was suspicious for infiltrative appearance into left cerebellum. Intratumoral hemorrhage was also noted. So, high grade meningioma or dural metastasis was suspected and surgery was planned.
The patient underwent left retrosigmoid craniotomy with navigation system. The tumor was combined with 2 components, whitish firm mass and gray colored soft & suckable mass. The mass was well-demarcated and attached to the dura with severe adhesion. The CN VII & VIII nerve complex and lower cranial nerve was preserved well. Additionally, tumorlike component at the base also removed with minimal lobectomy. Duroplasty with artificial dura was done. The procedure was well tolerated and the patient recovered without complication. The postoperative MRI showed no definite evidence of remaining enhancing tumor at the operation site. We examined the function of swallowing and gag reflex, and the results showed complete recovery of swallowing and gag reflex at the videofluoroscopic swallowing study.
On pathologic report, the final diagnosis was GS of WHO grade IV. Gliofibrillary cytoplasmic processes was positive in glial component, but negative in sarcomatous component. And S-100 protein and P53 was positive in both component. Immuno-histologic staining showed Ki-67 labeling index as high as 20% ().
After surgical treatment, the patient was discharged without any surgical complication. Before pathological confirmation, abdomen & pelvic CT with contrast was done for systemic evaluation and there was no abnormal finding. We recommended concurrent chemoradiotherapy as a standard protocol of GBM, but the patient rejected all treatment to get a home remedies. The patient survived for nine months without receiving any special treatment from the hospital.


A 77-year-old male patient with end-stage renal failure was admitted to our hospital for hemodialysis initiation. He was nondiabetic and had a 60-year smoking history from age 16 to 76 years, and had no ApoE4 (ε4 allele). His preexisting diseases were hypertension and hyperuricemia. On admission, initial investigation revealed high serum creatinine (Cr; 8.63 mg/dL) and blood urea nitrogen (87.8 g/dL) concentrations in the patient’s blood. Other results were as follows: white blood cells, 5,900/μL; hemoglobin, 9.4 g/dL; platelets, 23.7×104/μL; total protein, 5.7 g/dL; and albumin, 2.8 g/dL. Urinalysis revealed urinary protein (3+) and occult blood (1+). Ultrasonography showed atrophy of the kidneys. Although the reason for renal failure was unclear, we considered it to be nephrosclerosis. On the basis of these data, the patient was started on hemodialysis.
At the hemodialysis initiation, the patient was diagnosed with mild cognitive impairment per the criteria of Petersen et al. Although he exhibited mild memory impairment, he experienced no trouble in his routine life. His Mini-Mental State Examination (MMSE) score was 23 points (disorientation to time, recall, and calculation). In addition, the score of Wechsler Memory Scale-Revised was 14/50 for Logical Memory I and 13/50 for Logical Memory II (the period of his education was within 9–12 years), suggesting a score near the low border of the normal range. His score on the short Japanese version of the Geriatric Depression Scale (GDS-S-J; published by Sugishita and Asada with the permission of the copyright holder) was 6, indicating mild depressives. He exhibited no abnormality in the thyroid function, and vitamin B12 and serum calcium concentration levels. Furthermore, he displayed no signs and symptoms of any other psychological disorder.
The cranial magnetic resonance imaging (MRI; ) was performed 3 days before the hemodialysis initiation. The MRI revealed no apparent atrophy, and the patient’s hippocampus seemed to be normal. Regarding white matter lesions, the periventricular hyperintensity was grade 2, and deep white matter hyperintensity was grade 1, as evaluated using the scale of Fazekas et al. Furthermore, the Hachinski et al’s ischemic score of the patient was 3, suggesting a low possibility of vascular dementia. Hence, his cerebrovascular impairment was concluded as very mild and seemed not to affect his clinical symptoms.
Regarding the Aβ accumulation in the brain, three-dimensional static PET imaging for 50–70 minute after the intravenous injection of PiB was conducted using a PET–computed tomography camera, Biograph True V (Siemens Healthineers, Erlangen, Germany), as reported previously. PiB images were visually rated as PiB-positive or PiB-negative, as described previously. The first PiB/PET was performed 14 days after the hemodialysis initiation (, top), which showed a PiB-positive result. A quantitative analysis using the method of Australian Imaging, Biomarkers and Lifestyle (AIBL) showed 1.91 as the global standard uptake value ratio with whole cerebellum as reference (SUVRWCb). After the patient received maintenance hemodialysis (4 h/day, 3 days/week) for 6 months (visit 2), PiB/PET was performed again. After 6-month hemodialysis, the Aβ accumulation in the brain was decreased (, middle). The global SUVRWCb was 1.72, which was lower by “0.19” than that of visit 1. On visit 3, PiB/PET was performed again after maintenance hemodialysis of 12 months (, bottom). The global SUVRWCb was 1.78, which was lower by “0.13” than that of visit 1. The change in SUVRWCb is summarized in .
Regarding cognitive functions, MMSE scores were the lowest at 23 points at the hemodialysis initiation but gradually increased during 3 months of maintenance hemodialysis (). Then, the scores marginally increased (improved) and were maintained at 26 points after 194 and 285 days of the hemodialysis initiation, and at 27 points after 355, 453, and 719 days (the last data are not shown in ).
We measured the concentrations of Aβ monomers and oligomers in the plasma, as described previously (). At the hemodialysis initiation, both plasma Aβ1–40 and Aβ1–42 concentrations, measured with High Sensitive Human β Amyloid (1–40) and (1–42) ELISA Kit Wako II (WAKO Pure Chemical, Osaka, Japan), were as high as 971 and 73.7 pg/mL, respectively, because of renal failure. After the hemodialysis initiation, both plasma Aβ1–40 and Aβ1–42 concentrations decreased for around 6 months, but then increased and were maintained as 709–1,033 and 77.2–99.2 pg/mL, respectively. In addition, the ratios of Aβ1–40 to Aβ1–42 were 0.077 (Day 3; ) and 0.076 (Day 0) just before the hemodialysis initiation. However, the ratios increased up to 0.117 for 6 months after hemodialysis initiation, but then were maintained between 0.08 and 0.10 ().
Contrary to Aβ monomers, the concentrations of Aβ oligomers in the plasma, measured with Human Amyloid β Oligomers (82E1-specific) Assay Kit (IBL, Fujioka, Japan), were below the detection limit (0; ) at the hemodialysis initiation and were maintained at 0 for 194 days after hemodialysis initiation. Then, plasma Aβ oligomer concentrations increased to 13.6–33.8 pmol/L after 285 days of the hemodialysis initiation ().
Serum Cr and β2-microglobulin (β2MG) concentrations just before hemodialysis sessions are shown in (measured by clinical test companies such as SRL, Nagoya, Japan). The change in both Cr and β2MG concentrations was small compared to Aβ monomers and oligomers.


A 44-year-old Chinese woman was admitted because of an antral ‘polyp’ in the stomach for 5 months which had been found during a routine health examination with gastroscopy in her local hospital. The patient did not experience any gastric discomfort due to this ‘polyp.’ She has been diagnosed with type 2 diabetes for 3 year, and had undergone total thyroidectomy, bilateral lymph node dissection and parathyroid autotransplantation for papillary thyroid carcinoma 5 months ago. Review of tumor markers (CEA, CA125, CA153 and CA199), hemoglobin A1C and thyroid function was normal. A second gastroscopy in our hospital confirmed a 0.8 × 0.8 cm polyp-like mass with distinct border and without mucosal ulceration at the gastric antrum. Further endoscopic EUS revealed a homogeneous hyperechoic lesion protruding into the lumen which was oval and without a distinct border. Furthermore, the lesion seemed to originate from submucosa and muscularis propria and was clearly demarcated from the serosa (). Endoscopic submucosal dissection (ESD) was performed to remove this mass en bloc.
Histological examination revealed that the tumor was mainly occupied by myxoid matrix extending from mucosa to muscularis mucosa at antrum. It also exhibited a plexiform pattern with spindle-shaped bland tumor cells. In order to determine the final diagnosis of this tumor, a group of molecular markers was stained immunohistochemically on the biopsy slides. The tumor cells were positive for vimentin, a cluster of differentiation 34 (CD34) but negative for smooth muscle actin (SMA), desmin, cluster of differentiation 117(CD117), phosphoenolpyruvate carboxykinase (PCK) and S-100. Taken together, a final diagnosis of PAMT was made (). Our follow-up indicated that the patient made an uneventful recovery at 6 months after ESD.


An 11-year-old 1.93 kg female spayed domestic shorthair cat was originally presented for chronic weight loss in the face of a voracious appetite, and was diagnosed with hyperthyroidism. Referral blood work showed total thyroxine 17.1 (0.8–4.7) μg/dl and alanine aminotransferase 215 (12–130) U/l. Methimazole 2.5 mg q12h treatment was initiated; however, shortly after starting the medication, the cat began vomiting while maintaining a good appetite. No improvement was noted when the methimazole formulation was changed from tablet to liquid. Supportive care with maropitant citrate (Cerenia 1 mg/kg [Zoetis]) was instituted without controlling the cat’s signs. Orthogonal whole-body radiographs showed severe dilation of the upper and lower gastrointestinal tracts (), with an impression of esophageal fluid accumulation at the level of the carina, and moderate to marked generalized cardiomegaly. The cat was referred for further diagnostics and care for persistent vomiting, gastrointestinal stasis, and possible dysautonomia.
On presentation to the Foster Hospital for Small Animals at the Cummings School of Veterinary Medicine, Tufts University, USA the cat had severe muscle wasting with moderate cachexia. The cat had a gallop rhythm, a small right-sided thyroid slip, mild anisocoria (miosis of the left eye) and repeatedly regurgitated on abdominal palpation. No overt lesions involving the paws or digits were noted. Neurologic consultation revealed generalized weak reflexes and withdrawal, with good perianal tone and eye motor function.
Recheck lateral whole-body and dorsoventral thoracic radiographs were obtained (). Although, classically, abdominal radiographs are taken with a history of vomiting, whole-body radiographs, including the thorax, were chosen in this case so that all previously noted radiographic abnormalities in both the thorax and abdomen could be re-evaluated.
The cardiac silhouette was again moderately to markedly enlarged. The left cranial and caudal lung lobes were persistently collapsed, causing a leftward mediastinal shift. The right lung lobes were hyperinflated but otherwise normal in appearance. A focal, rounded, soft tissue opacity was noted overlying the esophagus at the level of the carina, visible only on the lateral view. The entire gastrointestinal tract, including the esophagus, was again diffusely gas-dilated; however, the volume of gas within the stomach and intestines was reduced compared with the previous referral images. Therefore aerophagia was thought a more likely cause than diffuse functional ileus. Cardiomegaly was attributed to thyrotoxic cardiomyopathy. Differentials for the left lung lobes’ collapse included chronic lower airway disease (although this was considered unlikely given the lack of evidence for lower airway disease in the aerated right lung), or a mass obstructing the left primary bronchus. The soft tissue structure at the carina was thought to represent either focal fluid within the esophagus or a mass, possibly of esophageal, ectopic thyroid or left-sided pulmonary origin.
After reviewing the history with the owner, the cat was assessed to be chronically regurgitating, not vomiting. Given the possible esophageal involvement with a mass based on clinical signs and radiographic findings, CT of the thorax and/or endoscopic evaluation of the esophagus were recommended. Prior to anesthesia for CT, an echocardiogram was performed to evaluate the cat’s cardiac murmur and cardiomegaly. Echocardiography detected a large mass adjacent to the heart base, compressing the pulmonary arteries, which was suspected to be producing a significant increase in right-sided cardiac pressures. Left ventricular hypertrophy was also noted. At the time of the examination, the cat was hypothermic at 96.3ºF and hypotensive at 40 mmHg (systolic). These findings were discussed with the owner and humane euthanasia, with necropsy, was elected.
Post-mortem examination revealed a focal esophageal stricture secondary to local invasion of the esophageal wall by a left-sided pulmonary mass (). The gastro intestinal tract was otherwise unremarkable besides moderate gas distention. Histopathology of the mass revealed a densely cellular, unencapsulated neoplasm composed of polygonal cells arranged in cords, islands and acini supported by a robust fibrovascular stroma (). The mitotic count was 19 per 10 high-power fields. Immunohistochemistry staining with thyroid transcription factor-1 revealed variable positive nuclear staining in the neoplastic cells, confirming a lung origin neoplasm and a morphologic diagnosis of pulmonary adenocarcinoma (). Immunohistochemistry staining with thyroglobulin was negative. The neoplastic cells were found invading the adjacent esophageal musculature, the right atrium and the wall of the main pulmonary artery by both direct and vascular invasion (). Findings were supportive of primary pulmonary adenocarcinoma with extensive regional tissue invasion causing secondary esophageal stricture.


A 23-year-old female with no previous psychiatric diagnosis presented to the emergency department (ED) brought in by mother for extremely agitated behavior. Upon interview, patient endorsed methamphetamine and marijuana use the prior night as well as attending a music festival a week prior where she used cocaine and multiple forms of 3,4-Methylenedioxyme-thamphetamine (MDMA). She mentioned that she had not gotten any sleep the previous night and usually sleeps 8 hours per night. She was dysphoric, paranoid, endorsed auditory hallucinations, and demonstrated extreme suspicion of the family pictures on the walls of her parent’s home. She repeatedly told her mother that “the pictures are not real”, and directly referred to her family as imposters. Patient endorsed symptoms of depression over the past six months, but denied low energy, lack of sleep, poor concentration, guilt, or change in appetite. After stating that she would shoot herself if she had a gun due to paranoia about her family being imposters she was ultimately admitted voluntarily due to high risk for imminent suicide with significant risk factors including recent drug use, impulsivity, disconnect from reality due to psychosis, and current suicidal ideation.
She was started on Aripiprazole 10 mg daily for psychosis and Clonazepam 0.5 mg twice a day as needed for anxiety. Over the course of several days insight and judgement improved and she appeared more linear and logical, able to attribute her polysubstance abuse as a probable instigator to her psychosis. As she continued to endorse intermittent suicidal ideations, Escitalopram 10 mg daily for depression and Omega-3 fatty acids 1g daily for mood were added. Clonazepam was discontinued over the next few days.
She then endorsed that the night prior to admission; she had visited a bar and met a man whom she later accompanied home. At his home, the patient used marijuana and methamphetamine after which the man became paranoid and showed the patient a picture of him on his phone and stating that the picture was not him. Rather, it was an imposter who had been following him. She then became paranoid regarding imposters of both herself and her family. When she returned home, she was immediately suspicious of her mom and believed the pictures on the wall were all “fake.” It took several days of Aripiprazole and daily visits from close family members to assuaged her concerns that her family members were imposters and that the home pictures were “fake”. As her paranoia resolved she became pleasant and appropriately engaging. Her suicidal ideation resolved over several days, prior to the timeline which Escitalopram would have played much of a therapeutic role. Therefore, it is probable that suicidal ideation was an indirect result of acute psychosis as well. Within a week, she was found to no longer be a danger to self, danger to others, or gravely disabled, and was discharged home.


A 31-year-old male presented to the emergency department complaining of abdominal pain and bloody diarrhea of 3 weeks' duration. He was in his usual state of health until 3 weeks before admission, when he started developing diffuse severe colicky abdominal pain. The pain was followed by over 5 episodes of diarrhea per day with streaks of blood, accompanied by weight loss, tenesmus, and chills. The patient did not report any previous similar episodes. His only medical history includes chronic plaque psoriasis; he was started on ixekizumab therapy 3 months prior to presentation and currently his symptoms are well controlled. There were no other relevant hospitalizations and home medications.
He has no family history of IBD and reports a 10 pack-years smoking history during his lifetime. He denies any blood transfusions, recent travel or high-risk sexual behavior in the past.
On presentation, the patient was hemodynamically stable and afebrile. His physical examination was significant for left lower quadrant tenderness with no rebound or guarding. His initial laboratory results revealed a white cell count of 14,000/mm3 (granulocytes 67%, lymphocytes 19%, monocytes 10%), hemoglobin 14.8 g/dL, platelets 359/mm3, albumin 3.9 g/dL, ESR 69 mm/h, and CRP 71.1 mg/L. Liver profile, HIV, hepatitis panel, and ANCA serology were unremarkable. Stool testing showed many white cells, although cultures were negative for pathogens including nucleic acid amplification test, enzyme immunoassay for C. difficile toxin A and B. A computed tomographic scan of his abdomen with intravenous contrast demonstrated pancolitis with no drainable fluid collection. Initial flexible sigmoidoscopy revealed an absent vascular pattern, erythematous friable mucosa with spontaneous bleeding, and severe ulcerative proctosigmoiditis (Fig. ). Colonic biopsy obtained from the ulcers revealed chronic lymphoplasmacytic infiltration (Fig. ). All these features in the above setting were consistent with the diagnosis of new-onset UC (Mayo Score 12).
The patient was started on oral mesalamine (4 g/day), intravenous methylprednisolone (60 mg/day), and parenteral fluids. After 2 weeks of hospitalization, he developed C. difficile infection and oral vancomycin 125 mg orally was given for a total of 10 days. Initially, he showed mild improvement; however, 2 weeks later, bloody diarrhea recurred with worsening abdominal pain and anorexia. He had a 10-pound weight loss since admission, along with severe hypoalbuminemia of 2.6 g/dL and hemoglobin dropped to 7.1 g/dL. He was started on total parenteral nutrition, also requiring 1 unit of packed red blood cells. A repeat flexible sigmoidoscopy at this point illustrated worsening erosions and deep ulcers with heaped-up margins. Repeat biopsy from the ulcers was positive for CMV inclusion bodies. His CMV PCR DNA level was 426 IU/mL (reference range < 200 IU/mL). Thus, establishing the diagnosis of steroid-refractory UC with superimposed CMV colitis. It is possible that the patient had a reactivation of latent CMV infection or acquiring an exogenous strain secondary to immunosuppression by glucocorticoids.
After screening for hepatitis B and latent tuberculosis, the patient was started on an induction therapy with infliximab infusion (5 mg/kg) for UC and simultaneously treated for CMV colitis with intravenous ganciclovir (5 mg/kg every 12 h). After 1 week, he experienced significant clinical improvement, tolerating oral diet, bowel movement less than 3 per day, and not requiring further blood transfusions. He was discharged on oral valganciclovir for 3 weeks and infliximab infusion every 8 weeks. Currently, the patient is in remission after 6 months and ixekizumab was stopped for his plaque psoriasis after consulting his dermatologist.


A 46-year-old man was admitted to the hospital with an acute anterior wall myocardial infarction. He was urgently taken to the catheterization lab where he was found to have a totally occluded proximal left anterior descending coronary artery (LAD). The LAD was successfully stented, following which the patient had a 40% mid-right coronary artery lesion and ejection fraction of approximately 40–45% with an apical wall motion abnormality, which was subsequently confirmed on an echocardiogram. He did well post intervention without any further chest pain, dyspnea, or symptoms consistent with myocardial ischemia. He had an unremarkable post-procedural course and was discharged on combined therapy of aspirin 325 mg a day, atorvastatin 80 mg a day, metoprolol 50 mg twice daily, prasugrel 10 mg a day, and ramipril 5 mg.
Two months after this successful cardiac procedure, the patient returned with a new chest mass. He now presented for preoperative clearance for a possible sarcoma of the left chest. The ejection fraction at the patient’s first presentation was 40%, and a subsequent repeat echocardiogram showed well-preserved left ventricular systolic function of 55%.
Due to his recent anterior wall myocardial infarction and placement of drug-eluting stent, the patient was currently taking prasugrel and aspirin. Surgeons in the General Surgery department were consulted, and they were not willing to operate on the patient while he was on aspirin and prasugrel given the invasive nature of the procedure and the high risk of bleeding. It was then decided to use cangrelor as a bridging agent for this procedure.
The patient discontinued prasugrel 2 days prior to being admitted to the hospital, but continued on aspirin. He was then started on 4 mcg/kg/min of cangrelor and continued this treatment for the next 3 days. The drug was stopped 1 h prior to entrance into the operating room where he underwent a biopsy and excision of the soft tissue sarcoma. The patient tolerated the procedure well. He was then started on 60 mg of prasugrel 48 h after the procedure and continued on this agent at a dose of 10 mg per day. He experienced no further issues. All of his post-operative checkups and tests were normal, and the patient experienced no complications.
Informed consent was obtained from the individual participant for inclusion in the study.


A seven-year-old girl, with a generalized erythematous squamous rash, was admitted to 2nd Pediatric Clinic, Emergency County Hospital Craiova (medical record no. 7885) in February 2015, being transferred from a county hospital.
Personal physiological antecedents. Fourth child, due time birth, natural childbirth, birth weight = 2200 g, Apgar score 8, breastfed until 4 months, correctly diversified after 4 months, weaned at 7 months, at present being fed with adult food. Normal psychomotor development.
Personal pathological antecedents: chicken pox at four years old.
Heredo-collateral antecedents: healthy parents, 3 healthy brothers, an aunt, related to her mother, with psoriasis.
Anamnesis. The onset was 2 weeks before, with an erythematous rash at the abdominal level. She went to the dermatologist who recommended a local treatment with Fluocinolone ointment and magistral prescription with salicylic acid, urea and jelly. The rash generalized: squamous patches appeared and subsequently she was admitted to our clinic.
When admitted: no fever, weight= 20 kg, fair general state, erythematous rash in patches, erythematous plaques covered with silvery, thick, easily exfoliating, not painful, non-pruriginous squamae, with the presence of Auspitz signs and white spots, at the level of scalp, earlobes, retro-auricular, anterior and posterior torso, abdomen, lower and upper limbs; pustules surrounded by red skin at the axillary, genital and inguinal level. Pulmonary – normal, normal heartbeat, CF=98/min, supple abdomen, liver 1 cm below costal margin, based-flared thorax, tooth caries (Fig.).
Investigations. Hemogram: Hb= 12.2g%, Tr= 236000/mm3, L= 16000/mm3, NS=62%, Ly=32%, M=6%, VSH= 7/14 mm after 1/2 hours, fibrinogen= 397 mg/dl, CRP= 0.4 mg/l, creatinine= 0.4 mg/dl, uric acid = 3.53 mg/dl, glycemia= 82 mg/dl, calcemia= 8 mg/dl, total serical proteins= 6.5 g/dl, sideremy= 103 mg/dl, GOT= 19 U/l, GPT= 14 U/l, negative coproparasitary examination, normal urine summary examination, ASLO= 116.86UI. Immunogram: IgA= 76.67 mg/dl, (N=70-400), IgG= 865.5 mg/dl (N=700-1600), IgM= 167.2 mg/dl (N=100-230), pharyngeal exudate: absent streptococcus, staphylococcus, nasal exudate: present staphylococcus aureus, sensitive to: Biseptol, Linezolid, Gentamicin, Vancomycin, resistant to: Penicillin, Clarithromycin, Oxacillin. Normal abdominal ultrasound.
Dermatologic examination: psoriasis vulgaris in patches and plaques. Cutaneous biopsy / histopathological examination - microscopic examination: epidermis with orthokeratosis, large areas of hypo- and agranulocytosis, acanthosis, mild perivascular chronic inflammatory infiltrate in the dermis. The HP aspect most probably suggests psoriasis vulgaris (Fig., Fig.).
The patient received a local treatment recommended by the dermatologist, with magistral prescription with salicylic acid, ihtiol, vitamin A, vitamin E, Advantan cream – applied once per day and Diprosalic scalp application.
Starting with the 3rd day of the treatment, the patient presented progressive desquamation of the squamae. She was discharged after 7 days, without squamae (Fig.). Discharge diagnosis: Psoriasis vulgaris in patches and plaques. Nasal staphylococcus aureus. Hypocalcemia. Hypoproteinemia. Tooth cavities. Weight hypotrophy.


A 50-year-old diabetic male with a history of trauma followed by multiple retinal surgeries in the right eye (OD) presented to us with diminution of vision in the left eye (OS) of 2-month duration. Previous records indicate on and off treatment with oral steroids with partial response started elsewhere. Ocular examination showed a phthisical OD. His best corrected visual acuity (BCVA) in OS was 6/12. Slit lamp and fundus examinations (OS) showed medium sized keratic precipitates, 2 + anterior chamber reaction, vitritis, peripapillary retinal elevation, disc hyperemia and multiple subretinal coin-shaped lesions in midperiphery [Fig. and ]. Intraocular pressures by applanation tonometry (OS) were 26 mm of Hg. Gonioscopy showed open angles with hyperpigmentation. Ultrasonography (OS) showed a choroidal thickness of 1.6 mm. Laboratory investigations including complete haemogram, serum angiotensin converting enzyme, venereal disease research laboratory test (VDRL), treponemal pallidum Haemagglutination test (TPHA), antinuclear antibodies, enzyme-linked immunosorbent assays (ELISA) for human immunodeficiency virus (HIV) and toxoplasmosis were negative. Mantoux test, chest radiology and ultrasonography of abdomen were negative. Multiplex polymerase chain reaction on the aqueous for eubacterial, panfungal, herpes viruses, toxoplasma and mycobacterium tuberculosis (MTb) were negative. Treatment included oral steroids (1 mg/kg body weight), azathioprine (2 mg/kg body wt), hourly instillation of topical prednisolone acetate1% eye drops, timolol eye drops 0.5% bd and brinzolamide eye drops 1% tid. Subsequent follow-up 2 weeks later showed decrease in vitritis. However, he developed herpes zoster (left thoracic dermatome) a month later. The steroids and immunosuppressives were discontinued for 2 weeks till the resolution of active zoster skin lesions. He came back a month later with worsening of inflammation and deterioration of vision to counting fingers close to face [Fig. and ]. A core vitrectomy (OS) was done and the vitreous was sent for a detailed histopathology and microbiology examination. Cytology showed few lymphocytes and macrophages suggestive of chronic inflammation. Microbiology including staining, culture and multiplex PCR were negative for bacteria, herpes viruses and toxoplasma. Enucleation of the right pthisical eye showed chronic granulomatous inflammation in the choroid. Immunohistochemistry showed CD20, CD3, CD45 positivity suggestive of both B- and T-cell response. The peripapillary elevation with multiple subretinal deposits [] and large confluent subretinal lesions with indistinct borders [] were visible more clearly after vitrectomy. These lesions subsequently showed fibrosis with demarcation of borders following treatment with oral steroids and azathioprine [Fig. and ]. His BCVA (OS) was counting fingers 3 m.
Multimodal imaging showed larger and more hypointense areas on indocyanine green angiography in comparison to fluorescein angiography [] and staining of confluent lesions on fluorescein angiography. OCT showed multiple intraretinal, subretinal hyperreflective lesions and retinal pigment epithelium (RPE) undulations []. Magnetic resonance imaging (MRI) orbit and cranium were not significant. Audiometry evaluations showed bilateral moderate to severe sensorineural hearing loss in right and left ears, respectively.
As his inflammation continued to worsen with deterioration of vision, pulse doses of intravenous methyl prednisolone (1 mg/kg/day for 3 days) and intravenous cyclophosphamide (six cycles) were given. He eventually developed no perception of light (OS) over 3 months.


A 54-year-old male with a history of trauma followed by multiple retinal surgeries in the left eye presented to us with pain and diminution of vision in OD of 3 months duration. He had a history of receiving antituberculosis therapy for pulmonary tuberculosis 20 years ago.
On examination, his BCVA (OD) was counting fingers close to face. Left eye was a pthisical eye. Slit lamp examination (OD) showed medium sized keratic precipitates and an anterior chamber reaction (2+). Fundus examination showed vitritis, disc hyperemia, peripapillary retinal elevation, a choroidal scar in the posterior pole and plenty of subretinal lesions, coalescing in some areas mimicking retinal necrosis [] Ultrasonography showed no significant choroidal thickening (1.6 mm). Fluorescein angiography showed disc leakage, multiple hyperfluorescent lesions in the mid and late phases and vascular wall staining. The large coalescent lesions showed staining in late phases. ICG showed multiple, hypointense choroidal lesions. Spectral OCT showed intraretinal and outer retinal hyper reflective lesions. RPE undulations were seen []. Laboratory investigations including complete haemogram, peripheral blood smear, ELISA for HIV, antinuclear antibodies, serum angiotensin converting enzyme, toxoplasmosis, VDRL, TPHA, Quantiferon TB gold test, liver function tests, serum creatinine, random blood sugars and urine routine were negative. Chest radiology showed collapse of the left lung due to the past pulmonary tuberculosis []. Three consecutive sputum samples for acid fast bacilli (AFB) were negative. Right eye underwent a vitreous biopsy []. Cytology showed few lymphocytes and macrophages suggestive of chronic inflammation. Microbiology including staining, culture and multiplex PCR were negative for bacteria, fungi, herpes viruses, toxoplasma and MTB. MRI orbits and cranium was normal. Under an infectious disease specialist's supervision, he was started on oral steroids (1 mg/kg body wt) and azathioprine (2 mg/kg body wt). As the steroids were tapered to 30 mg/day, he developed a worsening of inflammation and decrease in vision to perception of light. Under a pulmonologist and infectious disease specialist's supervision, intravenous methyl prednisolone (1 mg/kg body wt for 3 days) with posterior subtenon injection of triamcinolone acetonide and intravenous cyclophosphamide (four cycles) were given. However, his vision deteriorated to no perception of light. He refused further treatment and was lost to follow-up.


Informed consent was obtained from the patient prior to publication of this manuscript.
A 31-year-old Caucasian woman with a history of Marfan syndrome and an anterior chamber intraocular lens (IOL) in her left eye was referred to us for management of a subluxed crystalline lens in her right eye. She was complaining of floaters and photopsias in her right eye. On examination, a mild exotropia with left gaze preference was noted. Snellen visual acuity was 20/80 in the right eye, pinholing to 20/30 and 20/20 in the left eye. The right lens was superonasally subluxated with the lens still within the visual axis. The right eye was without intraocular inflammation, had an intraocular pressure (IOP) of 17 mmHg, and was without other abnormality aside from an area of peripheral congenital hypertrophy of the retinal pigment epithelium. The left eye had a centered anterior chamber IOL (ACIOL), IOP of 8 mmHg, a peripheral iridotomy, and a normal posterior segment.
Over the next 2 years, the patient’s vision worsened in the right eye attributed to progressive crystalline lens subluxation. She subsequently underwent lensectomy with ACIOL implantation, but experienced persistent visual symptoms attributed to implant instability. She sought removal of the ACIOL and placement of a scleral-fixated IOL. This was performed using two 25-gauge trocars that were passed through bare sclera at an angle and into the vitreous cavity. End-gripping 25-gauge forceps were used to grab the tip of the IOL haptic and pull it through the trocar. The trocar was then removed leaving the haptic in the scleral tunnel. Postoperatively, she healed well and her central vision improved to 20/40.
Approximately 5 months later, the patient reported a sudden onset of redness and pain in the right eye while participating at a Marfan patient care conference abroad. She was evaluated by a local ophthalmologist who prescribed a topical antibiotic drop. Within a week, the patient returned to our center complaining of sharp, persistent periocular pain. Evaluation revealed the right eye to be mildly injected with a tender 3 mm × 3 mm lesion with tan layered material (Figs. , ). There was no active leakage from the lesion and the anterior chamber of the right eye was deep and quiet. IOP and best corrected visual acuity (BCVA) were 15 mmHg and 20/200, respectively. The patient was referred to the glaucoma department for further management of a possibly infected inadvertent filtration bleb. Antibiotic therapy was switched to broad spectrum fortified antibiotics as well as oral antibiotics. Despite broadened antibiotic treatment the conjunctival injection and lesion appeared unchanged, with persistent tan material within. The patient’s periocular pain worsened over the course of 2 weeks. A stable appearance on antibiotics as well as normal intraocular pressure and examination led to a high suspicion for a conjunctival epithelial cyst. The lesion was surgically excised at the patient’s request to relieve the pain. Histopathologic analysis confirmed the diagnosis of conjunctival epithelial inclusion cyst (Fig. ). A month after cyst excision, the patient developed a similar lesion a few millimeters beyond the original site (Fig. ). BCVA in the right eye was 20/500 and the anterior chamber was deep and quiet. Again, to alleviate pain, the lesion was excised uneventfully with copious mechanical debridement of local epithelium. Histopathologic examination revealed a conjunctival epithelial inclusion cyst.


A 48-year-old HIV-positive woman with previously well-controlled type 2 diabetes mellitus presented on May 2017 to her family physician with high blood glucose levels [fasting blood sugars (FBS) of 173 mg/dl and HbA1c of 9.6%] and elevated liver enzymes (direct and indirect bilirubin, ALT, AST, and GGTP were raised and were 287 U/L, 337 U/L, and 726 U/L, respectively).
She was diagnosed with type 2 diabetes mellitus 4 years back. Prior to this visit her blood sugars were well controlled (previous reports on February 2017: FBS: 111 mg/dl, HbA1c: 5.7%; 7th July 2016: FBS: 100 mg/dl, HbA1c: 6%). She was on metformin-sustained release 500 mg BD and atorvastatin 10 mg daily.
The patient also stated that she was started on IPT on February 2017 with a dose of 300 mg and for a planned duration of 6 months of which she had completed 3 months. She was given pyridoxine 40 mg daily to prevent INH-induced peripheral neuritis, a well-known side effect. Additionally, fenofibrate was started for high blood triglyceride levels on January 2017.
The patient gives no history of other changes in her medication, no gross change in weight, no significant change in her diet, or fever. The patient claims to be compliant with her medication. There was no history of any other co-morbidities such as hypertension, TB, obesity, coronary heart disease, stroke, previous surgeries, or recent trauma. No history of substance abuse.
She was diagnosed with HIV-1 infection 7 years back after her husband tested positive. Her initial CD4 count was 377/mm3 (September 2010) and was started on antiretroviral therapy (ART) (lamivudine 150 mg, nevirapine 200 mg, and zidovudine 300 mg) on May 2011 after her CD4 count had dropped to 264/mm3. She has been compliant with her ART. She has been responsive to treatment with her latest CD4 count of 504/mm3 (December 2016).
On examination, she was moderately built and nourished. Her body mass index (BMI) was 23.45 kg/m2. Her vitals were within normal limits. No icterus was noted. Systemic examination was unremarkable.
Impression: The sudden worsening of her glycaemic control was a puzzle to her physician and was causing distress to the patient. Taking into account that the only recent significant change was the initiation of INH, we looked at the possibility of this being a result of drug-induced hyperglycaemia. Our literature review showed one other documented case of hyperglycaemia caused by INH, hyperglycaemia was also known as an uncommon side effect.
The hypothesis that hyperglycaemia was caused by INH, we stopped INH and found that after 6 weeks of stoppings her FBS was 140 mg/dl and AST 40 U/L. Three months after the treatment was stopped her HbA1c was 6.2%. This supported our hypothesis.


A 41-year-old man diagnosed with end-stage renal disease, secondary to Gout kidney disease, was hospitalized for preemptive living kidney transplantation. He underwent ABO-compatible living kidney transplantation. The kidney donor was his 45-year-old sister, and her right kidney was selected for allograft due to a split renal function with Tc-99m mercaptoacetyltriglycine-3 renography revealing superiority of contralateral kidney function. The right kidney consisted of a single artery and vein. Despite instruction of weight loss, his preoperative body mass index (BMI) was 33.4 kg/m2; thus, we handled the surgery with the greatest care to avoid complications. The surgery progressed smoothly (first warm ischemic time: 5 minutes, cold ischemic time: 29 minutes, and second warm ischemic time: 60 minutes), and urine output was observed immediately after reperfusion of the transplant renal artery and vein. Doppler US immediately before abdominal closure revealed sufficient blood flow throughout the allograft, without reversed or absent diastolic flow and an obvious elevated resistive index (RI). An allograft biopsy 1 hour after the allograft blood flow was restored, showing no specific changes. He was introduced to an immunosuppression regimen consisting of tacrolimus, MMF, prednisone, and basiliximab. On postoperative day (POD) 1, the serum creatinine levels decreased, the urine output gradually decreased, hematuria was recognized, and Doppler US revealed mild hydronephrosis in the allograft. Doppler US on POD 2 showed a decrease in the diastolic flow and an elevated RI without obvious evidence of TRVT (); thus, rejection was considered, and steroid pulse therapy was initiated. Despite this therapy, allograft function did not improve, hydronephrosis worsened, and urine output decreased. Unenhanced computed tomography (CT) on POD 4 revealed a hematoma with air in the urinary tract of the allograft (), and serum creatinine levels increased to 7.0 mg/dL. By washing ureteral catheter to check for obstraction was the reason why air accumulated in urinary tract. To remove the hematoma with clots in the urinary tract, a ureteral stent was placed, and the allograft was assessed for anastomotic stenosis and compression of the renal artery and vein; then, surgical exploration was performed. Perforation of the pelvis was detected, and evacuation of the hematoma with clots in the urinary tract was performed. Ureteral stent indwelling was performed, and the pelvis was repaired using bioabsorbable sutures. Vascular anastomoses were examined to determine whether there was arterial anastomotic stenosis, kinking of the artery, compression of the vein, and presence of thrombosis. Although there was no evidence of arterial anastomosis and kinks in the renal artery, one of the two branches of the proximal renal vein was compressed by the surrounding tissues, including the allograft, and TRVT was detected. Therefore, subsequent surgical thrombectomy was performed, and Doppler US revealed improved diastolic flow and RI (). Postoperative CT also showed that hydronephrosis and the urinary tract hematoma were no longer present (). Simultaneously, an allograft biopsy was performed and showed no evidence of rejection, calcineurin inhibitor toxicity, or tubular injury. After surgical thrombectomy, urine output increased, and serum creatinine levels decreased to 1.8 mg/dL ().


A 27-year-old female who had suffered from recurrent fractures for 17 years, visual decline for 12 years, and a gradually rounded face for 7 years was admitted to our hospital. For 17 years, she has often suffered from various fractures (involving almost every part of the body) after mild activity. Twelve years ago, she suffered ocular proptosis, widened eye distance, and decreased binocular vision. In recent years, she has slowly developed a rounded face and her weight has increased significantly. Three years ago, she developed amenorrhea, and both adrenals were found by abdominal computed tomography (CT) to have multiple nodules. Therefore, the patient underwent bilateral adrenalectomy, and primary pigmented nodular adrenocortical disease (PPNAD) was confirmed (Figure ). After the surgery, she regained her normal menstrual cycles. Physical examination revealed an overweight female patient with a full moon face, thin skin, multiple purple striae on both sides of the abdomen, and numerous punctate areas of black or brown pigmentation on her lips and buccal mucosa. Detailed enquiry found a family history of “facial asymmetry”, as demonstrated in Figure .
Laboratory tests revealed an abnormal rhythm of cortisol secretion and increased urine free cortisol. Both the low-dose and high-dose dexamethasone suppression tests were not inhibited, indicating primary hypercortisolism. Serum adrenocorticotropic hormone (ACTH) level was less than 5.00 pg/mL (normal range: 5-50 pg/mL).
Skull CT examination showed that the skull and maxillofacial bones were remarkably enlarged, with both sclerotic and lytic lesions (Figure and B). Head magnetic resonance imaging (MRI) revealed diffused bone lesions in the frontal, occipital, and sphenoid bones, with low to intermediate and high signal intensity on both T1-weighted (WI) and T2WI images. Some of these retained high signal intensity on fat saturated T1WI and were markedly enhanced after the injection of gadolinium (Figure -F). Spine MRI demonstrated multiple flatted vertebrae, with patchy bone lesions that were of low signal intensity on T1WI, mixed signal intensity on T2WI, and high signal intensity on fat saturated T2WI, with enhancement on gadolinium enhanced T1WI (Figure ).


A 26-year-old male with a gradually rounded face and increased abdominal circumference for 2 years was admitted to our hospital. For 2 years, he had noticed his face becoming rounder and redder, the abdominal circumference had increased slowly, and more and more purple lines had developed on both sides of the abdominal skin. Right adrenalectomy was performed because of bilateral adrenal nodular hyperplasia and the postoperative pathology proved to be PPNAD (Figure ). On physical examination, the patient had a full, sanguineous moon face and scattered spots of pigmentation on his lips and buccal mucosa, which existed at birth and were similar to his father’s (Figure ).
Laboratory tests confirmed hypercortisolism because both the low-dose and high-dose dexamethasone suppression tests were not inhibited. Serum ACTH level was less than 5.00 pg/mL (normal range: 5-50 pg/mL). An enlarged frontal bone of inhomogeneous density with scattered small lytic lesions was found on skull CT (Figure ). The sclerotic lesion on the left part of the frontal bone was of high density on CT and low intensity on T1WI and T2WI MRI. In contrast, the lytic lesion was of low density on CT, low intensity on T1WI, and high intensity on T2WI, and was enhanced on gadolinium enhanced T1WI (Figure -D).
Genetic testing was undertaken by both patients to detect the mutation of the PRKAR1A gene, which was negative in the first case and positive in the second case. According to the patients’ clinical findings, imaging manifestations, and gene mutation, the diagnosis of CNC was made. Both patients were regularly followed after discharge, which was uneventful.


A 57-year-old female was admitted to the hospital with a one-day history of left knee and left shoulder pain and swelling. The pain was severe, sharp in nature, and caused disturbed sleep. Associated swelling and warmth of the joints were observed. Her symptoms worsened with physical activity, preventing her from standing or walking. The patient also had a fever of 100.9°F.
The patient was diagnosed with SLE 30 years prior to admission, during which her disease manifestations included membranous nephritis, arthritis of the hips, wrists, hands, and knees, vasculitic skin rash, and mild pancytopenia. The patient’s nephritis had progressed to end-stage renal disease, and she was dependent on hemodialysis. Her history included non-ST elevation myocardial infarction, colectomy with ileostomy after an episode of intestinal ischemia, and cardiomyopathy. Moreover, she developed avascular necrosis of the right hip (which was replaced), hand osteoarthritis, and osteoporosis. Finally, two years prior to admission, she was diagnosed with common variable immune-deficiency.
At the time of her hospitalization, she was on hydroxychloroquine 200 mg and prednisone 5 mg daily for the treatment of SLE. Previously, she had been treated with azathioprine, which she could not tolerate, and mycophenelate mofetil, to which she developed an allergic reaction.
The physical exam was notable for a temperature of 102°F with otherwise stable vital signs. She had tenderness on palpation of her left shoulder with notable swelling, severe pain on passive and active abduction, external rotation, and to a lesser extent, internal rotation. Her left knee was tender to palpation as well, had a large effusion, and was painful on passive extension more than on flexion. There was also mild symmetric bilateral swelling and tenderness in her proximal interphalangeal and metacarpo-phalangeal joints. Heberden nodes were observed on both hands.
Laboratory analysis showed normocytic anemia with hemoglobin level of 6.1 g/dL (worse than her baseline of 7 g/dL), white blood cell count of 6,200/μL (which was higher than her baseline), and creatinine of 4.8 mg/dL. She had a marked elevation in her inflammatory markers with a CRP of 176 mg/L and an ESR of 128. Her IgG levels were low at 412 mg/dL (normal range, 700–1600), whereas her IgM levels were undetectable. Complement levels were normal, and the anti-dsDNA antibody test was negative.
Her knee () and shoulder x-rays showed extensive damage in the femoral condyles and humeral head. A knee arthrocentesis showed inflammatory fluid with a white cell count of 71500/μL (80% polymorphonuclear leucocytes). No crystals were seen. Gram stain was negative. Shoulder arthrocentesis resulted in less than 1cc of fluid that was sent for culture. She was started on intravenous antibiotic therapy.
The synovial fluid culture showed sparse growth of S. lugdunensis. Subsequently, both joints were surgically washed out, and anterior synovectomy was performed. The patient also received intravenous immunoglobulin and was ruled out for endocarditis with a trans-esophageal echocardiogram. She was discharged in a stable condition on cefazolin.


A 45-year-old-woman visited our hospital after an abnormality was detected on chest CT screening. She had no symptoms and no past history. The chest CT scan showed a tumor measuring 121 × 82 × 58 mm extending from the cervical region to the middle mediastinum with homogenous low density (Fig a). Fluoro-2-deoxyglucose positron emission tomography (FDG-PET)-CT revealed positive accumulation (maximum standardized uptake value [SUVmax] 1.93). Surgical resection via the cervical approach was performed followed by video-assisted thoracic surgery (VATS) on the right side. The tumor was completely resected and the patient had an uncomplicated postoperative course. A diagnosis of dedifferentiated liposarcoma was made, and Ki-67 immunostaining was < 10%. Chest CT showed solitary local recurrence in the middle mediastinum 51 months after surgical resection (Fig b). As no other recurrent lesions were detected on FDG-PET-CT, repeat surgical resection was performed by right-side thoracotomy. The pathological findings of the resected tumor were the same as those of the primary tumor. Although adjuvant therapy was not performed, the patient has shown no signs of recurrence 12 months after repeat surgery.


A 62-year-old woman with no symptoms visited our hospital after an abnormality was detected on CT screening. Chest CT showed a tumor measuring 66 × 88 mm in the middle mediastinum with homogenous density (Fig a). FDG-PET-CT revealed positive accumulation (SUVmax 2.5); mediastinal liposarcoma was suspected based on the radiographic findings. Surgical resection was performed via median sternotomy, and as much tumor and peripheral fat tissue were resected as possible. Histopathologically, the tumor was diagnosed as dedifferentiated liposarcoma. Ki-67 immunostaining was approximately 20%. Adjuvant therapy was not performed. After 28 months, tumor recurrence was detected on chest CT (Fig b), and proton beam therapy was performed. No evidence of recurrence has been observed as of 17 months after radiotherapy.


An 81-year-old man with an anterior mediastinum tumor detected on chest CT during follow-up of autoimmune pancreatitis was referred to our hospital. Chest CT showed a tumor measuring 66 × 30 mm in the anterior mediastinum, with heterogeneous low and high-density components (Fig a). FDG-PET-CT revealed positive accumulation in the solid component (SUVmax 9.2) and anterior mediastinal liposarcoma was suspected. Sternotomy was performed and the tumor was completely resected without composite resection of other great vessels or organs. The resected tumor was diagnosed as dedifferentiated liposarcoma. Atypical cells were detected in the peripheral fat tissue, which showed low density on chest CT. The positive ratio of Ki-67 immunostaining was 50%. After 28 months, follow-up chest CT showed recurrent tumors behind the sternum. Repeat surgical resection was performed, but local recurrence was observed after eight months (Fig b). Radiotherapy was performed and the disease was well controlled.
Typical pathological and immunohistological findings are shown in ***Figure . Hematoxylin and eosin staining in case 3 revealed spindle tumor cells proliferate with fibrous stroma. Immunohistochemical analysis was positive for CKD4 and slightly positive for MDM2.


A 75-year-old man visited our hospital after an abnormal shadow was detected on chest X-ray screening. He did not exhibit any symptoms but chest CT showed a huge tumor in the posterior mediastinum projecting on either side of the intrathoracic space (Fig ). The esophagus was surrounded by the tumor. The tumor was suspected to be mediastinal liposarcoma and radical surgical resection was performed by bilateral thoracotomy. First, left-side complete VATS was performed. The tumor was smooth with only mild adhesion between the tumor and lung, aorta, and diaphragm. Leaving only adhesion around the esophagus, surgery was performed on the right side with a 20 cm post lateral incision. Like the left side, the extent of adhesion between the tumor and surrounding tissue was minimal. The tumor surrounded the esophagus, as determined on preoperative chest CT. However, there was no invasion of the esophagus, and it was relatively easy to peel the tumor off the esophagus. The tumor was removed en bloc and complete resection was performed. The tumor was diagnosed as dedifferentiated liposarcoma and the rate of positive Ki-67 immunostaining was 3%. Chest CT has shown no recurrence in three months.


A 78-year-old man visited our hospital because of rapidly progressing hoarseness and dyspnea over a three-month period. Chest CT showed a giant tumor in the middle and posterior mediastinum extensively surrounding the trachea (Fig ). As radiographic findings were suspicious for mediastinal liposarcoma, chemotherapy with doxorubicin (60 mg/m2) was immediately commenced. However, it was not effective and he died two weeks later as a result of respiratory failure. Post-mortem pathological examination revealed that the tumor was dedifferentiated liposarcoma but had not directly invaded the esophagus, trachea, or great vessels.


A 60-year-old male presented to the emergency department in a state of altered sensorium. Exploration of history revealed that he has been suffering from hypertension and hypothyroidism for the last 15 years and was diagnosed with PD 13 years prior to presentation. Since being diagnosed with PD, he had been on a combination of levodopa and carbidopa combination (100 + 25 mg respectively thrice a day) and had been taking the medications with good compliance and following up regularly with the neurologist. A day prior to presentation to emergency department, the patient met a minor road traffic accident in which he sustained minor abrasions on the forearms. There was no associated history of head injury, vomiting, or any loss of consciousness. Due to the accident, he missed the afternoon dose of his antiparkinsonian medications. On the same day evening, he appeared a bit drowsy, confused, and also developed low-grade fever. He also started talking irrelevantly and misidentified the family members. Due to this, his antiparkinsonian medications were stopped by the family members; however, other medications were continued. By the next morning, his condition worsened further, and developed fever, altered sensorium, and respiratory difficulty, following which he was brought to the emergency department.
In the emergency department, on examination, he was found to have high-grade fever (103°F), cogwheel rigidity of all the four limbs, diaphoresis, and altered sensorium. In view of the history and examination findings, possibilities of encephalopathy and NMS were considered and he was investigated accordingly. There was no history of intake of any psychotropic medications or intake of any licit or illicit substance during this period. On investigation, his hemogram, liver function test, renal function test, serum electrolytes, blood culture, urine routine microscopy, and urine culture did not reveal any abnormality. Computerized tomography (CT) of the brain revealed diffuse cerebral atrophy. His serum Creatine Kinase (CK) level was raised, i.e., 3500 IU (normal range: 26–308 IU). Over the next 48 h, the patient's clinical condition worsened despite starting of bromocriptine 2.5 mg thrice a day. Due to respiratory difficulty, he required ventilatory support. In addition, his blood pressure fell down, and he required intravenous fluids and inotropes. He continued in the same state for another 48 h. In view of lack of response and inability to find any specific cause for his condition, his history was reviewed. Careful history revealed that his symptoms followed discontinuation of the antiparkinsonian agents and, as a result, PHP was suspected and he was restarted on antiparkinsonian medications, i.e., levodopa and carbidopa combination (100 + 25 mg respectively thrice a day) along with tablet bromocriptine 2.5 mg thrice daily along with continuation of supportive measures. Over the next 48 h, gradually, his condition started improving. His rigidity reduced significantly, fever subsided, did not require any ventilatory support, sensorium improved, started recognizing his family members, and the CK level came down to 700 IU. By the end of 5 days of reinstitution of antiparkinsonian medications, he recovered completely and his CK level came down to 29 IU. He was discharged in an improved state from the hospital and has been maintaining well on the antiparkinsonian medications for the last 6 months.


A 47-year-old male with a HeartWare ventricular assist device (HVAD; HeartWare, Inc., Framingham, MA, USA) implanted for dilated cardiomyopathy three years previously presented for undergoing evaluation of low-flow alarms. His past history was unremarkable. At the time of HVAD implantation, he was at Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) level 2. Since the time of implantation, he was maintained on warfarin and was intermittently maintained on aspirin. His INR usually remained in the therapeutic range since implantation. He was at home and made a call to an LVAD coordinator because of low-flow alarm. He was living 303 km away and was immediately transferred to our center by an air ambulance. His waveform history showed no HVAD flow. His measured flow rate was −0.1 Lpm (). The patient had moderate dyspnea that did not require mechanical ventilation. Hemodynamic monitoring revealed pulsatile blood pressure of 80/50 mm Hg. His central venous pressure was 12 mm Hg. Lactate levels were in the normal range, and blood gas analysis did not demonstrate hypoxia. The HVAD was heard during auscultation and was operating at 2500 rpm. Blood tests showed normal renal and liver function, and his INR was 3.5. Transthoracic echocardiography revealed a dilated left ventricle with an ejection fraction of 15%. There were no signs of inflow or left ventricular thrombus. Outflow cannula obstruction was suspected, and multislice thorax CT was performed. CT showed total occlusion in the outflow cannula. The outflow graft was also attached to the sternum and sternal wire sutures (). The patient underwent discussion with the heart failure team with interventional cardiology and percutaneous intervention planned because of the high risk of mortality and morbidity of a probable surgical treatment. After obtaining written informed consent from the patient and relatives, the patient was taken to an intervention laboratory.
A 6 F introducer was placed at the right femoral artery by the Seldinger technique. A 0.38-inch guide wire and a 6-F right Judkins coronary catheter were placed together to the ostium of the outflow graft. In the angiograms, stenosis was detected from the ostium of the outflow graft to the middle part (). A 6-F right coronary catheter with a 0.38-inch guide wire was advanced to the middle portion of the outflow graft. Then, a Nitrex 0.35×300-cm guidewire was replaced with the 0.38-inch guidewire. The right coronary catheter was removed by leaving the guide wire in the outflow graft. First, an EverCross 8×40-mm peripheral balloon was advanced over the guidewire, and successive predilatations were performed at 8 ATM pressures for 2 min from the ostium to the middle portion of the aortic cannula (). After balloon dilatation, HVAD was turned on under bilateral carotid compression, but no flow was observed. Then, in the angiograms taken, severe stenosis was detected at the junction of the graft with the device, and the same procedure was performed in this region. The delivered radiopaque material reached the left ventricular cavity, and the device was restarted under bilateral carotid compression; the flow rates gradually increased and reached their normal values. In control angiograms, there was no narrowing along the cannula and full lumen clearance was observed. The process was terminated after observing that the values associated with device flow returned to normal.
The patient was taken to the intensive care unit (ICU) after the procedure. He was hemodynamically stable. At 3 h post operatively, the patient complained of paresthesia and severe pain in both lower extremities. Duplex US showed a thrombotic occlusion in the distal abdominal aorta and iliac bifurcation. The patient then underwent embolectomy. Under local anesthesia, both common femoral arteries were explored. There was no antegrade flow in both sides. After heparinization and bilateral distal clamping of the femoral arteries, proximal embolectomy was performed with 5F Fogarty catheter. Fibrinous embolic material was taken from both sides, and antegrade flow was maintained. The embolic material was whitish pink and gelatinous in some places (). Retrograde flow was normal; arteriotomies were closed, and the patient was taken to the ICU. Heparin infusion was continued for 24 h, and ACT values were around 200 s. The patient was discharged from the ICU after 24 h and was discharged from hospital after an uneventful 3-day period. Warfarin and the ASA regimen were not changed on discharge. First mounth CT, showed the open outflow graft ().


A 59-year-old male patient was admitted to the Department of General Surgery in the Second Affiliated Hospital of Nanjing Medical University (Nanjing, China) due to intermittent lower abdominal pain and distension accompanied by defecation difficulties for 3 years. These symptoms were initially relieved by laxatives but recently started to exacerbate. The patient denied nausea, vomiting, fever, melena and hematochezia. He had undergone several medical examinations including gastroscopy in another hospital, which showed gastritis and duodenitis. His colonoscopy showed cecum deformation and cicatricial changes of the mucous membrane in the colon hepatic flexure. The patient had never underwent surgery. There was nothing remarkable in his past medical and family histories. His vital signs were unremarkable. Upon physical examination, no obvious cardiovascular or respiratory system abnormalities were found. His abdomen was flat and soft. There were no signs of obvious pressure pain, rebound tenderness or abdominal mass. Murphy’s sign was negative. Auscultation revealed normal bowel sounds. Blood, urine, stool, as well as liver and kidney function tests, coagulation studies, and electrocardiograms were all unremarkable. Chest X-rays revealed an abnormal gas shadow in the right sub-phrenic space and a segment of gaseous distended colon, which was interposed between the liver and the right diaphragm. A CT scan of the abdomen confirmed right hepatic atrophy and interposition of the colon (Figure ). Further imaging by CT simulation endoscopy identified a cystic dilatation in the colon hepatic flexure, where the maximum diameter was 8.2 cm. There was no evidence of bowel wall thickening or bowel obstruction (Figure ). These findings, together with the symptoms this patient was experiencing, indicated that the patient has Chilaiditi syndrome. There was no urgent indication for surgery. However, the patient was unable to endure his defecation difficulties and finally underwent laparoscope-assisted right hemicolectomy. Postoperative recovery was uneventful. He was discharged after 14 d of hospitalization with close follow-up. During a 4-wk follow-up period, he reported complete resolution of abdominal pain and distension. Moreover, defecation improved due to ameliorated regularity of bowel movements. During the subsequent 9-mo follow-up period, the patient remained symptom-free.


A 45-year-old male patient reported to the Department of Oral Medicine and Radiology, with the chief complaint of multiple decayed teeth. Clinical intraoral examination revealed dental caries in 17, fractured restoration in 26, root stump of 27, and deep dental caries in 36. Clinically 36, 37 were absent due to extraction a few years before because of pulpal involvement of the teeth. Orthopantomogram (OPG) confirmed the oral findings. The OPG also showed an impacted 18 and inverted 28 impaction. As shown in , the crown of the impacted molar was facing the maxillary sinus floor. The patient was informed, but he refused to have surgery to remove the impacted teeth. He was only interested in having the decayed teeth treated. The patient was, therefore, advised to report for periodic follow-up visits.


A 50-year-old female patient reported to the Department of Oral Medicine and Radiology with the chief complaint of multiple root stumps in the teeth (of 6 months’ duration) causing discomfort during mastication. Intraoral examination and OPG showed multiple root stumps of 17,14,13,12,11,21,22,23,24,25,32,31,41,42 and missing 16,15,26,27,37,36,35,34, 33,43,44, 45,46,47. In addition, OPG showed inverted 38 impaction with the crown quite close to the mandibular canal and the root apex near the alveolar crest []. The patient was advised to have all root stumps and impacted 38 removed to be followed by complete denture replacement. She, however, declined the surgical treatment.


A 25-year-old Saudi female with a known case of autoimmune thyroiditis (Hashimoto's thyroiditis) presented to the emergency room in stuporous condition. For the past 7 years, she had been treated at a different hospital and prescribed irregular thyroxine replacement to regulate her menstrual cycles. The patient presented with fever, sore throat, vomiting, abdominal pain and confusion of 2 days duration.
A blood sugar test by glucocheck revealed a blood sugar level of 1.7 mmols/l (30.6 mg/dl). The patient was resuscitated with intravenous glucose and her cognitive function promptly improved. Previously, she had experienced similar episodes of hypoglycemia following flu-like symptoms. The patient had a history of nausea, occasional vomiting, abdominal pain and weight loss of 20 kg over the past 2 years. There was no history of headache visual disturbance, galactorrhea, polyuria and polydipsia. The patient had a 6-year-old daughter and had been unsuccessful in conceiving since her daughter's birth. Following delivery, she had no history of postpartum hemorrhage but had experienced irregular menstrual cycles. There was no family history of autoimmune disease. Upon physical examination, the pulse was 102/min and the blood pressure was 100/64 mmHg. There was no hypo- or hyperpigmentation of the skin, hyperpigmentation of the buccal mucosa. The rest of physical examination revealed no abnormalities. The radiological imagings were normal; MRI of the pituitary fossa showed a partially empty sella with asymmetry of the residual pituitary gland [].
The patient was diagnosed with autoimmune thyroiditis, autoimmune thrombocytopenia, celiac disease (PAS III) and partial empty sella syndrome with hypopituitarism. Corticosteroids were initiated, followed by adjustment by adjustment of the Thyroxine. A gluten-free diet was advised by the dietician. The patient's symptoms improved and blood sugars were maintained within the normal range. Her thrombocytopenia responded quickly with steroid treatment [].


We report a case of a 24-year-old male with a left-sided anterior subcoracoid shoulder dislocation () following a road traffic accident. This was the first episode of dislocation. The shoulder was closed reduced by the Kocher’s technique within 3 hours of trauma, and a post-reduction radiograph was taken to confirm concentric reduction. The shoulder was immobilized for 3 weeks ( and ), following which rotator cuff strengthening exercises were initiated. The patient was followed up, after the shoulder was reduced at 3 weeks, 3 months, and 6 months, and then, the patient reported after 2 years. This patient was a non-alcoholic healthy college-going student who was not on any medications. At 6-month follow-up, the left shoulder radiograph showed a sclerotic sector of the head with cortical erosions near the greater tuberosity ( and ). A magnetic resonance imaging (MRI) was done which revealed a geographic area of the anterior part of humeral head with an altered marrow signal, which was iso- to hyper-intense on short tau inversion recovery sequence, with a hypointense rim on T1 sequence. The differential diagnosis was a bone bruise or osteonecrosis of the humeral head. However, due to the sclerotic changes on the radiographs, possibility of osteonecrosis could not be ruled out and this required displaced medially, outside the bicipital groove ( and ), and the rotator cuff was normal. The patient had a stable shoulder with mild pain at the extremes of motion. A radiograph of the pelvis with both hips was normal, without any sclerotic changes of the femoral head. The patient was treated with cuff strengthening exercises, and he resumed all routine activities including leisure sporting activities. Bisphosphonate was not administered. At the end of 2 years, the patient had no functional restriction and had an excellent UCLA score. The shoulder radiograph revealed a mixed sclerotic and lytic lesion in the humeral head without any cortical defect and a maintained a congruent articular surface. The greater tuberosity erosions seen on the earlier radiographs became sclerotic without any further undermining ( and ). A repeat MRI of the shoulder at 2 years revealed a 19 mm3×17 mm3×12mm3serpiginous, geographic area, larger in size than the previous MRI, which was consistent with osteonecrosis of the humeral head without any deformation of the articular surface. There was a partial thickness tear with medial retraction of the subscapularis. The long head of biceps tendon was torn and retracted. The rest of the rotator cuff and glenoid labrum was normal ( and ). An MR angiography of the shoulder was performed to know the status of the circumflex vessels (, , , ). It showed attenuation of the some of the branches of anterior circumflex humeral artery, but all the vessels around the humeral neck were patent, but their course was not clearly defined. To enable a better visualization of the arteries around the neck of the humerus and to localize the site of obstruction of the artery, if any, a computerized tomography angiography of the left shoulder was performed at 2 years (, , , and ). This study reported that the origin and proximal part of the anterior circumflex humeral artery was not opacified while the distal part of the artery was seen filling with the dye through the collaterals. The posterior circumflex humeral artery was normal. On clinical examination, the patient was able to perform 170° shoulder abduction, with a normal scapulothoracic rhythm. The power of internal rotation of the shoulder was 4/5 as per the Medical Research Council grading on the left side, and the power of the rest of the shoulder movements such as external rotation, abduction, forward flexion, and extension was 5/5. The patient was advised biceps tenodesis with subscapularis repair. However, the patient was not willing for the same.


A 30-year-old woman presented with intermittent, high-grade fever with chills for 5 days prior to admission associated with headache, myalgia and nausea. With the high frequency of fever, leucopenia and thrombocytopenia during rainy season, a provisional diagnosis of dengue infection was made at a nearby hospital. The patient started on intravenous fluids and supportive treatment, and was then referred to the Bangkok Hospital for Tropical Diseases, a referral centre for tropical diseases, for further investigations and management.
On the first day of admission to the hospital, she was mildly pale, febrile (37.8°C), with the heart rate of 84 beats/min and respiratory rate of 20 breaths/min without hepatosplenomegaly. Other examinations were unremarkable. P. vivax was detected in her peripheral blood smear. She was diagnosed as P. vivax infection and chloroquine was thus given.
On the fourth day of admission, although malaria peripheral blood smear was negative, she still had an intermittent, high-grade fever, and developed dyspnoea and oxygen desaturation (O2sat=91% on room air).


A 43-year-old man with documented IHES presented to the hospital with paroxysmal chest discomfort, exertional dyspnea, orthopnea, occasional fever, and skin rashes. He reported a ten-year history of hepatitis B and was on entecavir without history of parasitic infections, bronchial asthma, hypertension, or diabetes mellitus. Physical examination showed stable vital signs, distended jugular vein, cyanosed lips, increased cardiac borders, clear lungs, and increased P2 sound, but no cardiac murmurs, soft, non-tender abdomen, non-palpable liver and spleen, and moderate edema on the bilateral lower limbs. Routine blood test showed normal white blood cell (WBC) count with increased eosinophils 2.42 × 109/L (reference range = 0.02–0.52 × 109/L), red blood cell (RBC) count 3.86 × 109/L (reference range = 4.3–5.8 × 109/L), hemoglobin 124 g/L (reference range = 130–175 g/L), platelet 56 × 109/L (reference range = 125–350 × 109/L). Other lab reports consisted of: AST 59.1 U/L (reference range = 15–40 IU/L); ALT 112.7 U/L (reference range = 9–50 IU/L); ALP 178.2 U/L (reference range = 45–125 IU/L); albumin = 26.5 g/L (reference range = 40–55 g/L); globulin 43.9 g/L (reference range = 20–40 g/L); total bilirubin 56.6 umol/L (reference range = 6.8–30 umol/L); direct bilirubin 20.3 umol/L (reference range = 0–8.6 umol/L); indirect bilirubin 36.3 umol/L (reference range = 5.1–21.4 umol/L); PT 26.5 s (reference range = 9–23 s); INR 2.26 (reference range = 0.60–1.20); ESR 37/1 h (reference range = 0–15/1 h); BNP 2090 pg/mL (reference range = 0–100 pg/mL); D-dimer 3660 ng/mL (reference range = 100–600 g/mL); arterial blood gas with pH 7.46 (reference range = 7.35–7.45); pO2 106 mmHg (reference range = 83–108 mmHg); and pCO2 28 mmHg (reference range = 35–48 mmHg). Among anti-phospholipid antibodies, anti β2-glycoprotein I antibody 34 RU/mL (0–20 RU/mL) and anticardiolipin IgA antibody 24 U/mL (reference range = 0–10 U/mL), while anticardiolipin IgM antibody and anticardiolipin IgG antibody were within normal limits. Anti-nuclear antibody, anti-neutrophil antibody, and thyroid function tests were also within normal limits. We conducted routine urine and stool tests that did not show any evidence for parasitic infections.
ECG showed sinus tachycardia and right ventricular hypertrophy. Echocardiography revealed enlarged right atrium (67 × 55 mm), enlarged right ventricle (45 mm), normal left ventricle (38 mm), normal ejection fraction (62%), increased pulmonary artery systolic pressure (83 mmHg), decreased right ventricular systolic function (TAPSE 11 mm), and mild pericardial effusion. There were no valvular abnormalities found on echocardiography. Abdominal ultrasonography revealed hepatic congestion, gall bladder wall edema, splenomegaly, and ascites. Venous ultrasound of lower extremities was normal. Pulmonary artery CTA was negative for thrombus. The patient did not give consent for ventilation/perfusion scan. The pulmonary function test was normal. Bone marrow smear revealed significantly active nucleated cell proliferation, increased eosinophil line 38%, eosinophils in different stages with unbalanced development of nucleoplasm of some eosinophils like megaloblastic degeneration. Right heart catheterization (RHC) revealed right atrial pressure 22/18/20 mmHg, right ventricle pressure 91/23/53 mmHg, pulmonary artery pressure 91/47/67 mmHg, and mean pulmonary arterial wedge pressure 14 mmHg. Cardiac output and pulmonary vascular resistance were not measured due to limited lab support. Normal saline was used during RHC. Finally, the patient was further diagnosed with precapillary PH and right heart failure. Treatment included prednisolone 10 mg daily for hypereosinophilic syndrome, ambrisentan 10 mg daily for PH, and diuretics and digoxin for the right heart insufficiency. The patient could not appear for follow-up visits; hence, information was obtained over the phone that he had significant improvement of the exertional dyspnea and chest discomfort. The lower limb edema also subsided.
This case has been approved for reporting and publication by the Ethical Committee of the First Bethune Hospital of Jilin University.