Giant cell tumor of tendon sheath mimicking pyogenic granuloma in the index finger pulp: a case report.

We report a 75-year-old man who presented with a painless friable mass in the index finger pulp mimicking pyogenic granuloma. Complete excision of the mass was done. The radiological and the histopathological findings suggested giant cell tumor of the tendon sheath. The patient had no recurrence at the end of a two-year follow-up. This unusual clinical presentation of the giant cell tumor of the tendon sheath was our study base and adds up to its variant presentation in the literature.

Eosinophilic gastroenteritis: a diagnosis behind the curtains.

Eosinophilic gastroenteritis (EG) typically presents with a combination of chronic nonspecific gastrointestinal symptoms which include abdominal pain, nausea, vomiting, diarrhoea, weight loss, and abdominal distension. Approximately 80% of the patients have symptoms for several years. A high degree of clinical suspicion is often required to establish the diagnosis, as this disease is extremely rare.We are presenting the case of a 19 year old boy who presented with growth retardation and markedly decreased secondary sexual characteristics. Taking the full clinical history and a meticulous investigation finally led to the diagnosis.

Recombinant factor VIIa in a case of pontine hemorrhage.

A 59-year-old lady presented with hypertensive hemorrhage involving the pons. Since she presented within 3 hours of onset of the stroke, recombinant factor VIIa was administered. From a state of altered sensorium there was a rapid recovery of consciousness followed by gradual improvement in limb weakness. Serial CT scans of the brain revealed no further expansion of the hematoma. The hematoma progressively resolved. Recombinant factor VIIa could be an attractive therapeutic option in treating hemorrhages at critical sites like brainstem where expansion of hematoma could be fatal.

Recurrent venous thrombosis with factor V Leiden mutation.

A patient who presented with recurrent venous thrombosis is reported. Following an episode of spontaneous deep vein thrombosis of the lower limb he was started on oral anticoagulant therapy, which he discontinued. He presented with cerebral venous thrombosis and improved partially with anticoagulant therapy. Evaluation for hypercoagulable states revealed factor V Leiden mutation by polymerized chain reaction method. Long-term anticoagulation has been planned. Evaluation for factor V Leiden mutation is always warranted in patients presenting with spontaneous thrombosis, especially if there is recurrent thrombosis.

Cognitive dysfunction in cholesterol embolic disease.

A patient who developed neurological and renal complications following coronary angiogram and coronary artery bypass grafting is reported. Neurological involvement was in the form of fluctuating sensorium and a subcortical pattern of dementia. Renal failure was seen in the form of raised urea and creatinine levels. Renal biopsy revealed the cause of the renal failure to be due to cholesterol embolic disease. While the sensorium often improved following renal replacement therapy (dialysis), the dementia was poorly responsive to therapy. The patient succumbed due to progressive renal failure. Awareness of the protean manifestations and a high index of suspicion are essential for appropriate diagnosis in order to enable the clinician to accurately prognosticate in this often fatal disease.

Neuroacanthocytosis misdiagnosed as Huntington's disease: a case report.

A patient with the typical features of neuroacanthocytosis is reported. Chorea, tics, personality changes and caudate atrophy on cranial MRI resulted in an erroneous diagnosis of Huntington's disease elsewhere. Attention to other features viz., absence of ocular motility disturbances, amyotrophy, areflexia, EMG evidence of axonopathy, raised serum creatinine phosphokinase (CPK) levels and the typical erythrocytic acanthocytosis enabled us to establish the correct diagnosis. The typical features of the disease as seen in the patient are discussed. In view of the implications for genetic counseling, careful clinical and laboratory evaluation is always warranted to exclude neuroacanthocytosis in all suspected cases of Huntington's disease.