Biomedical subjects

Rohini Sridhar

Publications and source records attributed to Rohini Sridhar.

3 recordsLinked to original sources

PubMed2005

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.

Adult↗

PubMed2004

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.

Basal Ganglia↗

PubMed2004

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.

Adult↗