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Biomedical subjects

I V Nath

Publications and source records attributed to I V Nath.

14 recordsLinked to original sources
PubMed1987

Fusidic acid-induced hyperbilirubinemia.

A 72-year old man developed jaundice while on fusidic acid therapy for suspected osteomyelitis. Hyperbilirubinemia was predominantly of the conjugated variety and elevation in liver enzymes was mild and transient. Although serum bilirubin fell rapidly after fusidic acid was stopped, complete resolution of the hyperbilirubinemia took nearly a month. Other possible causes of jaundice were excluded. Light microscopy of a needle liver biopsy showed focal hepatocyte feathery degeneration, intracellular bile retention, and canalicular bile plugging, most prominent in perivenous regions. Electron microscopy revealed varying degrees of canalicular dilatation, loss of microvilli, and disruption of the canalicular membrane with vesicular bleb formation as well as canalicular bile plugs. Widening of the pericanalicular ectoplasmic zone with accumulation of cytoskeletal filaments was also noted. These findings are similar to those reported in experimental cholestasis induced by bile acids. Possible mechanisms of jaundice caused by fusidic acid are discussed.

Aged↗
PubMed1983

Renal lesions in leprosy amongst north Indian patients.

Sixty consecutive patients with leprosy were investigated for renal involvement. Clinically overt renal disease was present in 4 patients; 3 presented with a nephrotic state and one patient with progressive renal failure. Urinalysis showed daily protein loss ranging from 0.4 to 8.9 g in 8 patients and microscopic haematuria in 4 cases. Elevated levels of blood urea and creatinine were seen only in one patient with diffuse proliferative glomerulonephritis. Of the 36 patients in whom distal tubular functions were evaluated, concentration and/or acidification defects were detected in 9 patients (25%). Renal histology revealed no abnormality in any of these patients. Serum C3 levels were decreased in 5 patients with lepromatous leprosy and 3 patients with borderline leprosy. Histological evidence of renal involvement was detected in 9 patients (15%). Amyloid deposits were seen in 3 (5%) patients of whom 2 had lepromatous leprosy and one had tuberculoid leprosy with chronic trophic ulcers. Mesangial proliferative lesions were seen in 5 (8.3%) and diffuse proliferative lesions (with crescents in more than 70% of glomeruli) in one patient. All of them had lepromatous leprosy. Three of the 5 patients with mesangial proliferative glomerulonephritis had erythema nodosum leprosum at the time of biopsy. Immunofluorescence studies revealed granular deposits of IgA, IgM and C3 in one patient with mesangial proliferation and IgA/IgM with or without C3 in 3 more patients in whom renal histology was normal. Glomerulonephritis associated with leprosy appears to be immune mediated but confirmation requires identification of lepra antigen in the glomerular immune complex deposits.

Adolescent↗