ABSTRACT
Objective: We hypothesize that upper gastrointestinal symptoms in cerebral malaria are due to gastric motor dysfunction. But gastric motility studies in cerebral malaria are scarce. Methods: We determined gastric emptying half-time (GET½) of liquid meals quantitatively by radio isotope scintigraphy in 25 patients of cerebral malaria and 10 healthy controls. Results: GET½ was prolonged (46.5 ± 4.8 min) significantly (p <0.001) in patients of cerebral malaria compared to healthy controls (27.6 ± 5.3 min). Conclusion: Cerebral malaria can cause prolongation of gastric emptying time of liquid foods.
ABSTRACT
A prospective study among the patients (n = 301) belonging to the coastal districts of Orissa having complicated falciparum malaria with multiorgan failure fulfilling modified APACHE II criteria, for a period of two years in this hospital setting was carried out with particular emphasis on hepatic involvement. There were 206 males and the rest females. Hepatic involvement in the form of raised serum bilirubin levels > or = 6 mg% and prothombin time > 4 compared to controls was found in 192 cases (63.8%). On analysis out of 192 cases predominantly conjugated hyperbilirubinaemia, mixed patterns and unconjugated hyperbilirubinaemia were seen in 115 (59.9%), 64 (33.3%) and 13 (6.8%) cases respectively. Serum bilirubin ranged from 6 to 38 mg%. Aminotransferase aspartate (AST, SGOT) and aminotransferase alkaline (ALT, SGPT) were raised almost two-fold in 98% cases of multiorgan failure with hepatic failure with mean values of 78 +/- 30.4 IU/l and 81 +/- 29.06 IU/l respectively. Nearly three-fold elevation of alkaline phosphatase was observed in 80% cases with mean (315 +/- 39.4 IU/l). Prothombin time was prolonged with mean 7 +/- 3 seconds. Serum proteins and albumin/globulin ratio were normal. There was no difference in glycaemic status over controls. In selected cases, liver histopathological study showed abnormalities in the form of Kupffer cell hyperplasia, mononuclear cell infiltration, hepatocyte necrosis, fatty changes and cholestasis. Majority of patients in multiorgan failure who died, had hepatic failure.
Subject(s)
Adolescent , Adult , Female , Hepatitis/parasitology , Humans , Hyperbilirubinemia/parasitology , Liver/pathology , Malaria, Falciparum/complications , Male , Middle Aged , Multiple Organ Failure/parasitology , Prognosis , Prospective StudiesSubject(s)
Adult , Antineoplastic Agents, Alkylating/therapeutic use , Busulfan/therapeutic use , Cardiac Tamponade/complications , Female , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications , Pericardial Effusion/complications , Pericardiocentesis , Pleural Effusion/complicationsABSTRACT
Twenty two patients of subacute hepatic failure (SAHF), diagnosed when jaundice progressed for more than 8 weeks with appearance of ascites, with or without encephalopathy, along with biochemical evidence of hepatocellular damage, were studied. The male and female ratio was 4.5:1 and majority (45.4%) of cases were between the age group of 41-50. The mean biochemical values were: S.bilirubin; 9.2 +/- 3.8 mg/dl SGOT; 94.4 +/- 25.0 I.U./lit., SGPT; 107.8 +/- 32.7 I.U./lit., S.Protein; 5.2 +/- 3.5 secs. Ascitic fluid analysis showed transudate in 16 (72.7%) and exudate in 6 (27.2%) patients. Bacterial peritonitis was found in 5 (22.7%) patients. Liver biopsy showed bridging and submassive necrosis. The complications developed in the hospital were: renal failure (36.3%), infection (27.2%), G.I. bleeding (18.1%) and encephalopathy (13.6%). The mortality was (86.3%). Out of 3 (13.6%) patients who survived, only two recovered completely and one had biochemical evidence of hepatocellular necrosis after 6 months of follow up.