Upjeet Kaur

Hepatic outflow obstruction (Budd-Chiari syndrome). Experience with 177 patients and a review of the literature.

Budd-Chiari syndrome (BCS) may not be as uncommon as was once believed. Our study has substantiated the existence of 2 major clinical forms. The acute syndrome is invariably associated with extensive blockage of the major hepatic veins, resulting in congestive liver cell necrosis. In a small, but significant, number of patients the inferior vena cava (IVC) is also occluded. The important etiologic factors are related to hypercoagulability of blood. Immediate placement of a shunt improves survival. The chronic syndrome is characterized by portal hypertension and is associated with a variable abnormal vascular anatomy. The causes of the chronic syndrome are not clear, but a substantial number of cases are related to the presence of an IVC membrane. Shunt surgery is effective but procedures aimed at the primary pathology are likely to be even more so. The natural history of BCS should be viewed over a long period of time. The very long survival of several patients urges a more cautious approach to surgical remedies. Budd-Chiari syndrome probably represents a spectrum of disease caused primarily by a hypercoagulable state and having a varied presentation depending on the balance between rate of formation and the extent of the thrombosis and the bodys own rate of thrombolysis and recanalization. The extent and efficacy of the individuals collateral circulation and the rate of development of liver fibrosis are other determinants. It is thus possible to view BCS as a continuum of a single pathogenetic spectrum. Pregnancy-related BCS in India probably has strong social determinants, and is usually acute and fulminant. We have, however, documented a chronic form not described earlier. Children usually do not have acute BCS, but chronic BCS in children and adolescents is similar to that in adults. Membranous obstruction of the inferior vena cava (MOVC) is common and was found even at a young age. The association of MOVC with hepatocellular carcinoma, however, did not appear to be as clear as was previously believed. There has been a wide geographical variability in the causes and manifestations of BCS. Our study has clearly shown that--Kiplings categorical statement to the contrary--East and West do meet in India, in the Budd-Chiari syndrome.

Hepatitis E virus transmission to a volunteer

Hepatitis E virus (HEV) causes an enteric non-A, non-B hepatitis. The disease occurs in epidemic settings and sporadically, and viral transmission is thought to be faecal-oral. We present here a single volunteer study of HEV transmission followed by disease. Clinical and biochemical features of the infection correlated with HEV detection in the stools and sera by reverse transcription/polymerase chain amplification. IgG antibody has persisted for 2 years. The presence of HEV in serum before clinical signs appeared suggests that in endemic areas sporadic transmission of HEV may also occur parenterally.

Budd-Chiari syndrome : Our experience of 71 patients

Background : Hepatic venous outflow obstruction (Budd–Chiari syndrome) is frequently encountered as a cause of portal hypertension at our centre.

Common aetiological agent for epidemic and sporadic non-A, non-B hepatitis

Enterovirus-like particles have been reported in the acute phase of both epidemic and sporadic non-A, non-B (NANB) hepatitis. To examine whether these particles were the causative agent in the two types of disease, 29 patients with acute viral hepatitis in a north Indian epidemic outbreak and 9 with sporadic acute disease were investigated. 25 (86%) of 29 patients with epidemic hepatitis and 5 (56%) of 9 with sporadic disease were diagnosed as having enterically-transmitted-NANB hepatitis by exclusion. Virus-like particles (VLP) of 30-34 nm were detected in stool of 1 patient with epidemic and 1 with sporadic hepatitis. The VLPs crossreacted serologically and a specific IgM response was seen in acute epidemic and sporadic serum samples. After inoculation with infected stool rhesus monkeys had a mild rise in liver enzymes, and bile samples contained VLPs. These results suggest that the aetiological agent in epidemic and sporadic disease is the same.

Diminution in Parietal Cell Number in Experimental Portal Hypertensive Gastropathy

Portal hypertensive gastropathy is awell-established clinical entity. Although stimulatedacid secretion has been found to be decreased in portalhypertensive rats, the parietal cell mass has not been studied. Portal hypertension was produced inWistar rats either by partial portal vein ligation (N =16) or by common bile duct ligation (N = 23) andconfirmed by intrasplenic pulp pressure measurement. The parietal cells were isolated and counted in aNeubaur hemacytometer. The parietal cell count was alsodone in microscopic sections at direct histopathologicalexamination. The viable, isolated parietal cell count and parietal cell count onhistopathological examination were significantlydecreased in partial portal vein ligated rats.Similarly, in common bile duct ligated rats, theparietal cell count was decreased as compared to sham-operatedrats. In experimental portal hypertensive gastropathythere is a decrease in parietal cell number.

Anorexia nervosa in a patient with systemic lupus erythematosus

SummaryAnorexia nervosa has not been described in patients with systemic lupus erythematosus (SLE). The case of a patient with SLE who developed the classical features of anorexia nervosa is described. Although an impressive interplay between psychosocial and cultural factors was present, the possibility that this syndrome was produced by active CNS vasculitis remained.

Extrahepatic portal hypertensive gastropathy in Wistar rats. Modulation of acid secretion in isolated parietal cells

Stimulated acid secretion in portal hypertensivegastropathy is blunted and could be due to defectivesignal transduction in the parietal cell. Therefore, anattempt was made to study the levels of second messengers in parietal cells in experimentalextrahepatic portal hypertensive gastropathy. Our aimwas to measure acid secretion, intracellular freecalcium, calcium transport, cyclic AMP, and ATP levels in the parietal cells isolated from the gastricmucosa of portal hypertensive rats. Acid secretion usingacridine orange, intracellular free calcium usingFura-2/AM, calcium influx and efflux by45CaCl2 and cyclic AMP by RIA kits were measured inunstimulated and histamine- and carbachol-stimulatedisolated parietal cells in rats with partial portal veinligation and sham operation. ATP was measured by HPLC. In portal hypertensive gastropathy,stimulated acid secretion was blunted, and there was adecrease in basal intracellular free calcium. Calciuminflux and efflux were at a higher level, and there was a decrease in elevation of intracellularfree calcium and cyclic AMP levels with secretagogues.There was also a decrease in ATP. In conclusion, thereexists a low energy state in addition to multiple aberrations at the second messenger level inparietal cells in portal hypertensivegastropathy.

Modulation of acid secretion in common bile duct ligation-related gastropathy in Wistar rats

Background: Portal hypertensive gastropathy is associated with fundic gland atrophy, resulting in a decrease in chief and parietal cells, and diminished acid secretion.

Activity of brush border membrane enzymes in proximal jejunum of portal hypertensive rats

Purpose. Malabsorption accompanies portal hypertension, especially when associated with chronic liver disease. The development of portal hypertension is accompanied by significant alterations in the splanchnic microcirculation. In this study, the effect of extrahepatic and intrahepatic portal hypertension on brush border membrane enzymes was estimated. Methods. Portal hypertension was induced in rats by partial portal vein ligation (PPVL) (n = 6) and common bile duct ligation (CBDL) (n = 6), and the activity of sucrase, lactase, alkaline phosphatase, and leucine aminopeptidase (LAP) in the intestinal homogenate was measured. Results. Intrasplenic pulp pressure (ISPP) (in cm of saline) was found to be elevated in PPVL (21.3 ± 1.47) and CBDL animals (21.5 ± 1.79) as compared with findings in their respective sham-operated controls (12.74 ± 0.86, 11.83 ± 1.04). Only sucrase and LAP activity was significantly elevated (P < 0.05) in the PPVL group. No changes were observed in the CBDL group. Conclusion. Only sucrase and LAP activities were increased in PPVL rats.

Duodenal-Ulcer - Calcium Status in Isolated Parietal-Cells

Although the etiology of duodenal ulcer is not known, its treatment with drugs that reduce acid secretion is well accepted. The central role of calcium in stimulus-secretion coupling resulting in acid secretion by gastric parietal cells is documented. However, the status of intracellular calcium in gastric parietal cells in the basal state in patients with duodenal ulcer is not known. Multiple endoscopic gastric mucosal biopsies from the corpus of the stomach of 52 patients were processed and isolated parietal cells were studied. Intracellular calcium was estimated using fura-2-acetoxymethyl ester. Influx and efflux were determined by using radioactive calcium. Acridine orange retention was used to assess acid production. Only calcium influx at 20 min was significantly (P<0.01) more in patients with duodenal ulcer as compared to the control group. There was no difference between the groups in calcium influx at 0 and 60 min; calcium efflux at 0, 20, and 60 min; intracellular free calcium and acid secretion. We conclude that in the unstimulated state calcium homeostasis in isolated parietal cells of patients with duodenal ulcer shows only a minimal difference as compared to controls.