Acetylsalicylic acid-induced biochemical changes in gastric juice: a failure of adaptation?

BACKGROUND: Acetylsalicyclic acid (ASA) causes gastric mucosal damage which diminishes with continued use due to adaptation. METHODS: To determine the net effect of these processes on the gastric juice, we estimated acid, osmolality, bicarbonate concentration in nonparietal gastric juice, calcium, potassium and sodium in 18 patients (9 men; mean age 32 years, range 20-46) with irritable bowel syndrome, before and after 600 mg of ASA taken post-cibum thrice daily for 4 weeks. Osmolality was determined by an osmometer, acidity by titration, and Na+, K+ and Ca++ using a sodium-potassium-calcium analyzer; bicarbonate was derived from the two-component model of Feldman. RESULTS: Gastric juice K+ and Na+ increased significantly from mean (SE) 14.6 (0.5) and 197.5 (16.3) to 16.7 (0.4) and 256.8 (18.1) mEq/L, respectively. The other parameters remained unchanged. CONCLUSION: After four weeks of ASA ingestion there is a dichotomy of gastric mucosal injury and adaptation, with preservation of acid secretion but continued loss of Na+ and K+.

Sexual behaviour, drug use and hepatitis B infection in Chandigarh students.

BACKGROUND: The relationship of hepatitis B virus infection with drug use and sexual activity in Indian college students has not been studied earlier. METHODS: We studied this relationship in Chandigarh, using a prospective, cross-sectional questionnaire-based survey and blood tests for hepatitis B markers. The responders were assured of the confidentiality of their responses and blood test results. RESULTS: Of the 1311 students who participated, 192 (15%) were sexually active. Eight-four per cent of them were heterosexual, 7.3% homosexual and 8.7% bisexual. Thirty-seven per cent of heterosexuals and 36% of homosexuals had more than one partner. Condoms were used by 24% heterosexuals, 11% bisexuals and 7% homosexuals. Of the sera tested, 2.9% were hepatitis B surface antigen positive and 10.4% were positive for the antibody to hepatitis B surface antigen. Fifteen per cent consumed alcohol, but only 1.6% were addicted to other drugs. Two students were intravenous drug users. Eleven per cent had donated blood at least once and a third of these had suffered from jaundice in the past. CONCLUSION: The pattern of sexual behaviour, low condom use and the small but definite prevalence of hepatitis B virus infection in this population of students suggests that the human immunodeficiency virus infection may spread rapidly when it enters this community.

Sodium and potassium content of liquid antacids.

Sodium and potassium contents of 37 commercially available liquid antacid preparations were estimated. Only nine preparations had sodium content below 60 mmol/L. The potassium content was below 1 mmol/L in 26 preparations. We conclude that caution should be exercised in selecting liquid antacid preparations in whom critically ill patients for electrolyte overload could prove harmful.

Monoclonal antibodies which inhibit in vitro cytotoxicity of axenic Entamoeba histolytica.

A panel of 12 independent hybridoma cell lines secreting monoclonal antibodies to axenic E. histolytica (HM1) have been developed. A hybridoma cell line P4 C4 P2 F8 C8 (clone C8) produced monoclonal antibodies (MoAb C8) of IgG1 isotype which recognised a 29 KD surface associated antigen of amoebic trophozoites in Western immunoblot. Immunofluorescent probing with MoAb C8 employing live and acetone fixed amoebic trophozoites indicated 29 KD molecule on the surface plasma membrane of E. histolytica trophozoites. The MoAb C8 also agglutinated the live amoebic trophozoites. Pretreatment of amoebic trophozoites with anti 29 KD monoclonal antibody significantly (P less than 0.01) inhibited in vitro cytotoxicity of amoebic trophozoites to the cultured baby hamster kidney (BHK-21) cells. MoAb recognised a 29 KD molecule of E. histolytica trophozoites which mediated cytotoxic potentials of the parasite. The absence or variable degree of expression of cytotoxic 29 KD molecule may possibly serve as a marker to differentiate virulent/avirulent populations or strains of E. histolytica.

Hemostatic alterations in non-cirrhotic portal fibrosis, extrahepatic portal venous obstruction and Budd-Chiari syndrome.

We studied the coagulation function in ten patients each with non-cirrhotic portal fibrosis (NCPF), extrahepatic portal venous obstruction (EHPO) and Budd-Chiari syndrome (BCS), conditions where venous thrombosis in the hepatic vasculature is a common denominator. Prothrombin time, partial thromboplastin time with kaolin (PTTK) and thrombin time were normal in patients with NCPF and EHPO. However, in BCS the PTTK was prolonged, with a mean test/control ratio of 1.68 +/- 0.11. Fibrin degradation products were absent in all patients. Platelet aggregation tests showed hypoaggregability in all patients with NCPF. They were normal in patients with EHPO. However, two of ten BCS patients showed hyperaggregability, coinciding with a recent onset of illness in one patient. In conclusion, coagulation abnormalities appear unlikely to be the cause of thrombosis in patients with NCPF and EHPO. Further studies are required to substantiate the findings of hyperaggregability of platelets in BCS.