Summary
Under carefully controlled conditions, seven aspirin‐intolerant asthmatic patients were challenged with oral aspirin and experienced respiratory tract reactions with a decline in forced expiratory volume in 1 sec (FEV1), ranging from 26 to 64%. Venous blood samples, which were collected during the challenges, showed a rise in plasma histamine in all seven patients. The increase in plasma histamine occurred at the onset of their respiratory reactions and those patients with the most severe asthmatic responses were found to have the highest and most prolonged levels of plasma histamine. The same aspirin‐intolerant asthmatic patients were able to ingest Maalox® or sodium salicylate without untoward effects, decline in FEV1 values or changes in plasma histamine levels. Ten non‐asthmatic individuals and eight out of ten asthmatic control patients were able to ingest aspirin without any reactions or changes in their plasma histamine levels. However, two asthmatic control individuals, with severe asthma requiring treatment with moderate dosages of corticosteroids, were found to have elevated pre‐challenge plasma histamine levels which increased during their ASA challenges despite the absence of respiratory reactions or changes in FEV1 values. It is possible that these two individuals were unsuspected aspirin‐intolerant asthmatics. These studies demonstrate that asthmatic reactions to acetylsalicylates are associated with release of histamine into plasma in the subgroup of asthmatic patients with the aspirin‐intolerance syndrome. Such a finding suggests that histamine may be one of the mediators of bronchospasm in aspirin‐induced asthma.
Sequential therapy was significantly more effective than standard therapy for eradicating H. pylori infection in peptic ulcer disease in Asian patients. Side effects were similar.
BACKGROUND: Biliary pathology and alcoholism are responsible for 70 to 80% cases of acute pancreatitis. Viral etiology is not uncommon.
OBJECTIVE: To study association of nonfulmimant acute hepatitis with acute pancreatitis. METHODS: We undertook a prospective study over 3 years from Jan 2009 to Dec 2011, during which 950 patients got admitted as acute pancreatitis.
RESULTS: Four patients (4.2%) were diagnosed with acute pancreatitis which developed after acute hepatitis. All patients were young (15-36 years); three males and one female. Two patients had pancreatitis in first week and two in third week, after onset of jaundice. Three patients had mild pancreatitis and one had sever pancreatitis. The etiology of pancreatitis was hepatitis A in two, and hepatitis E and hepatitis B in one each. All patients were managed conservatively and recovered completely.
CONCLUSIONS: Association between acute pancreatitis and acute viral hepatitis is now more frequently recognized; more commonly in young males, between 1st and third week of hepatitis illness. JMS 2012;15(1):44-46.
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