Symptoms consistent with IBS and functional diarrhea occur more frequently in people after bacterial gastroenteritis compared with controls, even after careful exclusion of people with pre-existing FGIDs. The frequency is similar at 3 and 6 months. Our findings support the existence of postinfectious IBS and give an accurate estimate of its frequency.
Sulphasalazine prescribing is on the increase. Pulmonary toxicity and blood dyscrasias are rare side-effects. Numerous case reports have been published implicating sulphasalazine in pulmonary toxicity. The authors searched the literature for cases of sulphasalazine induced lung toxicity and the 50 cases identified are discussed here.All published case reports/letters referring to sulphasalazine and lung toxicity were studied. The search terms "sulphasalazine" and "sulfasalazine" were combined with the terms "lung", "pulmonary disease", "pneumonitis" and "pleuritis" using Medline and PubMed databases.Typical presentation of sulphasalazine-induced lung disease was with new onset dyspnoea and infiltrates on chest radiography. Common symptoms were cough and fever. Crepitations on auscultation and peripheral eosinophilia were noted in half of the cases. Sputum production, allergy history, rash, chest pain and weight loss were inconsistent findings. Pulmonary pathology was variable, the commonest being eosinophilic pneumonia with peripheral eosinophilia and interstitial inflammation with or without fibrosis. Fatal reports were infrequent. Most patients were managed by drug withdrawal with 40% prescribed corticosteroids.In conclusion, sulphasalazine lung disease should be distinguished from interstitial lung disease due to underlying primary disease. Despite the increase in sulphasalazine prescribing, pulmonary toxicity remains rare. The majority of patients with suspected sulphasalazine-induced lung disease improved within weeks of drug withdrawal and the need for corticosteroids is debatable. Sulphasalazine has been used worldwide since the 19409s when it was first prescribed for ulcerative colitis. Its use in the management of inflammatory bowel disease (IBD) is declining with the availability of newer nonsulphur containing aminosalicylates. Conversely, its use as a disease-modifying antirheumatoid drug (DMARD) in the treatment of rheumatoid arthritis is well known [1], its pattern of prescribing by rheumatologists is changing with the development of combination therapies and earlier prescribing of DMARD9s in the course of the disease [2,3]. Overall prescribing of sulphasalazine is on the increase. Information provided from the statistics division 1E of the Department of Health shows that in the decade 1980-1990 there were 4.3 million prescriptions for sulphasalazine with 652 million tablets prescribed. In the last decade to 1998 there were 4.6 million prescriptions with 698 million tablets prescribed.Sulphasalazine has clinically important side-effects in up to one-fifth of patients but these are mostly nausea and vomiting, skin rashes, arthralgia, fever and hepatic dysfunction. More serious side-effects include pulmonary toxicity and blood dyscrasias. Early case reports of adverse effects were published in the 19609s [4] and knowledge of adverse pulmonary effects is not new [5][6][7]. Numerous case reports have been published in the last 30 yrs implicating sulphasalazine in pulmonary toxicity. The presen...
Post-infectious FGIDs appear to be associated with smoking. Smoking is known to moderate gut immunity in other disorders such as ulcerative colitis and Crohn's disease. This study adds to increasing evidence for an organic basis to post-infectious FGIDs, perhaps moderated via inflammatory pathways.
Biliary casts are uncommon but are more frequently described in liver transplant patients. To our knowledge there have been only two published cases describing biliary casts in non-liver transplant patients. The aetiology of cast development is not fully known but is likely to be multifactorial with the presence of biliary sludge being a prerequisite for cast formation. Bile duct damage and ischaemia, biliary infection, fasting, parenteral nutrition, abdominal surgery and possibly other factors, are all thought to be implicated in cast pathogenesis via sludge development. Endoscopic management has been shown to be effective in a minority of cases and may act as a temporary measure in others but surgical removal of casts is usually necessary. With a greater understanding and improvement in liver transplant surgical techniques and the management of post-operative complications, the development and severity of biliary sludge and casts have decreased.
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