Clinical Spectrum of Pseudomembranous Colitis

Cammerer, Richard C.

doi:10.1001/jama.1976.03260490020012

Cited by 11 publications

(1 citation statement)

References 18 publications

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“…The development of the syndrome of pseudomembranous colitis is closely associated, however, with the antibiotics lincomycin, clindamycin and ampicillin, but the pathogenesis is by no means clearly established (Price and Davies, 1977). Pseudomembranous colitis usually presents as an acute illness, the patient is ill with fever, lower abdominal pain and profuse watery diarrhoea (Cammerer et al, 1976). Oral clindamycin has been found to produce diarrhoea and pseudomembranous colitis when given to orthopaedic patients as prophylaxis in joint replacement (Smart et al, 1976).…”

Section: Discussionmentioning

confidence: 99%

Penetration into bone and tissues of clindamycin phosphate

Baird

Hughes

Sullivan

et al. 1978

Postgraduate Medical Journal

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Section: Discussionmentioning

confidence: 99%

Penetration into bone and tissues of clindamycin phosphate

Baird

Hughes

Sullivan

et al. 1978

Postgraduate Medical Journal

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Medical Management of Antimicrobial‐Associated Diarrhea and Colitis

Gotz

Rand

1982

Pharmacotherapy

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Gastrointestinal complications, including diarrhea, may occur with virtually all antimicrobial agents. Such diarrhea may represent either a common, nonspecific adverse effect, or it may be one of the manifestations of antimicrobial-associated colitis (AAC), a potentially fatal complication. Clostridium difficile and a cytotoxin neutralized by Clostridium sordellii antitoxin has been isolated from the stools of nearly all patients with antibiotic-associated pseudomembranous colitis, many patients with AAC, and approximately 20% of those with antimicrobial-induced diarrhea. Demonstration that C. difficile is responsible for cytotoxin production has allowed for specific therapy for these disorders. General treatment measures include discontinuation of the causative antimicrobial agent(s), bowel rest, and supportive care with fluids, electrolytes and colloids, if necessary. Antiperistaltic agents and corticosteroids are not recommended. Various antimicrobials demonstrate potential efficacy in treating AAC in humans. Oral vancomycin is the most widely tested and is currently the treatment of choice. It achieves high concentrations in the feces and is very active against C. difficile in doses of 125-500 mg by mouth every six hours. Other potentially useful but inadequately tested antimicrobials include metronidazole (500 mg by mouth every eight hours) and bacitracin (25,000 units by mouth every six hours). Tetracycline has been employed with some success in nonspecific antibiotic-associated diarrhea, although it is as yet untested in humans with AAC and may induce diarrhea itself. Both miconazole and rifampin are highly effective against C. difficile in vitro but have not been evaluated in AAC. Anion-exchange resins bind the cytotoxin found in stools of patients with AAC. Cholestyramine has been used with variable response in oral doses of 4 g every six to eight hours. Since these resins may also bind vancomycin, resulting in lowered vancomycin concentrations in the stool, combination therapy should be used cautiously. With specific therapy directed against the toxin and aggressive supportive therapy, surgical intervention is rarely necessary. More recently, investigations have been directed at using bacterial preparations to suppress C. difficile by restoring the normal flora. The development of immunological agents (i.e., vaccines, toxoids, antitoxins) for the prevention or treatment of AAC would be a significant advance in therapy.

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