PubMed · 621832
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S Karpow, V Gotz, R D Lauper. 1978-01-30. Cimetidine.. https://doi.org/10.1001/jama.1978.03280320018006
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The term fasciitis-panniculitis syndrome (FPS) is proposed as a novel compilation encompassing several disorders, common to which is subcutaneous induration caused by cicatrizing fasciitis as well as septal and lobular panniculitis and perimysial fibrosis. Included herein are Shulman's eosinophilic fasciitis, morphea profunda, lupus profundus, venous lipodermatosclerosis, toxic oil syndrome, altered tryptophane-related eosinophilic myositis, graft-versus-host reaction, and fasciitis reactive to subjacent basal cell carcinoma. FPS should be differentiated from scleroderma, which primarily affects the dermal structures and in which arterioles are injured. In contrast, vasculopathy of the subcutaneous medium-sized veins accompanies the hypodermal lesions of FPS. The importance of recognizing and grouping these disorders lies in their different histopathology, characterization as reactive phenomena, enhanced responsiveness to treatment, and better prognosis than scleroderma. In view of the excellent prognosis of FPS, steroid treatment is not warranted. Long-term therapy with cimetidine appears to benefit the majority of patients.
Contrary to the general belief that cimetidine and ranitidine spare glucuronidation of drugs, some authors have indicated that both cimetidine and ranitidine could inhibit the glucuronidation of paracetamol (acetaminophen) by cultured rat hepatocytes. Thus, we tested the effect of three histamine H2-receptor blockers (cimetidine, ranitidine and famotidine) on the glucuronidation of 7-hydroxy-4-methylcoumarin (7-OH-4-MC) by human liver microsomes. None of the drugs studied produced significant inhibition of the glucuronidation of 7-OH-4-MC when used at concentrations up to 1.5 mM. Thus, even the new H2-receptor blocker, famotidine, spares glucuronidation. These findings further support the previous reports which suggest that glucuronide conjugation in humans is spared by H2-receptor blockers.
A total of 9928 cimetidine users were identified from prescriptions in four centres and followed for 10 years. The 'all-cause' mortality ratio fell from 1.9 in year 1 to 1.0 in years 8 to 10. Most of the early excess in mortality was attributable to cimetidine being given in the late stages of many diseases, often to counter adverse gastric effects of other drugs. Specific causes of mortality during years 5-10 of the study, were generally unremarkable. Significant increases in mortality ratios were apparent, however, for oesophageal cancer (years 5-7, 2.3; years 8-10, 1.9); lung cancer (years 5-7, 1.1; years 8-10, 1.7); diseases of the oesophagus, stomach, and duodenum (years 5-7, 3.3; years 8-10, 2.3); and chronic liver disease (years 5-7, 2.4; years 8-10, 3.3). None of these increases in mortality seems to be attributable to an adverse effect of cimetidine use. Data are also presented for mortality from diseases of the nervous system. Eight deaths (of which one was miscoded) were certified as being from motor neurone disease, representing a mortality ratio of 2.6 for years 2-10 of the study which is of borderline statistical significance. This study confirms that cimetidine is safe. Mortality from some diseases increased over the study period, but selection rather than any adverse effect of the drug is likely to be the explanation.