Lichenoid eruption due to chlorpropamide.

Dinsdale, R C; Ormerod, T P; Walker, A E

doi:10.1136/bmj.1.5584.100

Cited by 37 publications

(12 citation statements)

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“…Other drugs known to cause lichenoid eruptions include thiazides, diuretics, penicillamine, beta-blockers, quinine and quinidine, para-amino salicylic acid, phenothiazines, carbamazepine, allopurinol, lithium, lorazepam, ketoconazole, streptomycin, isoniazid, metopromazine, levopromazine, amiphenazole, pyrimethamine, levamisole, beta-blocking agents, cinnarizine, flunarizine, gold, cyanamide (calcium carbamide), and many others (Table 5) (Shatin et al, 1953;Groth, 1961;Baker et al, 1964;Dinsdale et al, 1966;Roberts and Marks, 1981;Chau et al, 1984;Hogan et al, 1985;Colvard et al, 1986;Markitziu et al, 1986;Torrelo et at., 1990). Occasionally, there are reactions to multiple drugs (Wiesenfeld et al, 1982).…”

Section: (3) Drugsmentioning

confidence: 99%

Update On Oral Lichen Planus: Etiopathogenesis and Management

Scully

Beyli²,

Ferreiro

et al. 1998

Critical Reviews in Oral Biology & Medicine

477

461

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Lichen planus (LP) is a relatively common disorder of the stratified squamous epithelia, which is, in many ways, an enigma. This paper is the consensus outcome of a workshop held in Switzerland in 1995, involving a selection of clinicians and scientists with an interest in the condition and its management. The oral (OLP) eruptions usually have a distinct clinical morphology and characteristic distribution, but OLP may also present a confusing array of patterns and forms, and other disorders may clinically simulate OLP. Lesions may affect other mucosae and/or skin. Lichen planus is probably of multifactorial origin, sometimes induced by drugs or dental materials, often idiopathic, and with an immunopathogenesis involving T-cells in particular. The etiopathogenesis appears to be complex, with interactions between and among genetic, environmental, and lifestyle factors, but much has now been clarified about the mechanisms involved, and interesting new associations, such as with liver disease, have emerged. The management of lichen planus is still not totally satisfactory, and there is as yet no definitive treatment, but there have been advances in the control of the condition. There is no curative treatment available; immunomodulation, however, can control the condition. Based on the observed increased risk of malignant development, OLP patients should be offered regular follow-up examination from two to four times annually and asked to report any changes in their lesions and/or symptoms. Follow-up may be particularly important in patients with atrophic/ulcerative/erosive affections of the tongue, the gingiva, or the buccal mucosa. Much more research is required into the genetic and environmental aspects of lichen planus, into the premalignant potential, and into the possible associations with chronic liver, and other, disorders. More clinical studies are required into the possible efficacy of immunomodulatory drugs such as pentoxifylline and thalidomide.

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Section: (3) Drugsmentioning

confidence: 99%

Update On Oral Lichen Planus: Etiopathogenesis and Management

Scully

Beyli²,

Ferreiro

et al. 1998

Critical Reviews in Oral Biology & Medicine

477

461

View full text Add to dashboard Cite

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“…Recently it has also been used with some success in the treatment of pitressin-sensitive diabetes insipidus [2,3,6,7,13], Skin rashes occur in 2-3% of patients receiving chlorpropamide. Most cases are of the exanthematic erythematous type [15], but rashes with the morphology of urticaria [I, 4], erythema exudativum multiforme [16,17], purpura [10] and lichen planus mucosae oris [5] have been reported. Hitsel-Feukrman/F rumkin berger and F o sn a u g h [11] have reported a case of photosensitivity with cross-reaction to tolbutamide.…”

Section: Discussionmentioning

confidence: 99%

Photodermatitis Induced by Chlorpropamide

Feuerman¹,

Frumkin²

1973

Dermatology

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Five diabetic patients developed photodermatitis following the ingestion of 250–500 mg chlorpropamide per day, from 3 weeks to 4 years after the onset of therapy. Four patients developed the rash in August and September and one in December. Four patients were treated successfully by withdrawing chlorpropamide, shielding from sunlight and administering local symptomatic therapy, while the fifth patient had to be given corticosteroids. In four patients, the skin ultimately cleared, but one patient developed a residual leukomelanoderma. In one patient the minimal erythema dose was found to be lowered a few hours after ingesting a small dose of chlorpropamide.

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“…A vast number of medications have been implicated in the onset of OLP. These include antihypertensives, antimalarials, antimicrobials, metals, non-steroidal anti-inflammatory drugs (NSAIDs), diuretics, oral hypoglycaemic agents, penicillamine, anxiolytics and antiretrovirals (Wilson, 1946;Dinsdale et al, 1968;Hay and Reade, 1978;Powell et al, 1983;Colvard et al, 1986;Markitziu et al, 1986;Potts et al, 1987;Lamey et al, 1990;West et al, 1990;Ficarra et al, 1993). In recent years, poor drug metabolism because of cytochrome P450-enzymes (CYPs) polymorphisms has been suggested as an explanation for the debut of OLP (Kragelund et al, 2003(Kragelund et al, , 2009).…”

Section: Introductionmentioning

confidence: 99%