Abstract:Observations were made of 12 cases of psoriasis that developed and three cases of psoriasis that became exacerbated during treatment with lithium compounds. Only two patients had a family history of psoriasis, and results of a search for increased frequencies of the histocompatibility antigens seen in psoriasis vulgaris were negative. The clinical features were identical to severe psoriasis vulgaris and the diagnosis was confirmed by histologic examination performed in six cases. However, the skin changes disa… Show more
“…For some drugs, possible mechanisms are presumed on the basis of their pharmacological actions. Beta blockers (6) and lithium (7) may induce a defective adenyl cyclase-cyclic AMP cascade, leading to decreased cyclic AMP and increased epidermal cell proliferation. Nonsteroidal anti-inflammatory drugs such as indomethacin may reduce cyclic AMP or inhibit prostaglandin synthesis and result in redirection of the arachidonic acid cascade to accumulation of hydroxy fatty acids including HETE, which has been reported to be increased in psoriatic epidermis (8).…”
We report a case of pustular psoriasis precipitated by acetazolamide, a carbonic anhydrase inhibitor. A 28-year-old man suffering from 20 years-standing generalized pustular psoriasis developed psoriatic arthritis and glaucoma and experienced a precipitation of pustular lesions and widespread erythema after initiation of oral acetazolamide for glaucoma. The cutaneous lesions and systemic symptoms improved after restriction of acetazolamide and administration of oral etretinate. Readministration of acetazolamide confirmed that generalized pustules arose within 24 hours.
“…For some drugs, possible mechanisms are presumed on the basis of their pharmacological actions. Beta blockers (6) and lithium (7) may induce a defective adenyl cyclase-cyclic AMP cascade, leading to decreased cyclic AMP and increased epidermal cell proliferation. Nonsteroidal anti-inflammatory drugs such as indomethacin may reduce cyclic AMP or inhibit prostaglandin synthesis and result in redirection of the arachidonic acid cascade to accumulation of hydroxy fatty acids including HETE, which has been reported to be increased in psoriatic epidermis (8).…”
We report a case of pustular psoriasis precipitated by acetazolamide, a carbonic anhydrase inhibitor. A 28-year-old man suffering from 20 years-standing generalized pustular psoriasis developed psoriatic arthritis and glaucoma and experienced a precipitation of pustular lesions and widespread erythema after initiation of oral acetazolamide for glaucoma. The cutaneous lesions and systemic symptoms improved after restriction of acetazolamide and administration of oral etretinate. Readministration of acetazolamide confirmed that generalized pustules arose within 24 hours.
“…Several drugs have been reported to induce psoriasis (or psoriasiform eruption) or its exacerbation; for example, {3-blockers (2, 3), lithium salts (4,5), and chloro- quine (6) indomethacin (7,8). However, so far as we can see from the literature, there are no reports regarding induction of psoriasis or its exacerbation by the administration of antibiotics such as ABPC.…”
Section: Discussionmentioning
confidence: 99%
“…However, so far as we can see from the literature, there are no reports regarding induction of psoriasis or its exacerbation by the administration of antibiotics such as ABPC. ,8-blockers and lithium salts are presumed to reduce cyclic AMP cascade activity by inducing abnormalities related to transmembranous signal transducing systems (2)(3)(4)(5). Lithium salts are also known to activate neutrophils, resulting in the increased protease activity which is usually found in psoriatic lesions.…”
We experienced a case of psoriasis with ABPC allergy which showed a psoriasiform intradermal test reaction to ABPC. A 22-year-old man with a history of psoriasis since the age of 17 was admitted to our department because he developed erythrodermic psoriasis after oral administration of ABPC. About 1 year later, he again developed erythroderma after administration of ABPC. Intradermal testing with 2% ABPC was performed. We found infiltrating erythema at day 2, followed by a gradually increasing psoriasiform reaction at 6 days on the site of ABPC skin test. We examined the infiltrating cells in the skin test reaction immunohistochemically. Most of the infiltrating cells in the dermis were activated helper/DTH-type T cells. Among the infiltrating cells in the epidermis, we observed more cytotoxic/suppressor-type T cells than helper/DTH-type T cells. A possible role of a DH reaction to ABPC in inducing the psoriatic lesion is discussed in relation to the pathomechanisms of psoriasis.
“…35,47 The refractory period for development of the lesions after the initiation of lithium therapy is variable, but may range from a few weeks to several months. 48 The incidence of psoriasis secondary to lithium treatment has been reported to be 1.8-6%. 6,7 Most cases of psoriasis in lithium-treated patients occur at the therapeutic level.…”
Section: Psoriasismentioning
confidence: 99%
“…In some cases, however, this may not be very effective. 48,64 In such resistant cases, dose reduction or discontinuation may be considered and the patient may be switched to another mood stabilizer. 47,65 In some double-blind, placebo-controlled studies, omega-3 fatty acids have been found to be very useful in clearing lithium-induced psoriasis, 66 and some authors have successfully used tumor necrosis factor-α inhibitors to alleviate severe, recalcitrant, lithium-induced psoriasis.…”
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