Treatment of generalized pustular psoriasis with methotrexate and colchicine

Horiguchi, M.

doi:10.1001/archderm.117.12.760

Cited by 11 publications

(6 citation statements)

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“…In addition to gout, it has become evident that colchicine is also effective for treating familial Mediterranean fever2930, Behçet’s disease3132, Sweet’s disease33, palmoplantar pustulosis3435, scleroderma36, and primary biliary cirrhosis37. Although colchicine was thought to act by inhibiting microtubule formation and cell division38, its anti-inflammatory effects were unclear.…”

Section: Discussionmentioning

confidence: 99%

Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome

Otani

Watanabe

Shimada

et al. 2016

Sci Rep

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The inflammasome is a large, multiprotein complex that consists of a nucleotide-binding oligomerization domain-like receptor (NLR), an apoptosis-associated speck-like protein containing a caspase recruitment domain, and pro-caspase-1. Activation of the inflammasome results in cleavage of pro-caspase-1 into cleaved caspase-1, which promotes the processing of pro-interleukin (IL)-1β into mature IL-1β. We investigated the effects of colchicine on non-steroidal anti-inflammatory drug (NSAID)-induced small intestinal injury and activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome. Colchicine treatment inhibited indomethacin-induced small intestinal injury by 86% (1 mg/kg) and 94% (3 mg/kg) as indicated by the lesion index 24 h after indomethacin administration. Colchicine inhibited the protein expression of cleaved caspase-1 and mature IL-1β, without affecting the mRNA expression of NLRP3 and IL-1β. Although treatment with recombinant IL-1β (0.1 μg/kg) did not change the severity of small intestinal damage, the preventive effects of colchicine were abolished by supplementation with the same dose of recombinant IL-1β. Indomethacin-induced small intestinal damage was reduced by 77%, as determined by the lesion index in NLRP3−/− mice, and colchicine treatment failed to inhibit small intestinal damage in NLRP3−/− mice. These results demonstrate that colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome.

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Section: Discussionmentioning

confidence: 99%

Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome

Otani

Watanabe

Shimada

et al. 2016

Sci Rep

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“…However, as the toxicity of MTX is well known, other medications or modalities have been tried. In one case of PP, which could not be controlled by MTX, colchicine was added; the response was dramatic (Horiguchi et a/., 1981). The effect of colchicine on PP appears to be variable.…”

Section: Discussionmentioning

confidence: 99%

“…, PUVA (Honigsmann et aL, 1977;Abel, Goldberg & Farber, 1980), systemic corticosteroids (Baker, 1976), and a combination of therapies (Horiguchi et aL, 1981;Lauharanta, Jurakoski & Lassus, 1981;Thivolet, Robart & Vignon, 1981;Kanerva et al, 1982) Various types of PP have been described (Baker & Ryan, 1968;Baker, 1971): dermatitis repens of Radcliffe-Crocker, acrodermatitis continua of Hallopeau, PP of palms and soles (Barber's type), von Zumbusch, impetigo herpetiformis, the exanthematous, the annular and its variant, the erythema annulare centrifugum-like type. Treatment may vary according to the types of PP.…”

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confidence: 99%

Treatment of generalized pustular psoriasis-clinical trials using different therapeutic modalities

1985

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Summary Treatment of various types of pustular psoriasis, using dressings wet with Burow's solution alone, resulted in the clearing of pustules in 67 of 115 severe attacks in 26 mates and 21 females. The average number of days until spontaneous clearing was between 20 and 42; approximately one third of these attacks cleared within 20 days. Antichcmotactic medications such as tetracycline, dapsone and colchicinc cleared one third of the remaining non‐spontaneously remitting attacks. The medications were ineffective in cases of chronic pustular eruption of the palms and soles for which a topical corticosteroid, with occlusion, was found to be useful. PUV A gave a favourable result in about half of cases of chronic drug‐resistant pustular eruption of the trunk. Methotrexate CMTX) with or without non‐steroidal anti‐inflammatory agents could control cases of arthritis. Etretinate was efficient in treating two recalcitrant attacks; subsidence of the pustules occurred in I week. In conclusion, pustular psoriasis is a self‐limited disease in cases of annular, exanthematous and impetigo herpetiformis, and in some cases of the von Zumbusch types. However, it may be a chronic, recurrent, progressive, intractable (especially the Hallopcau type), or rarely, even fatal disease. Methotrexate is not the drug of first choice for treating generalized pustular psoriasis.

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“…For example, methotrexate has been successfully used for the treatment of psoriasis since the 1950s 12,13 . Methotrexate has been combined with psoralen and ultraviolet A (PUVA), ultraviolet B (UVB), etretinate and cyclosporine with the aim of improving efficacy, reducing dosage and limiting associated toxicity 14–21 . Methotrexate and cyclosporine have been particularly successful in achieving this, although long‐term use has not been reported 21 .…”

Section: Introductionmentioning

confidence: 99%

Effective and sustainable biologic treatment of psoriasis: what can we learn from new clinical data?

Langley¹

2012

Acad Dermatol Venereol

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The introduction of the biologic agents, adalimumab, etanercept, infliximab and ustekinumab, has provided more options for the short-and long-term treatment of patients with psoriasis. Physicians are now able to achieve and maintain effective disease control in more patients using biologic therapies. Newly published clinical data support the introduction of novel optimization strategies to further improve outcomes in patients with psoriasis. Recent randomized controlled clinical trials have provided data on the efficacy of conventional therapies, including systemic agents, and biologics at specific time points. Switching from methotrexate to a tumour necrosis factor (TNF)-a antagonist after 16 weeks can improve response rates, as demonstrated in a study of patients with moderate-tosevere psoriasis, while the benefit of long-term methotrexate use remains unclear. In a separate study, psoriasis area and severity index (PASI) ‡75 response rates were maintained over time (>3 years for adalimumab), suggesting that long-term biologic therapy is an effective and sustainable treatment option for psoriasis. For each individual patient, the benefit of a particular treatment needs to be balanced with the risks. The lack of head-to-head trials of antipsoriatic therapies, particularly biologic therapies, does not help with making individualized treatment decisions.However, a benefit-risk assessment of TNF-a antagonists calculated from an integrated analysis of published literature in moderate-to-severe psoriasis can be used to aid clinical practice. The number needed to treat, number needed to harm and number of patient years of observation to detect an adverse event have been determined for adalimumab, etanercept and infliximab. The benefit-risk profiles generated demonstrated that, during the initial year of treatment, likelihood of success with TNF-a antagonists was several orders of magnitude greater than the likelihood of serious toxicity.

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Treatment of generalized pustular psoriasis with methotrexate and colchicine

Cited by 11 publications

References 0 publications

Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome

Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome

Treatment of generalized pustular psoriasis-clinical trials using different therapeutic modalities

Effective and sustainable biologic treatment of psoriasis: what can we learn from new clinical data?

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