Generalized Pustular Psoriasis (Von Zumbusch) with Episodic Hypocalcæmia

Copeman, P.W.M.; Bold, Adriana; Wallace, H. James

doi:10.1177/003591576505800615

Cited by 16 publications

(2 citation statements)

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“…Hypoparathyroidism may be cause of the onset or aggravation of psoriasis in patients with surgical hypoparathyroidism (Vickers & Sneddon, 1963;Montgomery, 1964), primary hypoparathyroidism (Risum, 1973) and pscudohypoparathyroidism (Laymon & Zelickson, 1959). Chronic and acute hypocalcemia were also shown repeatedly in patients with pustular psoriasis (Copeman & Bold, 1965;Baker & Ryan, 1968;Stewart, Battaglini-Sabetta & Millstone, 1984), and the pustular psoriasis subsided on restoration ofthe circulating Ca level to the normal range (Stewart, Battaglini-Sabetta & Millstone, 1984). The patients examined in this study did not have any history of endocrinological disorder, and their basal levels of serum Ca were within the normal range.…”

Section: Discussionmentioning

confidence: 96%

An open study of vitamin D3 treatment in psoriasis vulgaris

et al. 1986

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Active forms of vitamin D3, 1 alpha-hydroxyvitamin D3 and 1 alpha,25-dihydroxyvitamin D3, were administered in an open-design study to 40 patients with psoriasis vulgaris in three ways: to 17 patients 1 alpha-hydroxyvitamin D3 was given orally at a dose of 1.0 micrograms/day for 6 months, to four patients 1 alpha,25-dihydroxyvitamin D3 was given orally at a dose of 0.5 microgram/day for 6 months, and 19 patients were given 1 alpha,25-dihydroxyvitamin D3 applied topically at concentration of 0.5 microgram/g of base for 8 weeks. Improvement was observed at the end of the individual study periods in 13 (76%) patients in Group 1 with a mean period of treatment (+/- SD) of 2.7 +/- 0.6 months, in one patient in Group 2 at 3 months after the start of treatment, and in 16 (84%) patients in Group 3 when the chemical was applied for 3.3 +/- 1.2 weeks. No side-effects were observed in any of these trials. These data suggest that psoriasis may respond to active metabolites of vitamin D3 and that abnormalities in vitamin D metabolism or in responsiveness of the skin cells to active metabolites of vitamin D may be involved in the pathogenesis of this skin disease.

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