No abstract

Summary Of 231 patients evaluated for chronic urticaria and angioedema (CUA), 192 were diagnosed as having an idiopathic condition. The roles of serum IgE, complement (CH50), and immune complexes (IC) were investigated in 112 patients with idiopathic CUA. Immediate skin tests were not helpful, but total IgE was elevated in 13%, equally divided between dermographic (D) and non‐dermographic (ND) patients. Depressed haemolytic complement (CH50) was noted in 10% of CUA, all of whom were D. Serum IC were elevated in 38%, equally divided between D and ND patients. There was no relationship between depressed CH50 and elevated IC. Skin biopsies, evaluated by both light and immunofluorescent techniques, were negative for all specimens tested. The pathophysiology of idiopathic CUA is multifactorial, with a variety of immunological mechanisms involving serum IgE, CH50, and IC. The relationship between depressed CH50 and dermographism was noted but unexplained by serum or tissue studies.

Primary cultures of chick kidney cells convert 25-hydroxycholecalciferol into more-polar metabolites. Cells from vitamin D-deficient chicks have high 25-hydroxycholecalciferol 1 alpha-hydroxylase (1 alpha-hydroxylase) activity, but no 25-hydroxycholecalciferol 24-hydroxylase (24-hydroxylase) activity. Physiological concentrations of 1,25-dihydroxycholeclaciferol suppress 1 alpha-hydroxylase and induce 24-hydroxylase activity. The inhibition of 1 alpha-hydroxylase preceded the induction of 24-hydroxylase. In contrast, oestradiol-17 beta had no effect on the activity of either hydroxylase under a variety of experimental conditions. These results clearly demonstrate that 1,25-dihydroxycholecalciferol, but not oestrogen, acts directly on the kidney cells to regulate the metabolism of 25-hydroxycholecalciferol.