Elemental diet for refractory atopic eczema.

A total of 37 children with refractory wide-spread atopic eczema were treated with an antigen avoidance regimen comprising hospitalisation, exclusive feeding with an elemental formula for a median duration of 30 days, and measures to reduce exposure to pet and dust mite antigens at home. After the initial period of food exclusion, food challenges were performed at intervals of seven days, and the patients followed up for at least 12 months. Ten of the children (27%) either failed to respond to the regimen or relapsed within 12 months. Improvement in the eczema was seen in 27/37 (73%) patients, by discharge from hospital their disease severity score had fallen to a median of 27% of the pretreatment figure, and only 3/27 required topical corticosteroids. There were no clinical or laboratory findings which could be used to predict the outcome. Drawbacks to the regimen were prolonged hospitalisation (median 70 days), a fall in body weight and serum albumin concentration, and a risk of anaphylactic shock (4/37 cases). A strict antigen avoidance regimen may be associated with improvement of atopic eczema where conventional treatments have failed

Mast cells: the forgotten cells of renal fibrosis

Background/Aims—Mast cells, when activated, secrete a large number of fibrogenic factors and have been implicated in the development of fibrotic conditions of the liver, lung, and skin. There is evidence that renal fibrosis is closely linked with a chronic inflammatory cell infiltrate within the interstitium, but a potential role for mast cells in this process has yet to be defined. Therefore, the numbers of mast cells in normal and fibrotic kidneys with various pathologies were investigated. Methods—Mast cells were quantified in renal transplants showing acute and chronic rejection and cyclosporin toxicity, kidneys removed for chronic pyelonephritis, and renal biopsies from patients with IgA nephropathy, membranous nephropathy, and diabetic nephropathy. Mast cells were stained using two methods: acid toluidine blue detected less than 30% of the mast cells revealed by immunohistochemistry for mast cell tryptase. Results—Mast cells were scarce or absent in normal kidney (median, 1.6 mast cells/mm(2)) but numerous throughout the cortex and medulla in all specimens that showed fibrosis. They were almost entirely confined to the renal interstitium. Mast cells were present in large numbers in biopsies from patients with membranous nephropathy (median, 21.7 mast cells/mm(2)) and diabetic nephropathy (median, 29.2 mast cells/mm(2)), which were selected on the basis of showing chronic injury. In 24 unselected IgA nephropathy biopsies there was a close correlation between numbers of mast cells and the extent of interstitial fibrosis (r = 0.771; p < 0.0001). In renal transplant biopsies, mast cells were associated with allograft fibrosis in chronic rejection (median, 27.1 mast cells/mm(2)) and chronic cyclosporin toxicity (median, 10.6 mast cells/mm(2)) but not acute rejection (median, 2.7 mast cells/mm(2)) or acute cyclosporin toxicity (median, 2.0 mast cells/mm(2)). There was no detectable increase in mast cell numbers during acute rejection in those transplants that subsequently progressed to chronic rejection. In some biopsies the mast cells were largely intact, but in most cases some or all were degranulated. Conclusions—An increased number of mast cells is a consistent feature of renal fibrosis, whatever the underlying pathology, and the number of mast cells correlates with the extent of interstitial fibrosis. This suggests that mast cells might play a pathogenetic role in the fibrotic process. Key Words: mast cells • kidney • fibrosi