[Eczematous reactions after intravenous immunoglobulin therapy in two patients with Guillain-Barré syndrome and a patient with Miller Fisher syndrome].

The use of intravenous immunoglobulin (IVIG) has become an accepted treatment for patients with Guillain-Barré syndrome. Few patients develop adverse reactions to IVIG such as flushing, urticaria, eczema, chest tightness, wheezing, diaphoresis and hypotension. We report three patients who each received a five day course of IVIG at the standard dose of 0.4 g/kg/day. Two patients had Guillain-Barré syndrome, and the other had Miller Fisher syndrome. All developed eczematous reactions after 4 days from the start day of therapy to 5 days from the last day of therapy. One patient with GBS had widespread eczematous eruption with severe pompholyx lesions on the palms, fingers and soles, and spread over a period of 2 to 3 weeks to become generalized. That persisted for 4 weeks but gradually settled with desquamation by the use of topical steroids. None of our patients subsequently developed long-term or chronic eczema after the resolution of the initial cutaneous reaction. Eczematous reactions of our patients were similar to those reported in the literature and clinically typical as pompholyx. Although pompholyx has been recognized as a clinical entity, its cause remains obscure. Cutaneous reactions after IVIG infusion are recognized to be rare, but actually they may occur more frequently than our recognition, and its knowledge is essential to make the right clinical decision.

Cell-transforming activity and mutagenicity of 5 phytoestrogens in cultured mammalian cells.

For the simultaneous assessment of in vitro carcinogenicity and mutagenicity of phytoestrogens, the abilities of 5 phytoestrogens, daidzein, genistein, biochanin A, prunetin, and coumestrol, to induce cell transformation and genetic effects were examined using the Syrian hamster embryo (SHE) cell model. Cellular growth was inhibited by all phytoestrogens in a concentration-related manner. The growth inhibitory effect of the compounds was ranked: genistein, prunetin > coumestrol > biochanin A > daidzein, which did not correspond to their apoptosis-inducing abilities. Morphological transformation in SHE cells was elicited by all phytoestrogens, except, prunetin. The transforming activities were ranked as follows: genistein > coumestrol > daidzein > biochanin A. Somatic mutations in SHE cells at the Na(+)/K(+) ATPase and hprt loci were induced only by genistein, coumestrol, or daidzein. Chromosome aberrations were induced by genistein or coumestrol, and aneuploidy in the near diploid range was occurred by genistein or biochanin A. Genistein, biochanin A or daidzein induced DNA adduct formation in SHE cells with the abilities: genistein > biochanin A > daidzein. Prunetin was negative for any of these genetic endpoints. Our results provide evidence that genistein, coumestrol, daidzein and biochanin A induce cell transformation in SHE cells and that the transforming activities of these phytoestrogens correspond to at least 2 of the mutagenic effects by each phytoestrogen, i.e., gene mutations, chromosome aberrations, aneuploidy or DNA adduct formation, suggesting the possible involvement of mutagenicity in the initiation of phytoestrogen-induced carcinogenesis.