In a study of twenty-five patients with herpes gestationis we found that 80% possessed the HLA antigen DR3, which confers increased immune responsiveness and a predisposition to 'auto-immune disease'. In five patients the development of herpes gestationis coincided with a change in sexual partner, suggesting that the development of herpes gestationis may depend on exposure to an antigen derived from the father. This might share determinants with a component of the basement membrane zone of skin. Although anti-basement membrane zone antibodies are present in HG it is not clear whether they play a pathogenic role. The infrequency of neonatal involvement and the lack of correlation between immunofluorescence findings and clinical activity in our patients suggested that the antibodies might be a result of tissue damage rather than its cause. Two patients in our study were exceptional in that episodes of herpes gestationis were followed by normal pregnancies. In these patients the relationship of their DR antigens to those of the fetus may have been important in determining whether or not the pregnancy would be affected by herpes gestationis.
When lichen planus strikes families, a very rare happening, it is likely to afflict younger members, to erupt more acutely, extensively, and gravely, attacking also nails and mucous membranes, and to recur. Ten patients with familial lichen planus, two each from five distinct Caucasian families, the parents of whom were unrelated by birth, were found to be carrying HLA-B7 statistically more frequently than in the normal population or in those with the characteristic forms of lichen planus. We hint that their genotype might have rendered them susceptible to a pathogen that precipitated their disease.
Birth weight data for 356 pairs of newborn twins of known zygosity and placentation are presented. The combined weights of dizygotic twins are heavier than those of monozygotic twins. The significance of this finding is discussed in relation to the association between increased maternal height and dizygotic twinning.
We have searched the literature for data on the in vitro assessment of immune status in atopic eczema patients, and have found much confusion. The major findings are tabulated. It is concluded that atopic eczema is a form of immune deficiency, although it is unclear whether this is a primary or secondary defect. Most authors find a T-lymphocyte deficit while eosinophils, B lymphocytes and serum IgE are increased. Serum IgE levels appear to correlated with severity of eczema symptoms. We have previously suggested that T-lymphocyte levels are overestimated in eczema when fetal calf serum is used in the E-rosette assay. Analysis of the literature for the effect of this serum in the assay confirms that there is a T-lymphocyte deficit in atopic eczema, but that the serum masks it. Thus, much of the confusion surrounding this issue can be resolved.
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