A possible association between intrahepatic cholestasis of pregnancy (ICP) and human-leukocyte histocompatibility (HLA) antigens--used as genetic markers--was studied in 100 women with ICP compared to 100 multiparous women without a past history of the disease. Because we previously found a higher frequency of ICP in women with an overt Araucanian Indian descent than in Chilean Caucasoids, women from both ethnic groups were studied. Among the 37 specificities of the HLA system studied (17 of HLA-A, 16 of HLA-B, and 4 of HLA-C series), only HLA-BW16 showed a tendency to be more frequent in women with ICP rather than in control women. This finding appears to be related with ethnic origin and not ICP, HLA-BW16 was significantly more frequent in women with Araucanian Indian descent (43.4%) than in Chilean Caucasoids (16.3%) (p less than 0.01). The high frequency of HLA-BW16 in the predominantly Caucasoid population in Chile, in comparison with Caucasians in Europe and in North America, may be another indicator of their ethnic admixture with aborigine groups. The high frequency of HLA-BW16 reported in North American Indian-admixed groups (16%) suggests that HLA-BW16 may be a genetic characteristic common to some aboriginal populations in North and South America.

ABO Blood-Group System↗

PubMedDate not supplied

[Polyneuritis after use of perhexiline maleate: quantimetric and ultrastructural study (author's transl)].

The authors record a new case of polynevritis through a prolonged use of perhexiline maleate. The acute neurological episode occurred 14 months after the beginning of the treatment when the daily doses had been raised to 600 mg for 2 months. The biopsy of the peripheral nerve was carried out only 27 months later as the posology was brought down to 200 mg and the clinical symptomatology had almost completely diminished. This probably accounts for the unusual aspects observed on semi-thin and ultrathin sections: a very remarkable reduction of the number of myelinated fibers and the severity of the phenomena of Wallerian degeneration, contrasting with the rarity of intra-cytoplasmic multilamellar schwannian inclusions, classically observed in the course of polynevritis caused by perhexiline maleate. The direct toxic action of the drug upon the neuron has been discussed.

Humans↗

PubMedDate not supplied

An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of langerhans cells to UV light.

Actinic prurigo is an inflammatory disease of the skin that appears to be mediated by an abnormal immune response. Cell adhesion molecules play a key role in the induction of the immune response as well as in the pathogenesis of inflammation. We investigated the expression of cell adhesion and activation molecules, as well as the density of Langerhans cells in skin from patients with actinic prurigo. Skin biopsies from ultraviolet light-induced lesions, and non-irradiated areas from 10 actinic prurigo patients were studied; in addition, several spontaneous skin lesions were studied. Skin biopsies from normal individuals were used as controls. The expression of ICAM-1, ICAM-3, LFA-3, CD2, LFA-1, VLA-4, CD1a, VCAM-1, CD69, and activated b1 integrins were assessed by immunostaining. An increased expression of LFA-1, LFA-2, ICAM-3, VLA-4, and activated b1 integrins was observed in the cell infiltrate of actinic prurigo lesions and an up-regulated expression of ICAM-1 was detected in keratinocytes from these specimens. Interestingly, the number of Langerhans cells (CD1a + ) in actinic prurigo skin was not significantly affected by ultraviolet irradiation, a phenomenon that was not observed in normal controls. The increased expression of adhesion molecules in the cell infiltrate of actinic prurigo, indicates that these cells are activated and suggests that they are involved in the skin damage seen in these patients. The resistance of Langerhans cells from patients with actinic prurigo to ultraviolet light may have an important role in the pathogenesis of this condition. The involvement of keratinocytes in the pathogenesis of actinic prurigo is suggested by the expression of ICAM-1 on these cells.

Antibodies, Monoclonal↗