Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old SLE patient developed a xanthoma on her alopecia lesion. Histological examination showed typical lupus changes including immunofluorescence stainings. In addition, there were numerous xanthoma cells existed through the dermis, interlobular spaces of subcutaneous fat tissue, perivascular areas of small blood vessels, and subendothelial spaces and inside of intraluminal thrombosis of subcutaneous small arteries. These xanthoma cells contained granular materials in their cytoplasm. Histochemically, these materials are diastase resistant P.A.S. (+), immunoglobulin (+), Sudan BB (+), Sudan III (+), Nile blue (pinkish red), and yellowish orange autofluorescence suggesting that they are lipofuscin or lipid peroxidation products. Further histological findings showed destruction of sebaceus glands and peri-glandular++ infiltration of lymphocytes and histiocytes. These histiocytes contained phagocytic neutral lipid droplets in their cytoplasm. Very small lipid peroxides were also seen on surface and/or cytoplasm of infiltrating lymphocytes existing not only peri-lobular area but also intraluminal area of blood vessels. The marker profile of these infiltrating lymphocytes are B-cell predominant admixed with some CD8(+) T-cells. These data suggest that the mechanism of developing xanthoma is initiated by immune-complex deposition on basal lamina of sebaceus glands, followed by destruction of sebaceus glands by lympho-histiocytic cells infiltration with some antigen presenting and/or effector cells, and finally xanthoma cells were developed by phagocytosis of lipid peroxides caused by macrophage-derived oxygen radicals. Interestingly, our data suggest that the lipid peroxides, which may act as photosensitizer, may leave the skin and may enter the small vessels carried by lymphocytes. Furthermore the xanthoma cells may also enter the circulation through the small arteries.
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PMID:[Normolipemic xanthoma developed on alopecia lesion on a SLE patient--histological study]. 188 76

Isoniazid (INH) treatment can cause serious liver injury and autoimmunity. There are now several lines of evidence that INH-induced liver injury is immune mediated, but this type of liver injury has not been reproduced in animals, possibly because immune tolerance is the dominant response of the liver. In this study, we immunized mice with isonicotinic acid (INA)-modified proteins and Freund's adjuvant, which led to mild experimental autoimmune hepatitis (EAH) with an increase in cells staining positive for F4/80, CD11b, CD8, CD4, CD45R, and KI67. We expected that subsequent treatment of mice with oral INH would lead to more serious immune-mediated liver injury, but paradoxically it markedly attenuated the EAH caused by immunization with INA-modified hepatic proteins. In addition, patients of the slow acetylator phenotype are at increased risk of INH-induced liver injury. Treatment of arylamine N-acetyltransferase-deficient Nat1/2(-/-) mice with INH for up to 5 weeks produced mild increases in glutamate and sorbitol dehydrogenase activities, but not severe liver injury. Female Nat1/2(-/-) mice treated with INH for 1, 3, or 7 days developed steatosis, an increase in Oil Red O staining, and abnormal mitochondrial morphology in the liver. A decrease in M1 and an increase in M2a and M2b macrophages was observed in female Nat1/2(-/-) mice treated with INH for 1, 3, or 7 days; these changes returned to baseline levels by day 35. These data indicate that INH has immunosuppressive effects, even though it is also known to induce autoantibody production and a lupus-like autoimmune syndrome in humans.
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PMID:Paradoxical attenuation of autoimmune hepatitis by oral isoniazid in wild-type and N-acetyltransferase-deficient mice. 2462 63