Hydroxychloroquine-induced podocytopathy mimicking Fabry disease

Hydroxychloroquine (HCQ) is largely prescribed as an immunomodulator to prevent systemic diseases flares in patients with systemic lupus erythematous, rheumatoid arthritis, Sjogren’s disease. Among reported side effects, HCQ can accumulate in lysosomes and induced phospholipidosis. Here, we report an HCQ-induced podocytopathy mimicking Fabry disease (FD). They share the same histological lesions: cytoplasmic vacuolisation of the podocytes and zebra bodies on light and electronic microscopy. FD has been ruled out by measuring enzymatic activity and genetic test. The persistence of proteinuria after immunological remission of a systemic disease treated with HCQ could suggest this HCQ-induced podocytopathy.

Deoxynivalenol in the liver and lymphoid organs of rats: effects of dose and duration on immunohistological changes

Deoxynivalenol (DON) is one of the most prevalent type B trichothecenes present in food inducing adverse effects, including intestinal changes and immunosuppression. The aim of the present study was to investigate the effects of DON on rats exposed for 7, 14 and 28 days to mycotoxin-contaminated diets, using histological and immunohistochemical analyses on liver and lymphoid organs. Fifty rats received a control diet, or a diet contaminated with 1.75 mg/kg of DON for 30 days, or a diet contaminated with 11.4 mg/kg of DON for 7, 14 or 30 days. Ingestion of contaminated feed induced a significant increase in the lesional score in the liver, spleen, and lymph nodes. The main histological findings observed in the liver were cytoplasmic vacuolisation and hepatocelular megalocytosis. A significant increase in hepatocyte proliferation was observed in rats that received 1.75 mg/kg of DON. Lymphoid depletion was the main histological alteration observed in lymphoid organs, resulting in a significant increase in the lesional score in all groups that received the contaminated diets. The histological changes and lymphocyte apoptosis were more severe in lymph nodes of rats fed 11.4 mg/kg of DON during 30 days. The results of the morphological and immunohistochemical analyses suggest that the ingestion of DON can induce functional hepatic impairment and immunosuppression in a dose- and time-dependent manner.

Biochemical and Histological Changes in Rat Liver Caused by Cypermethrin and Beta-Cyfluthrin

Cypermethrin and beta-cyfluthrin are two most widely used multipurpose pyrethroids. After determining their oral LD50 (416.98 mg kg-1 and 354.8 mg kg-1 body weight, respectively), we assessed their hepatotoxicity in Wistar rats following acute (0.1 LD50 for 1 day) and sub-acute (0.1 LD50 for 7, 14, 21 or 28 days) poisoning. The assessment was based on hepatic marker enzymes AST, ALT, LDH, ALP, glycogen, total proteins, total lipids, cholesterol, free fatty acids, and phospholipids. AST, ALT, LDH, total lipids, cholesterol, phospholipids, and free fatty acids in hepatic homogenate increased following pyrethroid stress. In contrast, hepatic proteins, glycogen, and ALP activity decreased due to lysis of structural proteins and leakage of enzymes into the blood stream. Biochemical data were consistent with histological alterations (cytoplasmic vacuolisation, nuclear polymorphism, eccentric nucleus, karyolysis, karyorrhexis, and sinusoidal dilation). Comparatively greater hepatocellular damage was noted in beta-cyfluthrin than in cypermethrin-treated rats, which is probably related to the fluorine atom in beta-cyfluthrin.