Leptospirosis has a wide range of presentation which ranges from mild flu-like symptoms, to severe form including renal failure, liver failure, and hemorrhage. Pulmonary involvement can progress from subtle clinical features to life threatening pulmonary hemorrhage and acute respiratory distress syndrome. Although benefits of corticosteroids in adult respiratory distress syndrome have been proven and accepted, evidence for use of corticosteroids in pulmonary leptospirosis is still limited. Given the vasculitic nature of severe leptospirosis, it has been proposed that addition of intravenous corticosteroid therapy, particularly in cases of pulmonary involvement is beneficial. We report a case of leptospirosis with suspected pulmonary hemorrhage which deteriorates after a few days of admission in our tertiary hospital. We have demonstrated that the prescription of a lower dose of corticosteroid than what was widely reported in the literature can equally led to a satisfactory recovery of the pulmonary hemorrhage.
Hepatitis C virus (HCV) infection is known to cause acute and chronic active hepatitis. In addition, HCV also has systemic disorder involvement that links to various extra-hepatic complications. We report a case of a patient which has been diagnosed to have Hepatitis C Genotype 3A who has been started on antiviral. He achieved end treatment response and sustained virologic response. During routine follow up, he experienced acute kidney injury. Renal biopsy showed type III membranoproliferative glomerulonephritis. His proteinuria improved greatly with the addi- tion of angiotensin converting enzyme inhibitor. This case highlights the possibility of appearance of HCV related glomerulonephritis in patient who has sustained virological response.
Biologic sex influences the development of cardiovascular disease and modifies aldosterone (ALDO) and blood pressure (BP) phenotypes: females secrete more ALDO, and their adrenal glomerulosa cell is more sensitive to stimulation. Lysine-specific demethylase 1 (LSD1) variants in Africans and LSD1 deficiency in mice are associated with BP and/or ALDO phenotypes. This study, in 18- and 40-week-old wild type (WT) and LSD1+/- mice, was designed to determine whether (1) sex modifies ALDO biosynthetic enzymes; (2) LSD1 deficiency disrupts the effect of sex on these enzymes; (3) within each genotype, there is a positive relationship between ALDO biosynthesis (proximate phenotype), plasma ALDO (intermediate phenotype) and BP levels (distant phenotype); and (4) sex and LSD1 genotype interact on these phenotypes. In WT mice, female sex increases the expression of early enzymes in ALDO biosynthesis but not ALDO levels or systolic blood pressure (SBP). However, enzyme expressions are shifted downward in LSD1+/- females vs males, so that early enzyme levels are similar but the late enzymes are substantially lower. In both age groups, LSD1 deficiency modifies the adrenal enzyme expressions, circulating ALDO levels, and SBP in a sex-specific manner. Finally, significant sex/LSD1 genotype interactions modulate the three phenotypes in mice. In conclusion, biologic sex in mice interacts with LSD1 deficiency to modify several phenotypes: (1) proximal (ALDO biosynthetic enzymes); (2) intermediate (circulating ALDO); and (3) distant (SBP). These results provide entry to better understand the roles of biological sex and LSD1 in (1) hypertension heterogeneity and (2) providing more personalized treatment.