Anti-tubercular therapy (ATT) induced thrombocytopenia: A systematic review.

INTRODUCTION: Drug-induced thrombocytopenia is a known adverse event of several drugs. Antitubercular therapy (ATT) is rarely reported but important cause of thrombocytopenia. The present review aimed to understand the profile of thrombocytopenia caused by first-line ATT i.e. isoniazid, rifampicin, pyrazinamide, and ethambutol. MATERIALS AND METHODS: We screened case reports, case series, and letter-to-editor from databases, like Pubmed/MEDLINE, Ovid, and EMBASE from 1970 to 2021. The PRISMA guidelines were followed in the present systematic review. RESULTS: Categorical data were expressed as n (%) and quantitative data were expressed as median (IQR). After applying the inclusion/exclusion criteria, 17 case reports and 7 letters to the editor were selected for the present review. Rifampicin was most frequently associated with thrombocytopenia (65%). A median (IQR) drop to 20,000 (49,500) platelets/mm3 was observed. Anti-rifampicin associated antibodies and anti-dsDNA positivity were found in six studies. Except for two, all patients responded to symptomatic treatment. DISCUSSION: ATT-induced thrombocytopenia can be life-threatening and require hospitalization. Clinicians should be aware of the association of ATT with thrombocytopenia and should take appropriate measures for patient management. CONCLUSION: This review provides clinicians a comprehensive picture of adverse effects and their management in ATT induced thrombocytopenia.

Estrogen oversees the maintenance of the female genetic program in terminally differentiated gonochorists.

The sexual plasticity of the gonads is not retained after the completion of sex differentiation in vertebrates, except in some hermaphroditic species. Here, we report that the depletion of estradiol-17ß (E2) by aromatase inhibitors (AI) for up to six months resulted in a functional female-to-male sex reversal in sexually-mature adults of two gonochoristic fish species, Nile tilapia and medaka. The sex-reversed fish showed a typical male pattern of E2 and androgen levels, secondary sexual characteristics, and male-like sex behavior, producing fertile sperm. Conversely, co-treatment of E2 inhibited AI-induced sex reversal. In situ hybridization of medaka gonads during AI-induced sex reversal indicated that cysts on the dorsal side of the adult ovaries are the origin of germ cells and Sertoli cells in the newly formed testicular tissue. Gonochoristic fish maintain their sexual plasticity until adulthood and E2 plays a critical role in maintaining the female phenotype.

Sex change of adult initial-phase male wrasse, Halichoeres trimaculatus by estradiol-17 beta treatment.

Sex steroids are considered major regulators of sex change processes in fish. Estrogen depletion is shown to be crucial for female-male sex change initiation; however, its role in male-female sex change is largely unknown. In the present study, we examined the effects of estradiol-17 beta (E2) treatments on testes of initial-phase (IP) males of the three-spot wrasse (Halichoeres trimaculatus), which naturally do not undergo male-female sex change. Sexually mature IP males were fed a diet containing E2 (low, 20 microg/g feed; high, 200 microg/g feed) for 6 or 12 weeks, and changes in gonadal structures were examined. Percentage of sex change varied with the dosage of E2 and the duration of treatment. All individuals treated with high-dose E2 for 6 weeks had ovaries with many immature oocytes; whereas 75% of individuals treated with low-dose of E2 for 6 weeks and sampled on the 12th week had ovaries with yolky oocytes and an ovarian cavity indicating a typical mature ovary. No testicular tissue was observed in sex-reversed gonads in both treatment groups. Contrary to the previous assumptions, present results suggest that IP male wrasses have the potential to undergo male-female sex change in response to exogenous estrogen. How the presence or absence of estrogen creates sexual plasticity in gonadal germ and somatic cells remains to be clarified.

Adult subacute mountain sickness--a syndrome of congestive heart failure in man at very high altitude.

A new type of mountain sickness is described. 21 men (age 22.2, standard deviation [SD] 1.8 years) had severe congestive heart failure with oedema and ascites after 10.8 (SD 5.9) weeks at altitudes of 5800-6700 m. Investigation, within 3 days of transfer to 300 m, showed polycythaemia, cardiomegaly with right ventricular enlargement, and (in 17) pericardial effusion. The heart failure resolved rapidly after transfer from high altitude.