IntroductionEvidence on new-onset endocrine dysfunction and identifying whether the degree of this dysfunction is associated with the severity of disease in patients with COVID-19 is scarce.Patients and MethodsConsecutive patients enrolled at PGIMER Chandigarh were stratified on the basis of disease severity as group I (moderate-to-severe disease including oxygen saturation <94% on room air or those with comorbidities) (n= 35) and group II (mild disease, with oxygen saturation >94% and without comorbidities) (n=49). Hypothalamo-pituitary-adrenal, thyroid, gonadal axes, and lactotroph function were evaluated. Inflammatory and cell-injury markers were also analysed.ResultsPatients in group I had higher prevalence of hypocortisolism (38.5 vs 6.8%, p=0.012), lower ACTH (16.3 vs 32.1pg/ml, p=0.234) and DHEAS (86.29 vs 117.8µg/dl, p= 0.086) as compared to group II. Low T3 syndrome was a universal finding, irrespective of disease severity. Sick euthyroid syndrome (apart from low T3 syndrome) (80.9 vs 73.1%, p= 0.046) and atypical thyroiditis (low T3, high T4, low or normal TSH) (14.3 vs 2.4%, p= 0.046) were more frequent in group I than group II. Male hypogonadism was also more prevalent in group I (75.6% vs 20.6%, p=0.006) than group II, with higher prevalence of both secondary (56.8 vs 15.3%, p=0.006) and primary (18.8 vs 5.3%, p=0.006) hypogonadism. Hyperprolactinemia was observed in 42.4% of patients without significant difference between both groups.ConclusionCOVID-19 can involve multiple endocrine organs and axes, with a greater prevalence and degree of endocrine dysfunction in those with more severe disease.

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Background Clinicians have long been struggling to find an effective tool to predict onset of puberty. Objective To explore stimulability of inhibin B after exogenous FSH and it’s potential role for prediction of onset of puberty. Design and participants Study subjects were enrolled into “exploratory cohort”(n=42) and “validation cohort”(n=19). “Exploratory cohort” was further divided into Group-1(Healthy children with spontaneous puberty: SP, n=26) and Group-2 (Patients of hypogonadotropic hypogonadism: HH, n=16). “Validation cohort” included children who presented with complaints of delayed puberty. Intervention and outcome Participants were subjected to FSH stimulation test and GnRHa stimulation test. Cut-offs derived from “exploratory cohort” for basal and FSH stimulated inhibin B(FSH-iB) were applied on “validation cohort” .Basal LH, GnRHa stimulated LH, basal inhibin B and FSH-iB were compared with clinical outcome on prospective follow-up for prediction of onset of puberty. Results There was statistically significant increment in inhibin B after exogenous FSH in Group 1(SP) in both male(188.8 pg/ml;p-value-0.002) and female (1065 pg/ml;p-value-0.023) subjects. The increment was not statistically significant in Group 2(HH) in both genders. FSH-iB at a cut-off of 116.14 pg/ml in male and 116.50 pg/ml in female had 100% sensitivity and specificity for labelling entry into puberty. On application of these cut-offs on “validation cohort”, FSH-iB had 100% PPV, NPV and diagnostic accuracy for prediction of onset of puberty. Conclusion Inhibin B was stimulable in both male and female subjects. FSH-iB can be considered as novel and promising investigation for prediction of onset of puberty. Future studies are required for further validation.

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