A study to evaluate the prevalence of hypogonadism in Indian males with Type-2 diabetes mellitus.

BACKGROUND: A high prevalence of hypogonadism in men with Type-2 diabetes mellitus (T2DM) has been reported worldwide. OBJECTIVES: To evaluate the prevalence of hypogonadism in Indian males with T2DM and assess the primary and secondary hypogonadism along with androgen deficiency. MATERIALS AND METHODS: In this cross-sectional study, 900 men with T2DM were evaluated using androgen deficiency in aging male questionnaire. They were screened for demographic characteristics, gonadal hormone levels, lipid profile, and glycosylated hemoglobin. RESULTS: The prevalence of hypogonadism in T2DM patients was found to be 20.7% (186 out of 900). Hypogonadism was of testicular origin (primary) in 48/186 (25.8%) patients, of pituitary or hypothalamic origin (secondary) in 14/186 (7.53%), and remaining 124/186 (66.67%) patients were found to have low testosterone with the inappropriate normal level of luteinizing hormone and Follicle-stimulating hormone. 451/900 (50.1%) patients were only symptomatic but had normal testosterone levels. Further 263 patients out 900 were asymptomatic, of which 51/900 (5.7%) patients had low levels of testosterone and 212/900 (23.5%) patients had normal testosterone level without symptoms. There were no deaths or other serious adverse events except mild pyrexia which was not related to the study. CONCLUSION: Hypogonadism diagnosis, at times, might not be validated with the help of androgen deficiency questionnaire or symptoms only. Given the large number of patients of T2DM in India, the incidence of hypogonadism is more in diabetic patients as compared to the general population. Hence, implementation of screening programs in diabetic patients is necessary to understand and detect individuals with low serum total testosterone at any early stage and to supplement testosterone accordingly.

Adrenal insufficiency in patients with stable non-cystic fibrosis bronchiectasis.

BACKGROUND & OBJECTIVES: Suppressed adrenal responses associated with inhaled steroid use have been reported in patients with bronchiectasis and have been shown to be associated with poor quality of life. This study was undertaken to examine the prevalence of suppressed cortisol responses in stable bronchiectasis and determine their correlation with the use of inhaled corticosteroids, radiologic severity of bronchiectasis and quality of life (QOL) scores. METHODS: In this case-control study, cases were patients with bronchiectasis and suppressed cortisol responses and controls were healthy volunteers, and patients with bronchiectasis without suppressed cortisol responses. Symptoms, lung function test values, exercise capacity, HRCT severity scores for bronchiectasis, exacerbations, inhaled corticosteroid use and quality of life scores were compared between patients with and without suppressed cortisol values. RESULTS: Forty consecutive patients with bronchiectasis and 40 matched controls underwent 1-µg cosyntropin testing. Baseline cortisol (mean difference -2.0 µg/dl, P=0.04) and 30-minute stimulated cortisol (mean difference -3.73 µg/dl, P=0.001) were significantly lower in patients with bronchiectasis. One patient had absolute adrenal insufficiency and 39.5 per cent (15/38) patients with bronchiectasis had impaired stimulated responses. Baseline and stimulated cortisol responses were unaffected by inhaled steroids (O.R 1.03, P=0.96). SGRQ scores were negatively correlated with body mass (r= -0.51, P=0.001) and bronchiectasis severity (r=0.37, P=0.019), but not related to baseline or stimulated cortisol responses. INTERPRETATION & CONCLUSIONS: Our results showed that the impaired adrenal responses to 1-µg cosyntropin were common in patients with bronchiectasis. This was not associated with the use of inhaled steroids or severity of bronchiectasis. Poor health status was associated with advanced disease and not with cortisol responses to the 1-µg cosyntropin test.

The 1 µg cosyntropin test in normal individuals: A reappraisal.

BACKGROUND: The 1µg cosyntropin test has some advantages over the 250µg test as a test of adrenal function. One of the concerns regarding the 1 µg test includes stability of the cosyntropin when reconstituted and stored. Classically the 5(th) percentile responses to cosyntropin in normal individuals have been used to define a normal response. Recent studies have shown that these normative values should be determined for individual assays. MATERIALS AND METHODS: We performed a 1µg cosyntropin test using reconstituted and refrigerated (4-8(°) C) cosyntropin in saline solution in 49 non pregnant adults who were apparently healthy and had no exposure to exogenous glucocorticoids. The cosyntropin solution was stored for up to 60 days following reconstitution. We analysed the data for any association between duration of cosyntropin solution storage and the cortisol responses to cosyntropin administration. RESULTS: The mean ± SD cortisol level at baseline, 30 and 60 min were-12.19 ± 3 µg/dl, 20.72 ± 2.63 µg/dl, 16.86 ± 3.33 µg/dl. The 5(th) percentile cortisol response at 30 min was 16.5 µg/dl (16.33 µg/dl rounded off). The correlation coefficients between number of days of cosyntropin solution storage and the cortisol responses at 30 and 60 min were (Spear mans rho = 0.06,-0.24 respectively) (P = 0.69 and 0.41). There were no differences in cortisol values whether the storage was for less than 30 days or more than 30 days (mean difference 0.25 µg/dl P = 0.44). CONCLUSION: The 5(th) percentile normative values determined for our assay is lower than what is currently being used clinically and in research publications. Prolonged refrigerated storage of cosyntropin solution does not affect the validity of the 1 µg cosyntropin test.

Developmental origins of adult diseases.

There is considerable evidence for the fact that early life environment in human beings are associated with future development of various metabolic diseases. Fetal programming and perinatal events appear to exert effects on later life that are independent of environmental risk factors in adults. Our understanding of the underlying mechanisms are limited and remains unclear. However several animal models and epidemiological studies have shown this association, and it is assumed secondary to the penalties of developmental plasticity. In this review, we amalgamate facts from several disciplines to support this hypothesis.