Undernutrition is the leading risk factor for TB infection and death in India. We undertook a micro-costing analysis of a nutritional intervention for household contacts of people living with TB in Puducherry, India. We found that the total 6-month food cost for a family of four was USD4/day. We also identified several alternative regimens and cost-lowering strategies to encourage wider adoption of nutritional supplementation as a public health tool.

Setting India's National Tuberculosis Elimination Programme (NTEP) covers diagnostic and therapeutic costs of TB treatment. However, persons living with TB (PLWTB) continue to experience financial distress due to direct costs (payment for testing, treatment, travel, hospitalization, and nutritional supplements) and indirect costs (lost wages, loan interest, and cost of domestic helpers). Objective To analyze the magnitude and pattern of TB-related costs from the perspective of Indian PLWTB. Design We identified relevant articles using key search terms ('tuberculosis,' 'India,' 'cost,' 'expenditures,' 'financing,' 'catastrophic' and 'out of pocket') and calculated variance-weighted mean costs. Results Indian patients incur substantial direct costs (mean: US$46.8). Mean indirect costs (US$666.6) constitute 93.4% of the net costs. Mean direct costs before diagnosis can be up to four-fold that of costs during treatment. Treatment in the private sector can result in costs up to six-fold higher than in government facilities. As many as one in three PLWTB in India experience catastrophic costs. Conclusion PLWTB in India face high direct and indirect costs. Priority interventions to realize India's goal of eliminating catastrophic costs from TB include decreasing diagnostic delays through active case finding, reducing the need for travel, improving awareness and perception of NTEP services, and ensuring sufficient reimbursement for inpatient TB care.

Gonadal function in four patients with mosaic XO or XX/XY Turner's syndrome was reviewed. Luteinizing hormone (LH) levels were determined by double antibody radioimmunoassay. Urinary testosterone (UT) and plasma testosterone (T) levels were determined by either double isotope or competitive protein binding methods. Three patients had ambiguous genitalia and exploratory surgery revealed only medullary elements in the gonads. Two virilized at puberty and were studied prior to surgery. One had normal LH levels (11 mIU/ml), a normal excretion of UT (0.5 μg/24 hrs) but responded to human chorionic gonadotropin (HCG) with an ten-fold increase in UT. The other had castrate levels of LH (≧ 100 mIU/ml) and adult male levels of plasma T (208 mμg%) which did not increase with HCG. The third patient at age 41/2 years was found to have an undifferentiated streak and, contralaterally, a testis and epididymis. The fourth patient, 14 years of age, has no evidence of any adoloscent development. Prophylactic gonadectomy in mixed gonadal dysgenesis has been recommended because of the increased incidence of gonadal malignancy. Our patients support the recommendation for early surgery. It appears that waiting until post-puberty serves no purposes because if the gonads are to function at all, they are more likely to produce androgens.

Glucagon causes pituitary polypetide hormone release in patients with normal pituitary function. We have assessed the effect of a standard dose of glucagon, 0.5 mg. I.M., in 17 patients ages 9 mos. to 14 years who presesnted with short stature of various etiologies. Results reveal that glucagon induces growth hormone (GH) levels equal to or greater than those achieved by either an Insulin Tolerance Test (I.T.T.) or Arginine Tolerance Test (A.T.T.). A 17 mμg/ml difference in GH levels was noted at 90 to 120 mins. after the glucagon injection. Among the normal respondents (≥5.0 mμg/ml rise), there were neither false negative nor false positive tests when compared to a matched I.T.T. or A.T.T. One glucagon non-respondent (≤1.0 mμg/ml) also had a negative exercise tolerance test yet had a blunted A.T.T. One patient with a blunted G.S.T. had a normal I.T.T. After glucagon, the mean glucose levels of the growth hormone deficient patients were 20 mg% higher than in the normal patients. Their lowest blood sugar occurred later in the test than in the normal and subnormal respondents. A “back-to-back” A.T.T.-G.S.T. done the same day induces two peaks of growth hormone without risk of hypoglycemia, and may be the most reasonbale screen for this type of patients. Glucagon may be sued to further our understanding of the abnormalities of glucose homeostasis in growth hormone deficient patients.