Comparison of Indian Council for Medical Research and Lunar Databases for Categorization of Male Bone Mineral Density.

The mainstay of diagnosis of osteoporosis is dual-energy X-ray absorptiometry (DXA) scan measuring areal bone mineral density (BMD) (g/cm2). The aim of the present study was to compare the Indian Council of Medical Research database (ICMRD) and the Lunar ethnic reference database of DXA scans in the diagnosis of osteoporosis in male patients. In this retrospective study, all male patients who underwent a DXA scan were included. The areal BMD (g/cm2) was measured at either the lumbar spine (L1-L4) or the total hip using the Lunar DXA machine (software version 8.50) manufactured by GE Medical Systems (Shanghai, China). The Indian Council of Medical Research published a reference data for BMD in the Indian population derived from the population-based study conducted in healthy Indian individuals, which was used to analyze the BMD result by Lunar DXA scan. The 2 results were compared for various values using statistical software SPSS for Windows (version 16; SPSS Inc., Chicago, IL). A total 238 male patients with a mean age of 57.2 yr (standard deviation ±15.9) were included. Overall, 26.4% (66/250) and 2.8% (7/250) of the subjects were classified in the osteoporosis group according to the Lunar database and the ICMRD, respectively. Out of the 250 sites of the DXA scan, 28.8% (19/66) and 60.0% (40/66) of the cases classified as osteoporosis by the Lunar database were reclassified as normal and osteopenia by ICMRD, respectively. In conclusion, the Indian Council of Medical Research data underestimated the degree of osteoporosis in male subjects that might result in deferring of treatment. In view of the discrepancy, the decision on the treatment of osteoporosis should be based on the multiple fracture risk factors and less reliably on the BMD T-score.

Prevalence and severity of vitamin D deficiency in patients with diabetic foot infection.

The aim of the present research was to study the prevalence and severity of vitamin D deficiency in patients with diabetic foot infection. Patients were enrolled in two groups: diabetic patients with foot infection (n 125) as cases and diabetic patients without the infection as controls (n 164). Serum 25-hydroxyvitamin D (25(OH)D) was measured by RIA. Data were presented as means and standard deviations unless otherwise indicated and were analysed by SPSS. Results revealed that 25(OH)D (nmol/l) was significantly lower (40·25 (sd 38·35) v. 50·75 (sd 33·00); P < 0·001) in cases than in controls. Vitamin D inadequacy (25(OH)D < 75 nmol/l) was equally common in cases and controls (OR 1·45, 95 % CI 0·8, 3·0; P = 0·32), but cases had a greater risk of vitamin D deficiency (25(OH)D < 50 nmol/l) than controls (OR 1·8, 95 % CI 1·1, 3·0; P = 0·02). Risk of severe vitamin D deficiency (25(OH)D < 25 nmol/l) was significantly higher in cases than in controls (OR 4·0, 95 % CI 2·4, 6·9; P < 0·0001). Age, duration of diabetes and HbA1c were significantly higher in cases than in controls and therefore adjusted to nullify the effect of these variables, if any, on study outcome. The study concluded that vitamin D deficiency was more prevalent and severe in patients with diabetic foot infection. This study opens up the issue of recognising severe vitamin D deficiency (< 25 nmol/l) as a possible risk factor for diabetic foot infections and the need for vitamin D supplementation in such patients for a better clinical outcome. This could be substantiated by similar data from future studies.

Association of aldose reductase gene polymorphism (C-106T) in susceptibility of diabetic peripheral neuropathy among north Indian population.

AIM/HYPOTHESIS: Polymorphism in aldose reductase (ALR) gene at nucleotide C(-106)T (rs759853) in the promoter region is associated with susceptibility to development of diabetic peripheral neuropathy. The aim of this study was to detect the association of the C (-106)T polymorphism of ALR gene and its frequency among patients with type 2 diabetes mellitus with and without peripheral neuropathy. METHODS: The study subjects were divided into three groups. Group I included 356 patients with diabetes having peripheral neuropathy. Group II included 294 patients with diabetes without peripheral neuropathy and group III included 181 healthy subjects. Genotyping of ALR C(-106)T SNPs was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and direct sequencing methods. The genetic risk among the groups was compared and tested by calculating odds ratio with 95% class interval. RESULTS: ALR 106TT genotype was significantly higher in group I compared to group II with an odds ratio of 2.12 (95% CI: 1.22-3.67; p<0.01). Recessive model (CC+CT vs. TT), as well as T allele distribution also showed significant association to develop neuropathy with relative risk of 1.97 (95% CI: 1.16-3.35; p<0.01) and 1.36 (95% CI: 1.07-1.72; p=0.01) respectively. CONCLUSION/INTERPRETATION: In conclusion, the ALR C-106T polymorphism was associated with higher risk of peripheral neuropathy in patients with type 2 diabetes mellitus.

Reversal of nocturnal non-dipping of blood pressure after Levothyroxine therapy in patients with subclinical hypothyroidism.

AIMS: To study the loss of diurnal variation in blood pressure in normotensive patients with Subclinical/overt hypothyroidism and effect of Levothyroxine (L-T4) treatment. MATERIALS AND METHODS: In this interventional study Eighty patients between 17- 50 years with newly detected OH and SCH (74 women and 6 men) and nine euthyroid subjects (all men) with blood pressure <140/90 were recruited. All patients underwent 24h ambulatory blood pressure monitoring (ABPM) using ABPM machine before and after treatment with L-T4. Diurnal index (DI), Percent time elevation (PTE), Hyperbaric impact (HBI) were studied pre and post L-T4 treatment. RESULTS: Of the 89 subjects (22 SCH, 58 OH and 9 controls), 7 of the SCH and 30 of OH subjects reported back in follow up after L-T4 supplementation for evaluation. DI, HBI and PTE when compared at baseline between different groups (SCH- OH, SCH- control, OH- control) were insignificant. After L-T4 supplementation DI, HBI and PTE varied significantly with p value 0.007, 0.003 and 0.003 respectively between SCH- OH only. Post L-T4 analysis in SCH group was statistically insignificant (p-value 0.102) but a trend toward improvement in DI was noted (baseline and post treatment DI mean 7.00 and 13.00 respectively). CONCLUSION: Loss of nocturnal dipping was found in patients with OH and SCH which was restored after L-T4 therapy only in patients with SCH and not with OH. TREATMENT: of SCH patients with high cardiovascular risk may be beneficial in this setting and can be a new indication for LT4 therapy in SCH.

Parenteral vitamin D supplementation is superior to oral in vitamin D insufficient patients with type 2 diabetes mellitus.

BACKGROUND/OBJECTIVES: Oral vitamin D supplementation is better than parenteral in improving vitamin D deficiency in individuals with no systemic illness. Our aim was to compare the efficacy of oral and parenteral routes of vitamin D supplementation on circulating serum 25(OH) vitamin D level in patients with type 2 diabetes mellitus. METHODS: Total 85 cases of with type 2 diabetes mellitus were screened for vitamin D status of which 71 patients were vitamin D insufficient/deficient. They were randomized into two intent to treat groups with different vitamin D supplementation protocols (a) Oral-60000 IU per day for 5days (group I; n=40) and (b) injectable-300000 IU intramuscularly once (group II; n=31). Baseline and one month post supplementation 25(OH) vitamin D levels were measured in both the groups. RESULTS: Baseline clinical characteristics and 25(OH) vitamin D levels were comparable in both the groups. Post treatment 25(OH) vitamin D level in group I was 26.06±9.06ng/ml and in group II was 49.69±18.92ng/ml. After one month of vitamin D supplementation, increment in 25(OH) vitamin D level from baseline was significantly higher in group II than group I (p<0.001). INTERPRETATION & CONCLUSIONS: Injectable method of supplementation was better than oral route in improving serum 25 (OH) vitamin D status in patients with type 2 diabetes. The study suggested impaired absorption of vitamin D from the gastrointestinal tract in patients with type 2 diabetes mellitus and a need for parenteral route of vitamin D supplementation in deficient patients with type 2 diabetes mellitus.

Vascular calcification in diabetic foot and its association with calcium homeostasis.

INTRODUCTION: Vascular calcification (VC), long thought to result from passive degeneration, involves a complex process of biomineralization resembling osteogenesis, frequently observed in diabetes and is an indicator of diabetic peripheral vascular disease with variable implications. AIM AND OBJECTIVE: To study the association between vascular calcification and calcium homeostasis in diabetic patients with foot ulcers without stage 4, 5 chronic kidney disease. MATERIALS AND METHODS: A total of 74 patients with diabetic foot ulcer were enrolled, and VC was detected by X-ray and Doppler methods. Serum calcium, phosphate, alkaline phosphatase (ALKP), fasting and post-prandial glucose levels, and glycosylated hemoglobin (HbA1C) were recorded. Serum iPTH and 25 (OH) vitamin D were estimated by immune radiometric assay and radioimmunoassay, respectively. Data was analyzed by SPSS 16.0. RESULTS: Vascular calcification was present in 42% of patients. Significant difference in the mean (±SD) of vitamin D, HbA1C, and eGFR was observed in VC +ve compared to VC -ve. There was no significant association of age, duration, BMI, PTH, Ca, PO4, ALKP with that of VC incidence. Severe vitamin D deficiency was more common in VC +ve (51.6%) compared to in VC -ve (18.6%). Sub-group analysis showed that the risk of VC was significantly higher (RR = 2.4, P < 0.05, 95% C.I. = 0.058-2.88) in patients with vitamin D < 10 ng/ml compared to others. CONCLUSION: Vitamin D deficiency could be a risk for vascular calcification, which possibly act through receptors on vascular smooth muscle cells or modulates osteoprotegerin/RANKL system like other factors responsible for VC in diabetic foot patients.