OBJECTIVE -To determine the microbiological profile and antibiotic susceptibility patterns of organisms isolated from diabetic foot ulcers. Also, to assess potential risk factors for infection of ulcers with multidrug-resistant organisms (MDROs) and the outcome of these infections.RESEARCH DESIGN AND METHODS -Pus samples for bacterial culture were collected from 80 patients admitted with diabetic foot infections. All patients had ulcers with Wagner's grade 3-5. Fifty patients (62.5%) had coexisting osteomyelitis. Gram-negative bacilli were tested for extended spectrum ␤-lactamase (ESBL) production by double disc diffusion method. Staphylococcal isolates were tested for susceptibility to oxacillin by screen agar method, disc diffusion, and mec A-based PCR. Potential risk factors for MDRO-positive samples were explored.RESULTS -Gram-negative aerobes were most frequently isolated (51.4%), followed by gram-positive aerobes and anaerobes (33.3 and 15.3%, respectively). Seventy-two percent of patients were positive for MDROs. ESBL production and methicillin resistance was noted in 44.7 and 56.0% of bacterial isolates, respectively. MDRO-positive status was associated with presence of neuropathy (P ϭ 0.03), osteomyelitis (P ϭ 0.01), and ulcer size Ͼ4 cm 2 (P Ͻ 0.001) but not with patient characteristics, ulcer type and duration, or duration of hospital stay. MDRO-infected patients had poor glycemic control (P ϭ 0.01) and had to be surgically treated more often (P Ͻ 0.01). CONCLUSIONS -Infection withMDROs is common in diabetic foot ulcers and is associated with inadequate glycemic control and increased requirement for surgical treatment. There is a need for continuous surveillance of resistant bacteria to provide the basis for empirical therapy and reduce the risk of complications. Diabetes Care 29:1727-1732, 2006W orldwide, diabetic foot lesions are a major medical, social, and economic problem and are the leading cause of hospitalization for patients with diabetes. Infectious agents are associated with amputation of the infected foot if not treated promptly.Proper management of these infections requires appropriate antibiotic selection based on culture and antimicrobial susceptibility results; however, initial management comprises empirical antimicrobial therapy, which is often based on susceptibility data extrapolated from studies performed on general clinical isolates (1). Several studies found methicillin-resistant Staphylococcus aureus (MRSA) in as many as 15-30% of diabetic wounds (1-3). Infection with multidrug-resistant organisms (MDROs) may increase the duration of hospital stay and cost of management and may cause additional morbidity and mortality (4). Although increasing antimicrobial resistance is a pertinent problem in India, there is paucity of data on the frequency of MDRO infections and the outcome of such infections among diabetic foot ulcers in this region. The aim of this study was to determine the microbiological and antimicrobial susceptibility profile of organisms isolated from patients with diab...

BackgroundRenal failure in diabetes is mediated by multiple pathways. Experimental and clinical evidences suggest that renin-angiotensin-aldosterone system (RAAS) has a crucial role in diabetic kidney disease. A relationship between the RAAS genotypes and chronic renal insufficiency (CRI) among type 2 diabetes subjects has therefore been speculated. We investigated the contribution of selected RAAS gene polymorphisms to CRI among type 2 diabetic Asian Indian subjects.MethodsTwelve single nucleotide polymorphisms (SNPs) from six genes namely-renin (REN), angiotensinogen (ATG), angiotensin converting enzyme I (ACE), angiotensin II type 1 receptor (AT1) and aldosterone synthase (CYP11B2) gene from the RAAS pathway and one from chymase pathway were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and tested for their association with diabetic CRI using a case-control approach. Successive cases presenting to study centres with type 2 diabetes of ≥2 years duration and moderate CRI diagnosed by serum creatinine ≥3 mg/dl after exclusion of non-diabetic causes of CRI (n = 196) were compared with diabetes subjects with no evidence of renal disease (n = 225). Logistic regression analysis was carried out to correlate various clinical parameters with genotypes, and to study pair wise interactions between SNPs of different genes.ResultsOf the 12 SNPs genotyped, Glu53Stop in AGT and A>T (-777) in AT1 genes, were monomorphic and not included for further analysis. We observed a highly significant association of Met235Thr SNP in angiotensinogen gene with CRI (O.R. 2.68, 95%CI: 2.01–3.57 for Thr allele, O.R. 2.94, 95%CI: 1.88–4.59 for Thr/Thr genotype and O.R. 2.68, 95%CI: 1.97–3.64 for ACC haplotype). A significant allelic and genotypic association of T>C (-344) SNP in aldosterone synthase gene (O.R. 1.57, 95%CI: 1.16–2.14 and O.R. 1.81, 95%CI: 1.21–2.71 respectively), and genotypic association of GA genotype of G>A (-1903) in chymase gene (O.R. 2.06, 95%CI: 1.34–3.17) were also observed.ConclusionSNPs Met235Thr in angiotensinogen, T>C (-344) in aldosterone synthase, and G>A (-1903) in chymase genes are significantly associated with diabetic chronic renal insufficiency in Indian patients and warrant replication in larger sample sets. Use of such markers for prediction of susceptibility to diabetes specific renal disease in the ethnically Indian population appears promising.

Background: Cytokines play an important role in the development of diabetic chronic renal insufficiency (CRI). Transforming growth factor β1 (TGF β1) induces renal hypertrophy and fibrosis, and cytokines like tumor necrosis factor-alpha (TNFα), chemoattractant protein-1 (MCP-1), and regulated upon activation and normal T cell expressed and secreted (RANTES) mediate macrophage infiltration into kidney. Over expression of these chemokines leads to glomerulosclerosis and interstitial fibrosis. The effect of MCP-1 and RANTES on kidney is conferred by their receptors i.e., chemokine receptor (CCR)-2 and CCR-5 respectively. We tested association of nine single nucleotide polymorphisms (SNPs) from TGFβ1, TNFα, CCR2 and CCR5 genes among individuals with type-2 diabetes with and without renal insufficiency.

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We conducted a pilot study in 10 adult male schizophrenics, 5 with predominantly positive symptoms (group I) and 5 with predominantly negative symptoms (group II), and 10 healthy matched controls. No significant differences in serum levels of testosterone (T), dehydroepiandrosterone sulfate (DHEAS), estradiol, and cortisol were found between patients as a whole and controls, using radioimmunoassay. However, serum T and DHEAS levels were lower (P <0.05) in group II patients than in group I. Body hair and aggression scores also were lower (P <0.05) in group II. In a much larger sample, Shirayama and colleagues also showed that "moderate negative symptoms, but not low negative symptoms" correlated negatively with T (P <0.05), but positively with ACTH (P <0.05) and cortisol (P <0.01) levels in plasma. Neuroactive steroids, such as DHEAS, and other sex hormones, including their synthetic derivatives, may have an adjunctive role in reversing or slowing the progression of negative symptoms. Indeed, "DHEA augmentation" improved "negative (P <0.01), depressive (P <0.05), and anxiety (P <0.01) symptoms."

Reproductive endocrine functions were studied in men with primary hypothyroidism during the hypothyroid phase and after achieving euthyroid status with thyroxine substitution therapy. Hypergonadotropism [luteinising hormone (LH), 18.7 ± 7.3 IU/1; follicle-stimulating hormone (FSH), 6.3 ± 2.0 IU/1], low serum testosterone (6.1 ± 2.8 nmol/l), low serum sex-hormone-binding globulin (SHBG; 13.2 ± 2.0 nmol/l) and subnormal testosterone response to human chorionic gonadotropin hCG; (30% increase in serum testosterone following hCG) observed during the hypothyroid phase were restored to normal (LH, 7.2 ± 2.0 IU/1; FSH, 2.7 ± 0.9 IU/1; testosterone, 12.9 ± 2.7 nmol/l; SHBG, 26.5 ± 8.4 nmol/l, and 2-fold increase in serum testosterone following hCG) with thyroxine substitution therapy. Some improvement in sperm count and motility was also observed.

Background: Genetic markers conferring susceptibility to diabetes specific renal disease remains to be identified for early prediction and development of effective drugs and therapies. Inconsistent results obtained from analysis of genes from classical pathways generate need for examination of unconventional genetic markers having role in regulation of renal function. Experimental and clinical evidences suggest that dopamine is an important natriuretic hormone. Therefore, various genes involved in regulation of dopamine bioavailability could play a role in diabetic chronic renal insufficiency (CRI). We investigated the contribution of 12 polymorphisms from five Dopaminergic pathway genes to CRI among type-2 diabetic Asian Indian subjects.