The relationship between glycemic control and osteocalcin, type 1 collagen C-terminal telopeptide, bone-specific alkaline phosphatase and the effects of anti-diabetic regimens on circulating markers of bone turnover in newly diagnosed diabetic patients: Bone health in diabetics.

AIM: Bone mineral disorders are being increasingly seen among diabetic populations as the frequency of diabetes mellitus (DM) is rising at an alarming rate. Our aim is to examine the relationship between glycemic control and bone turnover markers like osteocalcin (OC), C-terminal carboxy telopeptide (CTX), and bone-specific alkaline phosphatase (ALP) in patients with type 2 diabetes, and the effects of anti-diabetic regimens on these markers. MATERIALS AND METHODS: A total of 80 newly diagnosed type 2 DM patients were enrolled into the study and divided into two groups according to glucose regulation (group 1 HbA1c < 7 and group 2 HbA1c ≥ 7). They were also classified into three groups according to antidiabetic regimen. Physical examination findings, demographic characteristics, and anti-diabetic regimens of the patients were recorded. Hemogram and biochemical parameters were studied after 12 hours of fasting. Serum levels OC and CTX were examined by ELISA method. Bone-specific ALP was examined by Chemiluminesence immuneassay (CLIA) method. Bone densitometry was performed on the 2016 model Stratos DR device of DMS brand, and T scores of the patients were recorded. All parameters were repeated at the 6th month of the study. RESULTS: Serum vitamin D and OC levels of group 1 were higher, while ALP was higher in group 2. However, we failed to determine a significant difference in CTX levels between the groups. OC levels were enhanced only in patients receiving metformin plus vildagliptin therapy. The CTX levels increased in all groups, whereas they decreased in the metformin plus DPP-4 group. CONCLUSION: Better glucose regulation is associated with better bone formation, and among three groups metformin plus vildagliptin therapy has a favorable effect on both bone formation and resorption.

Urotensin II levels in patients with chronic kidney disease and kidney transplants.

OBJECTIVE: Urotensin II is a potent vasoactive peptide that has been implicated in the pathophysiology of many diseases. There is no study reporting the role and level of this peptide in recipients of kidney transplant. So we aimed to study the plasma levels of urotensin II in this group of patients. METHODS: Plasma urotensin II levels were analyzed in 110 subjects, who were divided into three groups: group 1 (35 kidney transplant recipients), group 2 (36 patients with chronic kidney disease), and group 3 (39 healthy controls). RESULTS: Analysis of logarithmic transformation of urotensin II, i.e. log (urotensin II × 1000) levels, with a one-way analysis of variance yielded a P value of 0.001. Post-hoc analysis showed significantly higher log (urotensin II × 1000) levels in group 1 than groups 2 and 3 (P = 0.001 and 0.017, respectively). One of the important features of the subjects of this group was that they were taking immunosuppressive drugs because of renal transplantation. CONCLUSIONS: High urotensin II levels in recipients of kidney transplants could be drug-related (immunosuppressive drugs) and may be of practical importance that may be used to improve the long-term outcome of the patients.

Prevalence of gluten sensitive enteropathy antibodies in restless legs syndrome.

The prevalence of restless legs syndrome (RLS) is increased in gluten sensitive enteropathy (GSE); but prevalence of GSE is not known in RLS. 96 RLS patients and 97 healthy controls, both with or without iron deficiency were enrolled. All secondary RLS patients except iron deficiency were excluded. Subjects underwent a thorough biochemistry and routine blood analyses, and tissue transglutaminase antibodies (TTGA), endomysium antibodies (EMA) and gliadin antibodies (AGA) were also tested. In RLS patients positivity rates of all GSE antibodies were similar to those in controls. The rate of iron deficiency anaemia in RLS patients with at least one positive GSE antibody was significantly higher than that of RLS patients whose GSE antibodies were all negative. The prevalence of GSE antibodies in RLS patients is not increased. GSE might have a role in the aetiology of RLS in association with iron deficiency anaemia. Since the prevalence of GSE antibodies is not increased in RLS, it seems unlikely that GSE is involved in the aetiology of RLS through different mechanisms (e.g. immunological mechanisms) other than iron deficiency as proposed in some published papers.