ISRN endocrinology最新文献

Vitamin D and its analogues are widely used as treatments by clinical nephrologists, especially when treating chronic kidney disease (CKD) patients with secondary hyperparathyroidism. As CKD progresses, the ability to compensate for elevations in parathyroid hormone (PTH) and fibroblast growth factor-23 and for decreases in 1,25(OH)2D3 becomes inadequate, which results in hyperphosphatemia, abnormal bone disorders, and extra-skeletal calcification. In addition to its calciotropic effect on the regulation of calcium, phosphate, and parathyroid hormone, vitamin D has many other noncalciotropic effects, including controlling cell differentiation/proliferation and having immunomodulatory effects. There are several immune dysregulations that can be noted when renal function declines. Physicians need to know well both the classical and nonclassical functions of vitamin D. This review is an analysis from the nephrologist's viewpoint and focuses on the relationship between the vitamin D and the immune system, together with vitamin's clinical use to treat kidney diseases.

We aimed to observe the association between degree of obesity and metabolic syndrome and plasma thyrotropin levels in obese, euthyroid Turkish patients. 947 obese and overweight patients who admitted to our outpatient clinic were assessed retrospectively. 150 healthy euthyroid cases were also recruited as the control group. Cases with metabolic syndrome were determined. Patients were divided into various subgroups as overweight, obese, morbid obese, men, and women. No statistical significance was determined when all the patients' and subgroups' plasma thyrotropin levels were compared to normal weight control group. No association was shown between the presence of metabolic syndrome and plasma thyrotropin levels for both all patients and subgroups. Also there was not any association between each component of metabolic syndrome and plasma thyrotropin levels. In conclusion, we did not found any significant association between plasma thyrotropin levels and obesity and metabolic syndrome in our euthyroid subjects.

Background. Endothelial dysfunction and increased inflammation are precursors of cardiovascular disease in type 1 diabetes (T1D) and occur even in adolescents with T1D. The goal of this study was to determine the relationship of endothelial dysfunction to various measures of glycemia. Research Design and Methods. Forearm blood flow (FBF, venous occlusion plethysmography) was measured before and after 5 min of upper arm vascular occlusion in 17 adolescents with uncomplicated type 1 diabetes. Endothelial function was assessed as postocclusion FBF and forearm vascular resistance (FVR, mean arterial pressure/FBF). Fasting glucose, 72 hour mean glucose and standard deviation from continuous glucose monitoring, hemoglobin A1c, and hemoglobin A1c by duration area under the curve were used to assess immediate, short-term, and intermediate- and long-term glycemia. Results. Postocclusion FBF (r = -0.53, P = 0.030) negatively correlated and postocclusion FVR positively correlated (r = 0.52, P = 0.031) with hemoglobin A1c levels. FVR was positively associated with log 3 day mean glucose (r = 0.55, P = 0.027). Postocclusion FBF (2.8 ± 1.1 versus 3.4 ± 0.5 mL/dL/min, mean ± SE, P = 0.084) tended to be lower and FVR (31.4 ± 10.4 versus 23.9 ± 4.4 mmHg dL min/mL, P = 0.015) was significantly higher in subjects with hemoglobin A1c above the median (8.3%) compared to those with lower hemoglobin A1c levels. Conclusions. These results demonstrate that poor intermediate-term glycemic control is associated with impaired endothelial function.

Many studies have shown that carotid intima-media thickness (IMT) is associated with cardiovascular disease (CVD). Although it remains inconclusive whether assessment of carotid IMT is useful as a screening test for CVD in Japanese diabetic patients, a total of 271 patients (151 men aged 66 ± 10 (standard deviation) years and 220 women aged 71 ± 8 years) were divided into two groups based on the presence of CVD. We cross-sectionally assessed the ability of carotid IMT to identify CVD corresponding to treatment that was examined by receiver-operating characteristic (ROC) curve analyses. Among the 271 diabetic patients, 199 non-CVD and 72 CVD patients were examined. Multiple linear regression analysis using the presence of CVD as an objective variable showed that carotid IMT (β = 0.259, P < 0.001) as well as other confounding factors was a significant independent contributing factor. The ROC curve analysis showed that the best marker of CVD was carotid IMT, with an area under the ROC curve of 0.718 (95% confidence interval (CI), 0.650-0.785). The greatest sensitivity and specificity were obtained when the cut-off value of mean carotid IMT was set at 0.95 mm (sensitivity = 0.71, specificity = 0.60, and accuracy = 0.627). Our study suggests that carotid IMT may be useful for screening diabetic patients with CVD.

Methods of determining insulin sensitivity that use an oral challenge of glucose are preferred to those using intravenous administration since the measurement is made in conditions more akin to normal physiology. One previously reported protocol (ODILE) studies glucose uptake in isolation from absorption and endogenous production by the intravenous administration of tracer approximately forty-five minutes after the oral dose is given. However, this methodology has not been validated against other accredited procedures. This study utilizes the euglycemic hyperinsulinemic clamp in order to validate the ODILE method.

Impaired wound healing is a frequent problem in diabetes. Hyperglycemia may be an operative mechanism, but a link between glycemic control and wound healing has never been established. Wounds in db/db mice have been extensively studied. This study was undertaken to see if plasma glucose was a predictor of wound healing. An excisional wound was made (149 db/db mice). Wound closure was studied versus metabolic variables. The animals were 11.8 ± 0.2 weeks (mean ± standard error of the mean), obese (38.1 ± 0.5 g), and hyperglycemic (fasting plasma glucose 21.0 ± 0.7 mmol/L). Wound closure at day 13 was 30.1 ± 1.6%. In linear mixed model analyses neither fasting plasma glucose nor its change from start to end of experiment was a significant predictor of wound closure (β = 0.15, P = 0.07, 95% CI: -0.01 to 0.31 and β = 0.06, P = 0.5, 95% CI: -0.11 to 0.23, resp.). However, increase in body weight significantly and independently predicted wound closure (for weight change, β = 0.22, P = 0.008, 95% CI: 0.06 to 0.38). This study strongly suggests that wound healing in db/db mice is independent of prevailing glycemia but dependent on anabolic changes such as weight gain over time.

Aims. This study aims at assessing the relationship between 25 (OH) vitamin D (25-OHD) levels and microvascular complications in patients with type 2 diabetes mellitus (DM2). Methods. 136 patients (59 ± 11 years) with DM2 (disease duration 8.6 ± 7 years) participated in this cross-sectional study. Anthropometric data, HbA1c, 25-OHD levels, serum creatinine, and urine microalbumin/creatinine ratio were collected. Dilated retinal exam was performed, and diabetic neuropathy was assessed using the United Kingdom Screening Score. Results. Serum 25-OHD correlated negatively with HbA1c (r = -0.20,  P = 0.049). Mean 25-OHD levels were lower in subjects with diabetic retinopathy compared to those without retinopathy (12.3 ± 5.5 versus 21.8 ± 13.7, P < 0.001) and lower in subjects with diabetic neuropathy compared to those without neuropathy (16.4 ± 10.4 versus 23.5 ± 14.5, P = 0.004). After adjustment for BMI, diabetes duration, and smoking, 25-OHD was an independent predictor of HbA1c ( β   -0.14; P = 0.03). After adjustment for HbA1c, age, smoking, BMI and disease duration, 25-OHD were independent predictors for diabetic retinopathy: OR 2.8 [95% CI 2.1-8.0] and neuropathy: OR 4.5 [95% CI 1.6-12] for vitamin D < 20 versus vitamin D ≥ 20 ng/mL. Conclusion. Low serum 25-OHD level was an independent predictor of HbA1c, diabetic neuropathy, and diabetic retinopathy in patients with DM2.

Problem Statement. Thyroid gland in women undergoes functional changes during pregnancy. A few studies have described such changes in pregnant women residing in iodine deficient areas. Objective. To document these changes in pregnant women residing in Lahore, a low iodine intake urban area of Pakistan. Patients and Methods. In 254 pregnant women, data of FT4, FT3, and TSH during the first and subsequent trimesters were obtained and compared with those of 110 nonpregnant women. These hormones were determined in serum by radioimmunoassay (RIA) techniques using commercial kits. Results. Compared to nonpregnant women mean FT4 level was decreased, and FT3 and TSH increased significantly (P < 0.05) in pregnant women. A negative correlation of FT4 with TSH was observed in all three trimesters. Serum FT3 was positively correlated with TSH only during the third trimester. As a function of gestation time, FT4 levels progressively decreased, and FT3 and TSH levels increased significantly (one-way ANOVA F = 108.2, 17.3, and 44.8, resp.; all P < 0.05) exhibiting thyroid gland adaptations. Conclusion. Pregnancy is associated with significant alterations in thyroid function due to low iodine intake in women residing in study area. The compensated thyroid function poses a risk of thyroid failure in a number of pregnant women.

Studies showed suboptimal compliance rate of primary care physicians with microalbuminuria screening. This study evaluated impact of electronic medical records (EMR) and computerized physicians reminders on compliance rate and showed small to modest improvement. Combining EMR with quality control monitoring has significantly improved compliance [OR 1.556, 95% CI 1.251-1.935, P = 0.006].

Cancer is the second cause of death. Association of diabetes as a growing and costly disease with cancer is a major health concern. Meanwhile, preexisting diabetes is associated with an increased risk of all-cause and cancer-specific mortalities. Presence of diabetes related comorbidities, poorer response to cancer treatment, and excess mortality related to diabetes are among the most important explanations. Although diabetes appear to be a risk factor for cancer and is associated with the mortality risk in cancer patients, several factors such as diabetes duration, multiple drug therapy, and the presence of diabetes comorbidities make the assessment of the effect of diabetes treatment on cancer risk and mortality difficult. Metformin is the drug of choice for the treatment of type 2 diabetes. The available evidence from basic science, clinical, and population-based research supports the anticancer effect of metformin. However, randomized controlled clinical trials do not provide enough evidence for a strong protective effect of metformin on cancer incidence or mortality. One of the most important limitations of these trials is the short duration of the followup. Further long-term randomized controlled clinical trials specifically designed to determine metformin effect on cancer risk are needed to provide the best answer to this challenge.