ACTA ENDOCRINOLOGICA (BUC)

Background. Recent experimental data show that increased plasma adiponectin in chronic kidney disease could be a response to inflammation.\r\nObjective. To identify factors influencing adiponectinemia in patients with type 2 diabetes (T2DM) and microalbuminuria or low grade proteinuria.\r\nDesign. 32 patients with urinary albumin excretion rate (UAER)> 30 mg/g creatinine but without significant proteinuria (< trace COMBUR) were included and compared to 59 normalbuminuric T2DM controls. History, anthropometric measurements, laboratory analysis, total plasma adiponectin were obtained.\r\nResults. In our patients with UAER of 273.51?57.26 mg/g creatinine and estimated glomerular filtration rate (eGFR) 64.92?4.56 mL/min, in simple regression, adiponectinemia\r\ncorrelates inversely to eGFR (p=0.02, r= -0.38), triglyceridemia (p=0.03, r=-0.37) and hemoglobin\r\n(Hb -p= 0.01, r=-0.45) and positively to HDL cholesterol (p=0.001, r=0.54) and UAER (p<0.0001, r=0.71); the two latter parameters remain significant in multiple regression. In controls, adiponectinemia correlates inversely to age (p=0.04, r=-0.26) and BMI (p=0.04, r=-0.24); these and UAER predict adiponectinemia in multiple regression. 11 patients have UAE superior to 300 mg/g creatinine and 21 are strictly microalbuminuric (mean UAER 653.16?97.02 and 83.68?10.28mg albumin/g creatinine respectively). In microalbuminuric patients serum C reactive protein (CRP) correlates positively (p=0.0008, r=0.68) and Hb negatively (p=0.04, r=-0.41) to adiponectinemia; in multiple regression adiponectinemia only depends on CRP. In proteinuric patients CRP and\r\nglycated Hb correlate to adiponectinemia in stepwise multiple regression.\r\nConclusion. Adiponectinemia is mainly predicted by UAER in our cohort whereas it depends on age and BMI in normalbuminuric T2DM controls; in strictly microalbuminuric\r\npatients CRP is a major predictor of adiponectinemia.

Objective. Gestational diabetes mellitus (GDM) is defined as glucose intolerance that\r\nis detected for the first time during pregnancy. Normal pregnancy induces insulin resistance\r\nthrough the diabetogenic effects of placental hormones. Glucose tolerance test results in\r\ntwin and singleton pregnancies were compared in this study.\r\nSubjects and Methods. A total of 360 pregnant women were studied. 200 women\r\n(mean age 31.60?2.10 yr) had singleton pregnancies (Group I) and 160 women (mean age\r\n28.20?2.70 yr) had twin pregnancies (Group II). 50- g, 1- hour glucose tolerance test was\r\nconducted on the first prenatal visit. An abnormal glucose screen defined as glucose > 140\r\nmg/dL was followed by a 100g, 3-hour glucose tolerance test. Gestational diabetes was\r\ndefined as the presence of two or more abnormal values during the 3-hour test.\r\nResults. Gestational diabetes was found in 4 of the 200 (2%) singleton pregnant\r\nwomen and 8 of the 160 (5%) twin pregnant women. Group I (Singleton) was further\r\ndivided into two subgroups according to whether the 1-hr plasma glucose level was < 140\r\nmg/dl (Group Ia) or >140 mg/dL (Group Ib). Likewise, Group II pregnancies was also\r\ndivided into two subgoups on the same basis. Mean screening test glucose levels were found\r\nto be 127.8?14.94 mg/dL in Group Ia and 150.8 ? 18.1 mg/dL in Group Ib women. Mean\r\nscreening test glucose levels of Group IIa subjects was 92.80 ? 18.30 mg/dL while that of\r\nGroup IIb subjects was 154.8 ? 27.0 mg/dL. Mean 1st h glucose levels of 100-g glucose\r\ntolerance test was found to be 131.4 ? 32.58 mg/dL in Group I, and 112.5 ? 39.6 mg/dL in\r\nGroup II. Mean 2nd h glucose tolerance test values were 133.2 ? 28.8 mg/dL in Group I and\r\n100.6?28.8 mg/dL in Group II. Mean 3rd h glucose tolerance test values were 107.6 ? 23.58\r\nmg/dl in Group I and 72?16.9 mg/dL in Group II.\r\nConclusion: Glucose screening results and 100-g, 3- hour glucose tolerance test\r\nvalues have been found to be lower in twin pregnancies than in singleton pregnancies.\r\nTherefore, we suggest that these findings be taken into account in developing diagnostic\r\ncriteria for gestational diabetes in twin or more pregnancies.

Obesity is a well-recognized risk factor for type 2 diabetes, cardiovascular disease, and several types of cancer. However, a proportion of the obese individuals display a significantly lower risk for metabolic complications than expected for their degree of body mass index, and this subtype of obesity was described as “metabolically healthy obesity” (MHO). No universally accepted criteria for the diagnosis of MHO exists and the prevalence of this subtype of obesity varies largely according to criteria used. Broadly, MHO is characterized by a lower amount of visceral fat, a more favorable inflammatory profile, and less insulin resistance as compared to the metabolically unhealthy obesity. Currently, controversies exist regarding the risk of cardiovascular events and all-cause mortality associated with MHO as compared to metabolically-healthy non-obese individuals. Further research is needed in order to identify the MHO phenotype and if MHO is truly healthy for a long period of time or if it is a transient state from normal metabolic/normal weight to abnormal metabolic/obese state. This review will discuss the MHO definition criteria; the differences between MHO and metabolically unhealthy obesity; the possible underlying mechanisms and clinical implications of MHO.

Introduction. The functions of CD36 membrane receptor include removal of oxidized low-density lipoproteins from\r\nplasma. The aim of our study was to search association between the IVS3-6 C allele and hypercholesterolemia in overweight children.\r\nMaterial and Methods. The study groups comprised 55 Caucasian children with (33) and without hypercholesterolemia (22). Amplicons of exon 4 including\r\nfragments of introns 3 and 4 were studied using denaturing high-performance liquid chromatography (DHPLC).\r\nResults. Polymorphism detected by DHPLC was single nucleotide substitution in intron 3 (IVS3-6 T/C - rs3173798). The IVS3-6 T/C polymorphism is located in the\r\nregion encoding the oxidized LDL binding domain, at a conserved splice site. Total serum cholesterol concentrations were significantly lower in the IVS3-6 TC\r\nheterozygotes than in the TT patients. Furthermore we found tendency (p=0.06) to lower LDL-cholesterol level in IVS3-6 TC heterozygotes than in wild-type homozygotes.\r\nConclusion. The results of our preliminary study suggest that the IVS3-6 C allele of CD36 rs3173798 polymorphism\r\nmay be associated with lower serum total and LDL-cholesterol in overweight children diagnosed with hypercholesterolemia.

Background Supplementation of Lcarnitine is associated with improvement in some abnormalities present in hemodialysis (HD) patients. Objective. The study aim was to analyze the effect of oral L-carnitine supplementation on endothelial dysfunction (ED), oxidative stress (OS), inflammation and anemia in HD patients. Design. A prospective, longitudinal and observational study was performed in a single dialysis unit. Subjects and methods.We studied 31 HD patients: 21 patients formed the Lcarnitine supplementation group (group 1) and 10 entered the control group (group 2). At baseline and after 3 months of L-carnitine supplementation (500mg/day) we determined endothelial-dependent flow-mediated vasodilatation (FMD) and nitroglycerin induced endothelium independent vasodilatation, involving ultrasonographic brachial artery measurements, serum visfatin, malondialdehyde, body mass index, systolic blood pressure, diastolic blood pressure, interdialytic body weight gain, C-reactive protein, albumin, cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, ferritin, transferrin saturation, hemoglobin, erythropoietin dose, calcium (Ca), phosphorus (P), parathormone and Kt/V . Results. In group 1, FMD (8.9 (4.5-12.5) to 10.6 (6.7-18), p=0.04) and Ca (8.4±0.6 to 8.8±0.5 mg/dL, p<0.001) significantly increased after L-carnitine supplementation, while visfatin (1.0 (0.2-1.3) to 0.4 (0-0.9) pg/mL, p=0.03), malondialdehyde (2.8 (2.4- 3.2) to 1.3 (1.2-1.5) nmol/mL, p<0.001) and P (5.6±1.3 to 5.0±1.2 mg/dL, p=0.005) significantly decreased. Albumin increased significantly in both groups (3.9±0.3 to 4.2±0.3 mg/dL, p<0.001 in group 1 and 3.7±0.3 to 4.0±0.3 mg/dL, p=0.02 in group 2). There were no other significant variations of the studied parameters. Conclusions. L-carnitine supplementation reduces ED, visfatin levels and markers of OS, but has no effect on inflammation, nutrition and anemia in HD patients.

Primary hyperaldosteronism is the cause of approximately 0.05 to 2.2% of all\r\nunselected cases of hypertension. It was first described in 1955 by Conn in conjunction with\r\naldosterone-producing adrenal adenoma, which is the most frequent aetiology, in 65% of\r\ncases. Clinical features are usually non-specific and result from potassium depletion. We\r\nreport here the case of a 54-year-old woman who was admitted to the emergency department\r\ndue to coma (Glasgow score 6). The presence of severe potassium depletion (1.2 mmol/L)\r\nand metabolic alkalosis (PH=7.76, base excess>30 mmol/L) in a hypertensive patient\r\ndetermined the clinicians to search for a secondary cause of hypertension. This was\r\nconfirmed by localizing on computer tomography a right adrenal adenoma of 31-mm\r\ndiameter and on endocrine measurements that showed mineralocorticoid excess (plasma\r\naldosterone=764 pg/mL;N=14-193). Clinical evolution was slowly favourable after\r\nrestoring the electrolyte balance, with increasing of serum K up to 3.05 mmol/L. The patient\r\nbecame asymptomatic in 3 weeks and underwent laparoscopic right adrenalectomy. The\r\npatient had a good postoperatory evolution. Two weeks after laparoscopic right\r\nadrenalectomy, blood pressure normalized after the discontinuation of the antihypertension\r\ntreatment and the aldosterone measurement was normal (102 pg/mL).

Objective. This study aimed to evaluate the utility of C-peptide levels in the differentiation of monogenic forms of diabetes from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in clinical practice. Subjects and Methods. A total of 104 patients aged >16 who visited the Dicle University’s Faculty of Medicine between April 2011 and December 2020 and were diagnosed with monogenic diabetes by genetic analysis or with T1DM and T2DM were randomly selected for retrospective evaluation. The C-peptide levels of these patients at the time of diagnosis of diabetes were compared. Results. Of the 104 patients, 24 (23%) were diagnosed with maturity-onset diabetes of the young (MODY), 40 (38.5%) with T1DM, and 40 (38.5%) with T2DM. Median C-peptide levels (ng/mL) (interquartile range) were 1.78 (1.24–2.88) in MODY group, 0.86 (0.34– 1.22) in T1DM group, and 2.38 (1.58–4.27) in T2DM group. Conclusions. There was a difference in C-peptide levels between MODY and T1DM groups but not between MODY and T2DM groups. As per clinical evaluations, although C-peptide levels of patients with MODY are similar to those of patients with T2DM patients, the possibility of C-peptide levels being similar to those required for T1DM diagnosis should also be considered.

Objectives. The objective of this retrospective study was to evaluate weight gain at 3 months following insulin therapy initiation and to determine if it is due to fat or fat free tissue. Methods. Fifty-eight patients with T2DM and initiation of insulin therapy were evaluated. Body composition was assessed with InBody720 device (Biospace, Korea) before and 3 months after the initiation of insulin therapy. Results. The insulin therapy was initiated with basal insulin in 84.48% of the cases. The initial dose of insulin was 22.76±12.89 units/day and increased at 3 months to 30.81±18.49 units/day (p<0.001). The initial HbA1c was 9.86±2.02% and decreased to 7.58±1.19% (p<0.001). The body weight increased from 87.01±17.37 kg to 88.04±16.64 kg (p=0.026). The fat body mass and the percent of fat decreased with no statistical significance; the intracellular and extracellular body water increased significantly (intracellular: 26.30±5.96 vs. 27.26±6.16; extracellular: 16.61±3.63 vs. 17.03±3.84; p<0.001). Conclusion. During the first 3 months after initiation of insulin therapy a modest weight gain due to increase in the body water after restoration of the metabolic balance was observed.

Introduction. Recent studies suggest that nutritional status can modify the association\r\nbetween high iPTH and mortality, especially in diabetics and older hemodialysis patients (HDP).\r\nAim. To assess the impact of mineral metabolism parameters in the survival of HDP\r\nin our area and to evidence the factors that influence iPTH levels in our HDP, which are\r\nyounger and have less frequently diabetic nephropathy as the cause of chronic renal failure\r\nthan in most published studies.\r\nPatients and Methods. A prospective cohort study of 126 HDP was recorded for\r\ndemographic, clinical and laboratory data, and after 24 months, the general mortality. Patients\r\nwere divided in two groups, survivors and non-survivors, and each of groups classified according\r\nto the time on hemodialysis (THD). The groups of non-survivors and survivors with THD more\r\nthan 10 year-period were compared to the groups with less than 10 year vintage, regarding the\r\nalbumin levels, iPTH levels, phosphate-calcium metabolism markers, age and sex.\r\nResults. We observed the better survival only for calcium phosphate product less than 55\r\nmg?/dL? (p=0,02). The iPTH level seems to be conditioned by albumin levels. For THD<10\r\nyears, iPTH levels are greater in survivors (p=0.01); in this subgroup we observed higher levels\r\nof serum albumin (p<0.001), the patients were younger (p<0.001), and had 5-fold lower\r\nfrequency of diabetes. For THD>10 years, iPTH levels are greater in non-survivor patients\r\n(p=0.02), as well as calcium, phosphorus and calcium phosphorus product.\r\nConclusions. Calcium-Phosphorus product is a better indicator for survival in HDP in our\r\narea than immunoreactive PTH levels. Immunoreactive PTH as prognostic factor might be\r\nbetter evaluated in association with calcium phosphorus metabolism parameters and albumin\r\nlevels too, even in younger and lower percent-diabetic HDP groups.

Smith-Lemli-Opitz syndrome is an autosomal recessive disorder caused by mutations of 3-hydroxysterol &#8211;7reductase gene (DHCR7) which maps to 11q12-13 and was the first discovered defect in cholesterol biosynthesis resulting in a congenital dysmorphology syndrome. We present the case of a 46,XY newborn with ambiguous genitalia and multiple congenital anomalies (atrial septal defect, ventricular septal defect, syndactyly of the second and third toe, cleft palate, webbed neck, small fontanels, mesomelia, simian palmar crease, micrognathia, wide nasal bridge with anteverted nostrils, low set ears). Hormonal assessment performed at twelve days revealed a decreased testosterone level (0.03 ng/mL), a high estradiol level (448.8 pg/mL), normal LH (2.8UI/mL), DHEAS (86.61?g/dL), progesterone (1.34ng/mL) and 17 hydroxyprogesterone (1.08ng/mL) levels. Cholesterol was low (44mg/dL) confirming the diagnostic of Smith-Lemli-Opitz syndrome.