ACTA ENDOCRINOLOGICA (BUC)

Context. 18F-fluorocholine (FCH) has been used as a positron emission tomography (PET) tracer in the localization of hyper-functioning parathyroid glands (HPGs). Objective. We performed this methodological study to evaluate the diagnostic performance of 18F-FCH PET/computerized tomography (CT) and repeated ultrasonography (USG) in detecting unidentified lesions in patients with primary hyperparathyroidism (PHPT). Design. In this retrospective methodological study, we studied the diagnostic performance of 18F-FCH PET/CT and a repeated USG in detecting unidentified parathyroid lesions. Subjects and Methods. Twenty-eight patients who were diagnosed with PHPT, had an indication for surgery following the current guidelines and had no identified lesion on 99mTc-MIBI SPECT/CT, USG, or other imaging methods than 18F-FCH PET/CT, included in the study. Results. While lesions were detected in 26 patients via 18F-FCH PET/CT among 28 patients [92.9% (95% CI: 76.6%-99.1%)], the lesion detection rate was 95.7% (95% CI: 78.1%-99.9%) in 23 patients who underwent a repeated USG. The sensitivity and the accuracy of both 18F-FCH PET/CT and repeated USG were 95.2% (95% CI: 76.2%- 99.9%) and 95.0 (95% CI: 75.1%-99.9%), respectively. Conclusions. This study supports that the combination of 18F-FCH PET/CT and repeated USG has promising potential for being an imaging technique for early detection and localization of HPGs.

important role in insulin signaling and the common Gly971Arg polymorphism is related to type 2 diabetes (T2D). IRS-1 Gly971Arg polymorphism can modify tyrosine phosphorylation at a specific site of IRS-1 and may have a critical role in the development of insulin resistance (IR). Objective. The purpose of this study was to investigate the association between this polymorphism and IR in Iranian patients with newly-diagnosed type 2 diabetes. Design. The study was conducted on 114 individuals with newly-diagnosed T2D and 118 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin were measured by the enzymatic method and enzyme-linked immunosorbent assay, respectively. Insulin-resistance was calculated by homeostasis model assessment estimatedinsulin resistance (HOMA-IR). The gene polymorphism was examined by polymerase chain reaction-restriction fragment length polymorphism. Results. There are significant differences between IRS1 Gly971Arg polymorphism and studied individuals (P<0.0001). The findings showed that the risk of developing T2D in individuals who had R-alleles was 3.74 folds higher than those without R-alleles. However, IRS1 Gly971Arg polymorphism was not associated with high HOMA-IR, high BMI and familial history of diabetes. Conclusions. Even though there was not a significant relationship between IRS-1 G971R polymorphism with insulin resistance and high BMI, this polymorphism was correlated to newly-diagnosed diabetic patients. Thus, the evaluation of IRS-1 G971R polymorphism may be helpful for predicting T2D new cases.

Background. Primary hyperparathyroidism and vitamin D deficiency are both associated with increased prevalence\r\nof anemia. Relationship of hemoglobin and parathyroid hormone in normal ranges were not investigated appropriately.\r\nMethods. We analysed laboratory data of 476 patients without primary hyperparathyroidism. The patients had concurrent measurements of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, 25-OH vitamin D and hemoglobin.\r\nResults. Parathyroid hormone was negatively correlated with hemoglobin (p=0.01), the correlation persisted after\r\ncorrection for vitamin D levels (p=0.045), and in sub-group of normal (>20 ng/mL) 25-OH vitamin D levels (p=0.005). Parathyroid hormone was also correlated negatively with\r\nferritin (p=0.02), correlation persisted after being adjusted to vitamin D (p=0.021). In anemic patients, these with low ferritin (<12 ng/mL) had higher PTH levels than these with higher ferritin despite having similar calcium\r\nand vitamin D levels (p=0.014).\r\nConclusion. Interaction of parathyroid hormone and erythropoiesis seems to be present in normal ranges where\r\nerythropoietin may mediate key roles regulating both.

Background and Aim. The house sparrow (Passer domesticus) is a seasonal breeder\r\nforming monogamous pairs like majority of the sub-tropical birds. Less is known about its\r\nreproductive endocrinology during different phases of the breeding cycle. In the present\r\nstudy, the house sparrows were analysed to shed light onto their breeding physiology.\r\nMethods. Seasonal changes in body weight, gonad morphology and plasma\r\nconcentration of testosterone and progesterone (by ELISA) were evaluated in 40 males and\r\n40 females respectively, using 10 birds for each season.\r\nResults. Testosterone in males was minimal during the non-breeding phase at 0.41 ? 0.17\r\nng/mL increasing at 2.35 ? 0.12 ng/mL during the onset of the pre-breeding phase,increased in the\r\nbreeding period at 5.65 ? 0.16 ng/mL, while in the post-breeding phase it was 3.83 ? 0.20 ng/mL.\r\nIn females, testosterone levels during the non-breeding phase were 0.11 ? 0.07 ng/mL, which rose\r\nsignificantly during the pre-breeding phase to 0.45 ? 0.10 ng/mL, a level equivalent to the one in\r\nmales during the non-breeding phase. During the breeding phase the values increased to 1.25 ?\r\n0.09 ng/mL, which later decreased in the post-breeding phase to 0.96 ? 0.12 ng/mL.\r\nProgesterone basal levels in females during the non-breeding phase were maintained at\r\n1.80 ? 0.10 ng/mL. A significant increase (p<0.001) is seen with the onset of pre-breeding\r\nphase which continues in the breeding phase at 2.20 ? 0.13 ng/mL and 6.23 ? 0.12 ng/mL,\r\nrespectively. During the post-breeding phase the levels significantly (P<0.001) decreased to\r\n4.73 ? 0.10 ng/mL. In males, the levels of this hormone vary less during all the phases of\r\nbreeding. The progesterone titres during the non-breeding phase were 0.85 ? 0.17 ng/mL\r\nincreasing with the onset of the pre-breeding season at 1.12 ? 0.13 ng/mL and continued to rise\r\nin breeding phase at 2.76 ? 0.16 ng/mL. Later during the post-breeding phase the levels\r\ndecreased significantly 1.45 ? 0.18 ng/mL (p<0.001).\r\nConclusion. The present study reveals cyclicity in the breeding and cyclic changes taking\r\nplace in the titers of the two hormones during different phases of the breeding in both sexes.

The pathogenesis of type 1 diabetes became a history longer and longer. There are 40 years since the immunogenetic theory of type 1 diabetes has been launched. Near this anniversary a challenge of this theory was recently published. We give here our interpretation of primary cause of type 1 diabetes which must be connected with the pathogenesis of other phenotypes of diabetes which has a main similar mechanism: the β-cell dysfunction.

Context. In addition to traditional risk factors for cardiovascular diseases, there are new risk factors with potentially relevant prognostic, such as vitamin D deficiency. Objective. The study aims to analyze the relationship between vitamin D deficiency and the occurrence of cardiovascular disease, in patients who already have at least one cardiovascular risk factor. Design. It is a prospective, observational study. Follow- up time was 24 months. Subjects and methods. A total of 77 patients were included in the study, aged over 18 years, who had at least one cardiovascular risk factor. Their vitamin D levels were measured and they were monitored for a period of 2 years, in order to see which one developed cardiovascular diseases. Results. Of the 77 patients, 56 (72.7%) had serum deficient levels of vitamin D and the mean serum level was 16 ng/mL (± 8.6 ng/mL). Statistically significant differences were observed only in the case of dyslipidemia (p=0.0334). The evolution to cardiovascular disease occurred in 39 of the cases (50.6%). The only independent risk factors for progression to cardiovascular disease demonstrated in this study were serum vitamin D (OR = 0.9024, 95% CI: 0.83- 0.97 and age (OR = 1.1313, 95% CI: 1.05-1.21). Conclusion. The results shows that patients with cardiovascular risk factors and advanced age are at a higher risk of developing cardiovascular disease, if they also have vitamin D deficiency.

Introduction. Biotin treatment causes false-low or false-high results in some immunoassays methods. This phenomenon is called as biotin interference. In the present article, a seven-month-old male, with renal failure and laboratory hyperthyroidism due to biotin interference is presented. Case report. High free T4 (fT4), free T3 (fT3), antithyroid peroxidase antibody (anti-TPO), anti-thyroglobulin antibody (anti-TG) and low thyroid stimulating hormone (TSH) levels were detected in a seven-month-old male patient who has metabolic acidosis, renal failure, and suspected of metabolic disease. Anti-thyroid drug therapy was started. However, when he was re-evaluated due to the absence of euthyroidism with anti-thyroid therapy (methimazole 0.8 mg/ kg /day), it was found that the patient had been given 20 mg/ day biotin for acidosis for two months. Biotin interference was considered in hormone measurement. Thyroid function tests were found to be normal 12 days after discontinuation of biotin therapy. Conclusion. Immunoassay measurements which use biotin should be done 2-7days after the last dose of biotin in patients under biotin treatment, but this time may need be much longer in renal failure patients. During this period or if the biotin therapy cannot be stopped, alternative methods should be preferred for analysis.

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Background. Myocardial involvement is frequent in patients with systemic lupus erythematosus (SLE), and its early detection assures the prognosis improvement. Objective. To assess the NT-proBNP levels and its correlation with systolic longitudinal performance, during exercise testing in a SLE population Subjects and Methods. The study included 30 SLE patients (80 % females), with a mean age of 44.8 ± 9.91 years. All subjects were submitted to an echo Doppler examination, including the determination of the global longitudinal strain (GLS). Also, they performed a cardiopulmonary exercise testing (CPE) on cycloergometer, assessing the peak oxygen uptake. Venous blood samples were taken and NT-proBNP levels were determined before exercise, at peak effort and two hours after exercise. Results. The left ventricular ejection fraction was normal but GLS was low in SLE patients ( -16.96 ± 3.12%, vs. -19.5 ± 3.05% normal range) and much lower in those with diastolic dysfunction (-14.5 ± 2.3% vs. - 19.2± 1.85%, p=0.0014). During CPE, the patients performed a mean 71.96% ± 13.9% of predicted VO2 max. The mean values of NT-proBNP were: 186.84 ± 186.8 pg/mL at rest, 221.68 ± 245.76 pg/mL at peak effort and 412.48 ± 400.28 pg/mL post effort. No correlation was registered between GLS and peak VO2. We found a negative correlation between GLS ant NT-proBNP at peak effort (r = -0.508) and post exercise (r=-0.623). Conclusion. The exercise NT-proBNP levels can be used together with GLS for an early detection of systolic dysfunction in SLE patients.

An 18 years old, tall man presented for circumoral numbness, paresthesias, and hypocalcaemia, without carpopedal spasm or seizures. Previous medical history revealed bilateral cataract and osseous cysts on limbs at the age of 12. Hypocalcaemia resistant to calcium treatment and mild increased TSH levels were present. At diagnosis, we noticed a normal phenotype with tall stature, moderate hypocalcaemia (5.8 mg/dL), hyperphosphatemia (5.08 mg/dL) and significantly higher than normal intact parathormone (PTH) levels (518 pg/mL), in the presence of normal serum levels of 25-hydroxy vitamin D (53.56 ng/mL). The mother and the family members have been found in good health. All these data strongly suggested sporadic pseudohypoparathyroidism type Ib (PHP-Ib), but with some features of PHP - type Ia, like the osseous cysts. We were not able to perform molecular genetic tests. The nearly complete recovery of clinical and biochemical signs (normalization of PTH, calcaemia, phosphatemia, and a normal DXA osteodensitometry) after 2 years of chronic treatment with activated 1,25- dihydroxycholecalciferol (2.00-0.75 &#956;g/day) indirectly, but strongly confirmed the diagnosis of pseudohypoparathyroidism. The patient may have resistance to TSH evidenced by high TSH\r\n(range 4.8-7.5 mIU/L), with normal thyroid hormone levels, absence of goiter and normal TPO antibodies. The TRH test (400 &#956;g i.v.) showed a response of TSH, and also of serum thyroxine and triiodothyronine in a range that did not clarify the diagnosis. This association of the resistance to TSH with type Ib PHP was relatively recently reported by two groups (17,20) and before them it was reported only in PHP-Ia. Our patient also showed mild thrombocytopenia, with normal bleeding time, indicating also a possible Gs&#945; deficiency in platelets. In conclusion, our patient with sporadic pseudohypoparathyroidism without clinical phenotype of Albright hereditary osteodystrophy is highly suggestive for the type Ib PHP. A possible resistance to TSH and thrombocytopenia associated are features related to the genetic mechanisms found also in type Ia PHP. It is tempting to suggest that this case is one of the new variants of pseudohypoparathyroidism-Ib, recently reported.