ACTA ENDOCRINOLOGICA (BUC)

Objectives. To determine whether levonorgestrel releasing intrauterine device (LNGIUD) in association with oestradiol subdermic implant is an efficient and safe therapy for neurovegetative disturbances in climacterium, for the patients who had previous metrorrhagia in preclimax.\r\nPatients and method. We performed a prospective study on 18 menopausal patients (group A) with a mean age of 50.2 ? 1.5 years with LNG-IUD, inserted in preclimacterium for dysfunctional uterine bleeding (biopsy showed us simple endometrial hyperplasia) and 20 menopausal women with neurovegetative symptoms that refused hormonal replacement therapy (HRT) as control group B. In group A, patients had amenorrhea after 6.8 ? 1.7 months from IUD insertion. Our criteria for selection were: presence of neurovegetative disturbances, FSH >25 UI/L, no contraindication for hormonal replacement therapy. Group A patients had a subdermic implant with estradiol 25 mg every six months. All patients were regularly followed: first visit after one month, the next visits every three months for three years. At each visit we observed neurovegetative symptoms, uterine bleeding, endometrial thickness assessed by transvaginal ultrasonography. The Kupperman test of menopausal distress index was calculated at each visit.\r\nResults. All patients reported the absence of neurovegetative symptoms after 4.5 ? 1.8 months of therapy. Fifteen of them (83.33%) had no vaginal bleeding during the study, three patients presented minor uterine bleeding during the first six months of follow-up. Transvaginal ultrasonography showed endometrial thickness < 5mm in all our subjects. Four patients presented breast discomfort for a short period.\r\nConclusion. LNG-IUD in association with estradiol subdermic implant proved to be an efficient therapy in climacterium. The capacity of LNG-IUD to determine endometrial atrophy contributes to local safety of this hormonal replacement therapy.

Context. Detection of parathyroid incidentalomas (PTIs) by ultrasonography (US) generally depends on clinical experience and it can be usually confused with perithyroidal lymph nodes. Objective. We aimed to evaluate the role of US for the detection of PTIs and define clinicopathologic features of PTIs detected during routine neck US. Design. In this retrospective study, we studied PTIs in a multidisciplinary clinical approach of nuclear medicine and general surgery clinics. Subjects and Methods. US indications and reports of 41275 were reviewed retrospectively. Of these patients, PTI was suspected in 66 (0.16%) patients. Those with a pathology-confirmed diagnosis after surgery formed Group PCD and those without a pathology-confirmed diagnosis and operation Group NPCD. These groups were compared statistically according to demographic data, laboratory tests, imaging results and postoperative findings. Results. The diagnosis of PTI was confirmed pathologically in 31 operated patients. Other pathologies rather than PTI on US were multinodular goiter, thyroiditis, thyroid nodule and perithyroidal lymph node. PTH and calcium levels were significantly higher in PCD Group;anti- TPO and anti-TG levels were significantly higher in NPCD Group. Conclusions. Lesions suspected of PTI on US should be followed-up with further evaluation by laboratory tests and imaging methods and a multidisciplinary working environment should be established.

A certain degree of insulin resistance in patients with Gaucher disease type 1 (GD) under enzyme replacement therapy (ERT) was reported. Data on insulin sensitivity in treatment naïve patients are inconsistent. Objective. To analyse prospectively changes in parameters of insulin resistance under ERT and to estimate when they occur. Design. prospective, controlled study; three years follow-up. Patients and methods. 12 treatment naïve patients with GD type 1 (M/W 8/4), 29.5±12.9 years, without overweight, diagnosed enzymatically and by genotyping, without previous diabetes mellitus. Patients were evaluated before and every 6 months up to 3 years under ERT and compared at baseline and after 3 years with matched healthy controls. Fasting-glucose (FG), - insulin (FI), C-peptide, HOMA-IR, IRI, HOMA-B, blood count, hepatic and splenic volume, chitotriosidase, severity score index di Rocco (SSI) were assessed. Results. Baseline glycemic parameters did not differ from controls. FG increased from baseline after two years of ERT (+16.4%,p<0.010), FI (+40.3%,p=0.030), HOMA-IR (+61.2%,p=0.007) and IRI (+9.1%,p=0.010) after 18 months, HOMA-B after 2.5 years (+51%, p=0.015. After 3 years of ERT patients were more insulin resistant compared to controls (p<0.001): FG (96.0±6.2 vs. 73.2±6.4 mg/dL), FI (11.2±2.4 vs. 5.6±1.3 μU/L), HOMA-IR (2.7±0.6 vs. 1.0+0.3), IRI (3.02±0.10 vs. 2.62±0.13). FG, FI, HOMAIR, IRI, HOMA-B correlated with disease severity markers. Conclusions. This is the first controlled study which evaluates prospectively insulin resistance in GD patients, finding significant differences compared to baseline starting with 18 months ERT.

Context. Idiopathic male infertility is evident in half of infertile males. Vitamin D receptors are expressed throughout male reproductive tract, including spermatozoa, promoting motility. Epidemiological studies revealed the positive association between serum vitamin D and semen quality. However, there are no clinical studies examining the differential role of vitamin D in idiopathic male infertility. Objectives. 1) To investigate the association between vitamin D deficiency and idiopathic male infertility, and 2) To determine whether vitamin D deficient males would show restoration of semen quality parameters upon supplementation with vitamin D. Design. This was a year-long case-control study from November 2015 to November 2016. A therapeutic intervention cohort for 2 months was also performed. Subjects and Methods. 117 Jordanian males were enrolled. Following a clinical evaluation by a urologist, baseline serum vitamin D and semen fluid analyses were collected. Participants were stratified into 3 groups: controls (n=30), idiopathic infertility (n=67), and secondary infertility (n=20). Idiopathic infertility patients with low vitamin D (n= 45) were supplemented with oral vitamin D, 5000 IU, once daily for two months. Thereafter, serum vitamin D and semen fluid analyses were reassessed (n= 34; 11 patients were lost to follow up). Results. Vitamin D was significantly lower in patients with idiopathic infertility than in both controls and men with secondary infertility. Significant improvement of progressive and total sperm motility was observed after vitamin D treatment. Vitamin D correlated significantly with semen quality in the study population. However, no correlation was found between vitamin D and any of the semen quality parameters in the idiopathic infertility group. Conclusions. Vitamin D supplementation improves sperm motility in idiopathic male infertility patients with low vitamin D. Larger and longer clinical trials are warranted to validate the use of vitamin D in these cases.

Context. Inhibin B could be a good marker in predicting spermatogenetic activities and in discriminating men with spermatogenesis impairment, especially azoospermia and it would be considered as a current clinical tool in the future. Objective. This study aimed to investigate the clinical value of serum Inhibin B and AMH levels in subfertile men particularly in those with non-obstructive azoospermia (NOA). We conducted a prospective study to assess the role of inhibin B in the evaluation of male factor infertility. Patients and Methods. Thirty fertile men and three groups of infertile patients (n=91): normozoospermia (n = 40), oligozoospermia (n = 19) and NOA (n = 32), from Faculty of Medicine (Sfax, Tunisia) were investigated. Serum levels were measured by ELISA and by ELFA (FSH). Results. Inhibin B and AMH levels were significantly lower in NOA patients than in normozoospermic ones (72.6±76.8 pg/mL vs. 242.4± 124.7 pg/mL; p<0.001 and 3.7±2.9 ng/mL vs. 5.3±2.3 ng/mL; p<0.001). Only Inhibin B levels were significantly lower in NOA than in oligozoospermic (72.6±76.8 pg/mL vs. 141.3± 81.9 pg/mL;p<0.001) and were negatively correlated with FSH concentrations (r = -0.56, p = 0.001). But both Inhibin B and AMH were positively correlated with sperm count (r = 0.44, p < 0.0001and r = 0.26, p = 0.03 respectively). Conclusions. We conclude that our results support the literature data showing that serum Inhibin B level is strongly correlated with sperm count and suggesting that it could be a good marker in discriminating men with spermatogenesis impairment, especially NOA.

Objective. We aimed to examine the auxological findings of girls diagnosed with idiopathic central precocious puberty (CPP) at the end of the GnRHa treatment and to investigate the effect of related factors on the height gain of those patients. Design. Single-center, descriptive, cross-sectional retrospective study. Method. A total of 43 patients who were diagnosed with idiopathic CPP and treated with GnRHa between 2012 - 2021 were included in to the study. Results. A decline in height standard deviation score (SDS) from 1.20 ± 0.14 to 1.02 ± 0.06 during the therapy was observed (P<0.001). The bone age/chronological age ratio was decreased and predictive adult height was increased at the end of the therapy (P<0.001; P=0.001). Both the rates of being overweight and obesity were increased (38.6% to 50% and 9% to 15.9%) when the treatment onset compared to the end of therapy. At the end of the treatment, the mean body mass index (BMI) SDS of the overweight patients was still higher compared to the normal-weight group (P<0.001). Conclusion. We observed a positive effect of GnRHa therapy on height potential. An increase in BMI during the therapy has been also demonstrated especially in subjects who were overweight before treatment.

Background. There is no immunohistochemical study to show luteinizing hormone receptor (LHR), estrogen receptor (ER) and progesterone receptor (PR) in the pregnant Fallopian tubes (FT). Objective. To study LHR, ER, PR expression in FT containing an ectopic pregnancy (EP) and during the menstrual phase. Design. Thirty FT were obtained from women diagnosed with EP and twenty FT collected by hysterectomy performed for benign diseases not affecting the tubes were included in this study. Assessment of immunohistochemical expression staining LHR, ER, PR in epithelium, smooth muscle cell and blood vessel endothelium in FT containing an EP and during the different phases of menstrual cycle. Results. In ectopic pregnancy group we found LHR expression in epithelium in 30 cases, muscle cell in 28 cases, and endothelium in 9 cases in FT. In menstrual cycle group we noted LHR expression in FT in epithelium in all cases, muscle cell in 4 cases. Conclusion. There is a significant difference in the proportions of the existence of LH receptor immunostaining in the muscle cells for ectopic pregnancy group as compared to the menstrual cycle groups (p < 0.001). Our findings may suggest that the women who have increased LH receptors on muscle cells in Fallopian tubes are at increased risk for having external pregnancy.

Secondary hyperparathyroidism, i.e. increased synthesis and secretion of parathyroid hormone and gland hyperplasia, is commonly found in chronic kidney disease. Although it is, at first, an adaptive response to the loss of renal functions in order to maintain the calcium/phosphate homeostasis and normal bone turnover, it is also an important cause of increased morbidity in this clinical setting by leading to renal osteodystrophy and cardiovascular complications. Recent advances in the knowledge on the pathogenesis of parathyroid-related complications in renal failure allowed for new therapeutic approaches. However, many problems remain to be solved in the future. This paper briefly presents the current understanding of pathogenic mechanisms of hyperparathyroidism, bone disease and vascular calcification during chronic kidney disease. In addition, it summarizes the main therapeutic methods available today for controlling secondary hyperparathyroidism and the challenges of practitioners concerning this issue. Finally, the current status of secondary hyperparathyroidism management is analyzed, with emphasis on the Romanian experience.

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.