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ACTA ENDOCRINOLOGICA (BUC)
The International Journal of Romanian Society of Endocrinology / Registered in 1938in Web of Science Master Journal List
Acta Endocrinologica(Bucharest) is live in PubMed Central
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General Endocrinology
Kalhori Z, Azadbakht M
Hydrostatic Pressure Improves Maturation of Oocyte in Cultures of Follicles Derived from Mouse Polycystic OvaryActa Endo (Buc) 2015 11(1): 26-31 doi: 10.4183/aeb.2015.26
AbstractPolycystic ovary is a common cause of infertility due to anovulation. Objective. The aim of this study was to improve maturation of oocyte in cultures of follicles derived from mouse polycystic ovary by hydrostatic pressure. Subjects and Methods. Female NMRI mice 12-14 days old were injected daily with testosterone enanthate 1 mg/100g body weight dissolved in sesame oil (PCO group), for inducing polycystic ovary (PCO) while non-PCO group were injected only with vehicle for 2 and 4 weeks. The ovaries were fixed and then were used for histological studies. The isolated preantral follicles were cultured for 12 days. Follicles with good quality have been induced using human chorionic gonadotropin (HCG) for in vitro maturation. Then follicles from each group either were transferred to pressure chamber and subjected to 20 mmHg pressure for 30 min or no treated by hydrostatic pressure. Follicles from two groups were cultured for 24 and 48 h and the in vitro maturation of oocytes was assessed. Results. Testosterone enanthate treatment causes the histological changes in mouse ovary and significantly increased the percentage of cystic follicles and decreased the percentage of preantral and antral follicles in PCO group, in comparison to non-PCO group after four-week treatment) (P<0.05). (The in vitro maturation rate in hydrostatic pressure treated follicles was higher than in those not treated by hydrostatic pressure (P < 0.05). Conclusions. This study demonstrated that hydrostatic pressure can improve maturation of oocyte in cultures of follicles derived from mouse polycystic ovary. -
General Endocrinology
Beyca HH, Mesci B, Telci O Caklili, Mutlu HH, Oguz A
Neuropathy Associated with Hypertriglyceridemia in Patients with Metabolic SyndromeActa Endo (Buc) 2016 12(1): 26-29 doi: 10.4183/aeb.2016.26
AbstractContext. With more studies investigating effects of high serum lipid levels, new findings are emerging regarding the damage these biomolecules may cause. Aim. In this study we aimed to find a relation between neuropathy and hypertriglyceridemia in patients with metabolic syndrome (MS). Material and methods. One hundred and twenty subjects (Ninety subjects with metabolic syndrome and 30 healthy controls) were included in the study. Subjects with MS were divided into three groups. HbA1C levels of the subjects were < 5.7% in group A, ≥ 5.7% - < 6.5% in group B, and ≥ 6.5% - < 8.0% in group C. Pin-Prick test and Semmes- Weinstein Monofilament were used for neurological examination. Electromyography was performed to patients with neuropathy to support the diagnosis. Results. Neuropathy prevalence was found to be higher in the subjects with metabolic syndrome compared to control group. (9.9 %; 16.65 %; 23.31 % vs. 3.3%; in group A, group B, group C vs. healthy control group respectively) (p=0.003 for group A, p=0.0002 for group B, p=0.0002 for group C). There was an association between triglyceride levels and neuropathy in group C. Conclusion. Patients with MS may have more neuropathy risk than we estimate. -
General Endocrinology
Gurban C, Zosin I, Sfrijan F, Cojocaru M, Vermesan H, Vermesan D, Savescu I, Radulov I, Drugarin D, Erdelean V
The OPG/sRANKL system and the low bone mineral density in postmenopausal osteoporosisActa Endo (Buc) 2009 5(1): 27-40 doi: 10.4183/aeb.2009.27
AbstractBackground. sRANKL (soluble receptor activator of nuclear factor-kB ligand) and OPG (osteoprotegerin) represent a novel cytokine system with pleiotropic effects on bone remodeling.\r\nAim. The aim of this study was to assess the implications of serum levels of sRANKL, OPG and E2 (estradiol) in the process of bone remodeling of postmenopausal women with osteoporosis.\r\nMethods. The study was performed on 74 patients with postmenopausal osteoporosis, divided into two groups of patients according to the duration of estrogenic deprivation, compared with a control group (n= 20 postmenopausal women without osteoporosis). The serum levels of the enunciated markers were measured by ELISA technique.\r\nResults. In the group I (n= 48, bellow 15 yrs of estrogenic deprivation) the serum levels of sRANKL were 67.63?3.55 pg/mL (p<0.002), those of OPG were 42.15?0.55 pg/mL (p<0.002) and the levels of E2 were 28.32?1.78 pg/mL (p<0.004). In the group II (n= 26, over 15 yrs of estrogenic deprivation) the serum levels of sRANKL were 49.26?2.85 pg/mL (p<0.003), those of OPG 27.78?1.04 pg/mL (p<0.003) and the serum levels of E2 were 19.66?1.23 pg/mL (p<0.002). In the control group (n=20), the serum levels of sRANKL were 32.48?3.03 pg/mL, those of OPG 38.05?4.89 pg/mL and the serum levels of E2 were 43.07?4.04 pg/mL.\r\nConclusions. The serum levels of sRANKL are significantly higher in postmenopausal women with osteoporosis versus postmenopausal women without osteoporosis, attesting osteoclasts activation. The serum levels of OPG in postmenopausal women with osteoporosis were increased in group I, suggesting the osteoblastic activation and decreased in group II, probably secondary to the stimulation of osteoblastic apoptosis. -
General Endocrinology
Gurban C, Zosin I, Gotia S, Sfrijan F, Gotia L, Radulov I, Savescu I, Drugarin D
Correlations between the markers of bone remodeling and bone mineral density in postmenopausal osteoporosisActa Endo (Buc) 2010 6(1): 27-34 doi: 10.4183/aeb.2010.27
AbstractAim. To assess the levels of s BGP and BAP and correlate them with the rate of bone remodelling.\r\nPatients and Methods. The study was performed on 74 cases with postmenopausal osteoporosis, divided into two groups, according to the duration of estrogenic deprivation, compared with a control group (n= 20, postmenopausal women without osteoporosis). The serum levels of the discussed markers were measured by ELISA technique. BMD was measured using the DXA technique with the assessment of T score.\r\nResults. In the group I: BGP were 20.12?0.87ng/mL (p<0.03), those of BAP 13.76?0.6μg/mL (p<0.001) and sT spine were -3.63?0.65DS (p<0.001). In the group II: BGP were 15.12?1.55ng/mL (p<0.05), those of BAP 11.88?0.38μg/mL (p<0.001) and sT spine were -3.78?0.36DS (p<0.001). The control group presented: BGP of 16.22?1.62ng/mL, those of BAP of 8.68?0.44μg/mL and sT spine of -1.78?0.11DS. The serum levels of BGP in postmenopausal osteoporosis cases were increased in group I (suggesting an osteoblastic activation) and decreased in group II (probably secondary to the stimulation of osteoblastic apoptosis). The serum levels of BAP are significantly increased\r\nin postmenopausal osteoporosis versus control group, attesting osteoblastic activation.\r\nConclusion. Bone resorption begins gradually to outrun a new bone formation rhythm associated with low BMD. -
Endocrine Care
Saftencu M, Barbus E, Pestean C, Piciu A, Piciu D
Evaluation of Cardiovascular Risk and Myocardial Perfusion in Patients with Radically Treated Differentiated Thyroid Carcinoma and Repeated Episodes of Iatrogenic HypothyroidismActa Endo (Buc) 2016 12(1): 30-34 doi: 10.4183/aeb.2016.30
AbstractContext. Patients with radically treated differentiated thyroid carcinoma (DTC) undergo multiple episodes of iatrogenously-acquired hypothyroidism for the oncological follow-up. In some patients, this elevates high-sensitive C-reactive protein (hsCRP), a cardiovascular risk biomarker. Objective. We wanted to determine if there is any correlation between repeated hypothyroidism episodes, elevated hsCRP and an increased cardiovascular risk as stated through myocardial perfusion. Design. Between July 2014-January 2015, we analyzed serological levels of hsCRP for identifying our patients’ cardiovascular risk; we performed a myocardial perfusion scintigraphy to observe the alterations. Subjects and Methods. We included 27 patients (n=27), mean age of 52±10: CI (95%),14 female, all diseasefree after thyroidectomy, radioiodine ablation and chronic thyroid hormone treatment. We assigned the cardiovascular risk category for each patient according to hsCRP levels; all patients underwent a myocardial perfusion scintigraphy in order to determine the cardiac perfusion index (CPI). Results. hsCRP has been higher in > 65 years old male patients with more than 5 thyroid hormone withholdings. hsCRP is significantly associated with CPI (p=0.001). Spearman’s rank correlation indicates a strongly positive linear correlation between these two parameters (r=0.745). Conclusions. Repeated thyroid hormonal withdrawals in patients with DTC during the long-term follow-up elevated hsCRP at cardiovascular risk levels, having an impact on myocardial perfusion. -
General Endocrinology
Keshavarzi Z, Mohebbati R, Mohammadzadeh N, Alikhani V
The Protective Role of Estradiol and Progesterone in Male Rats, Following Gastric Ischemia-ReperfusionActa Endo (Buc) 2018 14(1): 30-35 doi: 10.4183/aeb.2018.30
AbstractBackground and Aim. Ischemia-reperfusion (I/R) injury frequently occurs in different situations. Female sex hormones have a protective function. The purpose of this study was to determine the function of female sexual hormones on the gastric damage induced by I/R in male rats. Methods. Forty (40) Wistar rats were randomized into five groups: intact, ischemia- reperfusion (IR), IR + estradiol (1mg/kg), IR + progesterone (16 mg / kg) and IR + combination of estradiol (1mg / kg) and progesterone (16 mg/ kg). Before the onset of ischemia and before reperfusion all treatments were done by intraperitoneal (IP) injection. After animal anesthesia and laparotomy, celiac artery was occluded for 30 minutes and then circulation was established for 24 hours. Results expressed as mean ± SEM and P <0.05 were considered statistically significant. Results. The Glutathione (GSH) concentration significantly decreased after induction of gastric IR (P<0.001). Estradiol (P<0.001) and combined estradiol and progesterone (P<0.001) significantly increased GSH levels. The myeloperoxidase (MPO) concentration significantly increased after induction of gastric IR (P<0.001). Different treatments significantly reduced MPO levels (P<0.001). The gastric acid concentration significantly increased after induction of gastric IR (P<0.001). Treatment with estradiol, progesterone (P<0.05) and combined estradiol and progesterone (P<0.01) significantly reduced gastric acid levels. Superoxide dismutase (SOD) concentration decreased after induction of gastric IR. The SOD levels were not significant. Conclusion. These data suggested that female sexual steroids have a therapeutic effect on gastrointestinal ischemic disorders by reduction of MPO and gastric acid, and increasing gastric GSH & SOD levels following gastric IR. -
General Endocrinology
Baraka A, Korayem H. , Baraka M
Metformin as a Potential Therapeutic Agent for Osteoporosis in Ovariectomized RatsActa Endo (Buc) 2014 10(1): 31-40 doi: 10.4183/aeb.2014.31
AbstractIntroduction. There is increasing evidence that 5’ adenosine monophosphateactivated protein kinase (AMPK) signaling pathway plays a role in bone physiology. The aim of the present study was to investigate the effect of a drug activating AMPK, namely metformin, on ovariectomy-induced osteoporosis in the rat. Methods. The present study was conducted on 40 female Wistar albino rats that were divided into 4 groups of 10 rats each, Group I: sham operated, Group II: non-treated ovarictomized (OVX) rats, while groups III and IV were OVX rats treated with metformin and metformin plus a substance that inhibits AMPK, namely compound C, respectively. At the end of the experimental period, urine and blood samples were collected and used for determination of urinary deoxypyridinoline (DPD) serum: osteocalcin, calcium and phosphorus concentrations and serum alkaline phosphatase activity. Biochemical assessment of AMPK activity in isolated fourth lumbar vertebrae (LV4) was carried out. The tibia, left femur and third lumbar vertebrae (LV3) were weighed and biomechanical study on LV3 was carried out. Immune histochemical studies of right femur and the forth-lumbar vertebrae (LV4) were carried out using anti-Fas antibodies to detect apoptotic osteoclastic and osteoblastic cells. Evaluation of cortical bone morphometric indices was done by CT-Scanning technique. Results. The results of the present study demonstrated that metfromin protected against biochemical, histological, biomechanical and histomorphometric osteoporotic changes. Compound C, an inhibitor of AMPK, blocked metformininduced changes in assessed parameters suggesting that the effect of metformin was mediated mainly through activation of AMPK. Conclusions. Drugs modulating AMPK could be effective in ameliorating OVX-induced osteoporotic changes. -
General Endocrinology
Galoiu SA, Kertesz G, Somma C, Coculescu M, Brue T
Clinical expression of big-big prolactin and influence of macroprolactinemia upon immunodiagnostic testsActa Endo (Buc) 2005 1(1): 31-41 doi: 10.4183/aeb.2005.31
Abstract ReferencesIn some humans, the big and big-big prolactin variants represent the majority of circulating prolactin, considered to be without biological activity. Aims: to establish the clinical expression of macroprolactinemia and the interference with immunodiagnostic tests\r\nin a randomized group of 84 consecutive patients with hyperprolactinemia. IRMA and electrochemiluminescence (Elecsys) were used for PRL assay; gel filtration chromatography (GFC) and protein A precipitation test were used to reveal macroprolactinemia. Results: Macroprolactinemia was found in 16 out of 84 patients (group A), 62 patients had hyperprolactinemia of other causes (group B) and 6 had normal PRL levels and normal GFC (group C). Of 16 patients with macroprolactinemia, 6 showed normal PRL with IRMA and hyperprolactinemia with Elecsys. The difference between the two methods used (∆ = PRL determined by Elecsys, -PRL determined by IRMA) correlated with big big PRL level determined by GFC with Elecsys in all patients. The strongest correlation was found in patients with macroprolactinemia (group A, r=0.82, p<0.01) as compared with group B, without macroprolactinemia (r=0.39, p<0.01). Menstrual disorders were expressed, but less frequent in group A versus B (3/15 vs. 28/56, p=0.04), and the appearance of galactorrhea and infertility were not statistically different. Conclusions: In these patients, macroprolactinemia had clinical expression, but weaker than in true hyperprolactinemic patients. It determines high apparent variability of serum PRL level in current commercial assays.1. Ben Jonathan N, Liby K, McFarland M, Zinger M. Prolactin as an autocrine/paracrine growth factor in human cancer. Trends Endocrinol Metab 2002; 13(6):245-250. [CrossRef]2. Jackson RD, Wortsman J, Malarkey WB. Characterization of a large molecular weight prolactin in women with idiopathic hyperprolactinemia and normal menses. J Clin Endocrinol Metab 1985; 61(2):258-264. [CrossRef]3. Kline JB, Clevenger CV. Identification and characterization of the prolactin-binding protein in human serum and milk. J Biol Chem 2001; 276(27):24760-24766. [CrossRef]4. Piketty M-L, Lancelin F, Poirier-Begue E, Coussieu C. Le dosage de la prolactine et ses pieges. Reproduction Humaine et Hormones 2002; XV(1-2):7-16.5. Hattori N, Ishihara T, Ikekubo K, Moridera K, Hino M, Kurahachi H. Autoantibody to human prolactin in patients with idiopathic hyperprolactinemia. J Clin Endocrinol Metab 1992; 75(5):1226- 1229. [CrossRef]6. Bonhoff A, Vuille JC, Gomez F, Gellersen B. Identification of macroprolactin in a patient with asymptomatic hyperprolactinemia as a stable PRL-IgG complex. Exp Clin Endocrinol Diabetes 1995; 103(4):252-255. [CrossRef]7. Cacavo B, Leite V, Santos MA, Arranhado E, Sobrinho LG. Some forms of big big prolactin behave as a complex of monomeric prolactin with an immunoglobulin G in patients with macroprolactinemia or prolactinoma. J Clin Endocrinol Metab 1995; 80(8):2342-234 [CrossRef]8. De Schepper J, Schiettecatte J, Velkeniers B, Blumenfeld Z, Shteinberg M, Devroey P et al. Clinical and biological characterization of macroprolactinemia with and without prolactin-IgG complexes. Eur J Endocrinol 2003; 149(3):201-207. [CrossRef]9. Hattori N. The frequency of macroprolactinemia in pregnant women and the heterogeneity of its etiologies. J Clin Endocrinol Metab 1996; 81(2):586-590. [CrossRef]10. Cavaco B, Prazeres S, Santos MA, Sobrinho LG, Leite V. Hyperprolactinemia due to big big prolactin is differently detected by commercially available immunoassays. J Endocrinol Invest 1999; 22(3):203-208.11. Ahlquist JA, Fahie-Wilson MN, Cameron J. Variable detection of macroprolactin: a cause of apparent change in serum prolactin levels. Clin Endocrinol (Oxf) 1998; 48(1):123-124. [CrossRef]12. Ahlquist JA, Fahie-Wilson MN, Cameron J. Variable detection of macroprolactin: a cause of apparent change in serum prolactin levels. Clin Endocrinol (Oxf) 1998; 48(1):123-124. [CrossRef]13. Vallette-Kasic S, Morange-Ramos I, Selim A, Gunz G, Morange S, Enjalbert A et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab 2002; 87(2):581-588. [CrossRef]14. Fahie-Wilson MN, Soule SG. Macroprolactinaemia: contribution to hyperprolactinaemia in a district general hospital and evaluation of a screening test based on precipitation with polyethylene glycol. Ann Clin Biochem 1997; 34 ( Pt 3):252-258.15. Garcia ML, Diez HA, Ciriza de los RC, Delgado GM, Orejas GA, Fernandez Erales AL et al. Macroprolactin as etiology of hyperprolactinemia. Method for detection and clinical characterization of the entity in 39 patients. Rev Clin Esp 2003; 203(10):459-46416. Hauache OM, Rocha AJ, Maia AC, Maciel RM, Vieira JG. Screening for macroprolactinaemia and pituitary imaging studies. Clin Endocrinol (Oxf) 2002; 57(3):327-331. [CrossRef]17. Leanos A, Pascoe D, Fraga A, Blanco-Favela F. Anti-prolactin autoantibodies in systemic lupus erythematosus patients with associated hyperprolactinemia. Lupus 1998; 7(6):398-403. [CrossRef]18. Pacilio M, Migliaresi S, Meli R, Ambrosone L, Bigliardo B, Di Carlo R. Elevated bioactive prolactin levels in systemic lupus erythematosus?association with disease activity. J Rheumatol 2001; 28(10):2216-2221.19. Rogol AD, Eastman RC, Manolio T, Rosen SW. Unusual heterogeneity of circulating prolactin in an acromegalic. J Endocrinol Invest 1981; 4(2):221-2220. Andersen AN, Pedersen H, Larsen JF, Djursing H. Preserved prolactin fluctuations and response to metoclopramide in ovulatory, infertile, hyperprolactinemic women. Acta Obstet Gynecol Scand 1984; 63(2):141-144. [CrossRef]21. Andino NA, Bidot C, Valdes M, Machado AJ. Chromatographic pattern of circulating prolactin in ovulatory hyperprolactinemia. Fertil Steril 1985; 44(5):600-605.22. Colon JM, Ginsburg F, Schmidt CL, Weiss G. Hyperprolactinemia in clinically asymptomatic, fertile men: report of two cases. Obstet Gynecol 1989; 74(3 Pt 2):510-513.23. Guay AT, Sabharwal P, Varma S, Malarkey WB. Delayed diagnosis of psychological erectile dysfunction because of the presence of macroprolactinemia. J Clin Endocrinol Metab 1996; 81(7):2512-2514. [CrossRef]24. Guitelman M, Colombani-Vidal ME, Zylbersztein CC, Fiszlejder L, Zeller M, Levalle O et al. Hyperprolactinemia in asymptomatic patients is related to high molecular weight posttranslational variants or glycosylated forms. Pituitary 2002; 5(4):255-260. [CrossRef]25. Vallette-Kasic S, Morange-Ramos I, Selim A, Gunz G, Morange S, Enjalbert A et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab 2002; 87(2):581-588. [CrossRef]26. Suliman AM, Smith TP, Gibney J, McKenna TJ. Frequent misdiagnosis and mismanagement of hyperprolactinemic patients before the introduction of macroprolactin screening: application of a new strict laboratory definition of macroprolactinemia. Clin Chem 20 [CrossRef]27. Olukoga AO, Kane JW. Macroprolactinaemia: validation and application of the polyethylene glycol precipitation test and clinical characterization of the condition. Clin Endocrinol (Oxf) 1999; 51(1):119-126. [CrossRef]28. Cavaco B, Leite V, Santos MA, Arranhado E, Sobrinho LG. Some forms of big big prolactin behave as a complex of monomeric prolactin with an immunoglobulin G in patients with macroprolactinemia or prolactinoma. J Clin Endocrinol Metab 1995; 80(8):2342-234 [CrossRef]29. Strachan MW, Teoh WL, Don-Wauchope AC, Seth J, Stoddart M, Beckett GJ. Clinical and radiological features of patients with macroprolactinaemia. Clin Endocrinol (Oxf) 2003; 59(3):339- 346. [CrossRef]30. Vallette-Kasic S, Morange-Ramos I, Selim A, Gunz G, Morange S, Enjalbert A et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab 2002; 87(2):581-588. [CrossRef]31. Pacilio M, Migliaresi S, Meli R, Ambrosone L, Bigliardo B, Di Carlo R. Elevated bioactive prolactin levels in systemic lupus erythematosus?association with disease activity. J Rheumatol 2001; 28(10):2216-2221.32. Jackson RD, Wortsman J, Malarkey WB. Characterization of a large molecular weight prolactin in women with idiopathic hyperprolactinemia and normal menses. J Clin Endocrinol Metab 1985; 61(2):258-264. [CrossRef]33. Andino NA, Bidot C, Valdes M, Machado AJ. Chromatographic pattern of circulating prolactin in ovulatory hyperprolactinemia. Fertil Steril 1985; 44(5):600-605.34. Fraser IS, Lun ZG, Zhou JP, Herington AC, McCarron G, Caterson I et al. Detailed assessment of big big prolactin in women with hyperprolactinemia and normal ovarian function. J Clin Endocrinol Metab 1989; 69(3):585-592. [CrossRef]35. Hattori N, Ikekubo K, Ishihara T, Moridera K, Hino M, Kurahachi H. A normal ovulatory woman with hyperprolactinemia: presence of anti-prolactin autoantibody and the regulation of prolactin secretion. Acta Endocrinol (Copenh) 1992; 126(6):497-500.36. Andino NA, Bidot C, Valdes M, Machado AJ. Chromatographic pattern of circulating prolactin in ovulatory hyperprolactinemia. Fertil Steril 1985; 44(5):600-605.37. Whittaker PG, Wilcox T, Lind T. Maintained fertility in a patient with hyperprolactinemia due to big, big prolactin. J Clin Endocrinol Metab 1981; 53(4):863-866. [CrossRef]38. Jackson RD, Wortsman J, Malarkey WB. Characterization of a large molecular weight prolactin in women with idiopathic hyperprolactinemia and normal menses. J Clin Endocrinol Metab 1985; 61(2):258-264. [CrossRef]39. Colon JM, Ginsburg F, Schmidt CL, Weiss G. Hyperprolactinemia in clinically asymptomatic, fertile men: report of two cases. Obstet Gynecol 1989; 74(3 Pt 2):510-513.40. Hattori N, Ikekubo K, Ishihara T, Moridera K, Hino M, Kurahachi H. A normal ovulatory woman with hyperprolactinemia: presence of anti-prolactin autoantibody and the regulation of prolactin secretion. Acta Endocrinol (Copenh) 1992; 126(6):497-500.41. Leite V, Cosby H, Sobrinho LG, Fresnoza MA, Santos MA, Friesen HG. Characterization of big, big prolactin in patients with hyperprolactinaemia. Clin Endocrinol (Oxf) 1992; 37(4):365-372. [CrossRef]42. Leslie H, Courtney CH, Bell PM, Hadden DR, McCance DR, Ellis PK et al. Laboratory and clinical experience in 55 patients with macroprolactinemia identified by a simple polyethylene glycol precipitation method. J Clin Endocrinol Metab 2001; 86(6):2743-27 [CrossRef]43. Vallette-Kasic S, Morange-Ramos I, Selim A, Gunz G, Morange S, Enjalbert A et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab 2002; 87(2):581-588. [CrossRef]44. Suliman AM, Smith TP, Gibney J, McKenna TJ. Frequent misdiagnosis and mismanagement of hyperprolactinemic patients before the introduction of macroprolactin screening: application of a new strict laboratory definition of macroprolactinemia. Clin Chem 20 [CrossRef]45. De Schepper J, Schiettecatte J, Velkeniers B, Blumenfeld Z, Shteinberg M, Devroey P et al. Clinical and biological characterization of macroprolactinemia with and without prolactin-IgG complexes. Eur J Endocrinol 2003; 149(3):201-207. [CrossRef]46. Leite V, Cosby H, Sobrinho LG, Fresnoza MA, Santos MA, Friesen HG. Characterization of big, big prolactin in patients with hyperprolactinaemia. Clin Endocrinol (Oxf) 1992; 37(4):365-372. [CrossRef]47. Leite V, Cosby H, Sobrinho LG, Fresnoza MA, Santos MA, Friesen HG. Characterization of big, big prolactin in patients with hyperprolactinaemia. Clin Endocrinol (Oxf) 1992; 37(4):365-372. [CrossRef]48. Hattori N, Inagaki C. Anti-prolactin (PRL) autoantibodies cause asymptomatic hyperprolactinemia: bioassay and clearance studies of PRL-immunoglobulin G complex. J Clin Endocrinol Metab 1997; 82(9):3107-3110. [CrossRef]49. Hattori N, Inagaki C. Anti-prolactin (PRL) autoantibodies cause asymptomatic hyperprolactinemia: bioassay and clearance studies of PRL-immunoglobulin G complex. J Clin Endocrinol Metab 1997; 82(9):3107-3110. [CrossRef]50. Jackson RD, Wortsman J, Malarkey WB. Macroprolactinemia presenting like a pituitary tumor. Am J Med 1985; 78(2):346-350. [CrossRef]51. Mounier C, Trouillas J, Claustrat B, Duthel R, Estour B. Macroprolactinaemia associated with prolactin adenoma. Hum Reprod 2003; 18(4):853-857. [CrossRef]52. John R, McDowell IF, Scanlon MF, Ellis AR. Macroprolactin reactivities in prolactin assays: an issue for clinical laboratories and equipment manufacturers. Clin Chem 2000; 46(6 Pt 1):884-885.53. Gilson G, Schmit P, Thix J, Hoffman JP, Humbel RL. Prolactin results for samples containing macroprolactin are method and sample dependent. Clin Chem 2001; 47(2):331-333.54. Gilson G, Schmit P, Thix J, Hoffman JP, Humbel RL. Prolactin results for samples containing macroprolactin are method and sample dependent. Clin Chem 2001; 47(2):331-333. -
General Endocrinology
Can B, Ozturk S, Gungor K, Sargin M
C-Peptide as an Inflammatory Marker in Obese WomenActa Endo (Buc) 2023 19(1): 31-35 doi: 10.4183/aeb.2023.31
AbstractBackground. Insulin resistance (IR) is a component of type 2 diabetes and metabolic syndrome and it increases in the presence of chronic inflammation. Lately, “neutrophilto- lymphocyte ratio” (NLR) has been used as an indicator of inflammation. This study evaluates the association between IR and NLR in obese women. Material and methods. Obese female patients who were followed up in a university hospital for the last two years were included in the study. Homeostasis model assessment of IR (HOMA-IR), C-peptide, NLR, bioelectrical impedance measurements of 83 patients were analyzed. Results. The C-peptide levels of our patients showed a highly significant correlation with HOMA-IR (p<0.001). A significant positive correlation was found between fasting plasma C-peptide levels and NLR (r=0.36 and p<0.003) in obese women. The increase in C-peptide levels had a significant effect on the increase in NLR (r2=0.31, p=0.002), however insulin had no similar effect on NLR (r2=0.01, p=0.544). Conclusion. Plasma C-peptide levels are better correlated with NLR compared to other parameters of IR. C-peptide may be used as an efficient laboratory marker with high relevance in IR and chronic inflammatory conditions in obese women. -
General Endocrinology
Ademoglu E, Berberoglu Z, Dellal FD, Keskin Ariel M, Kose A, Candan Z, Bekdemir H, Erdamar H, Culha C, Aral Y
Higher Levels of Circulating Chemerin in Obese Women with Gestational Diabetes MellitusActa Endo (Buc) 2015 11(1): 32-38 doi: 10.4183/aeb.2015.32
AbstractObjective. To characterize serum chemerin levels in obese patients with gestational diabetes mellitus (GDM). Design. Case–control study. Subjects and Methods. Forty seven obese women with newly diagnosed GDM at 24-28 weeks of pregnancy and 32 age, body mass index- and gestational age-matched, normal pregnant women were included. Metabolic patterns and serum chemerin concentrations were measured. Results. Serum chemerin levels were significantly higher in subjects with GDM as compared to healthy pregnant controls (p < 0.05). Fasting insulin was similar between the two groups. HOMA-IR tended to be higher in GDM group but did not reach statistical significance. Women with GDM had significantly higher triglyceride (p < 0.01) and lower highdensity lipoprotein cholesterol (p < 0.001) than controls. In multiple linear regression analyses, chemerin was significantly associated with BMI (beta-coefficient = 0.274, p = 0.01), HbA1c (beta-coefficient = 0.327, p < 0.01), HDL-cholesterol (beta-coefficient = -0.307, p < 0.01), triglyceride (betacoefficient = 0.236, p < 0.05), insulin levels (beta-coefficient = 0.236, p < 0.05) and HOMA index (beta-coefficient = 0.283, p = 0.01). Conclusions. Maternal chemerin levels were significantly increased in GDM at 24-28 weeks of pregnancy. The physiological significance of elevated serum chemerin in GDM remains unclear.