There is an increased incidence of autoimmune thyroid disease (AITD) in women with infertility. We hypothesized that serum anti-Müllerian hormone (AMH) levels will be lower in premenopausal women with AITD than controls. We evaluated ovarian reserve in women with AITD (n = 85) and healthy controls (n = 80), all <40 years old. Detailed data on reproductive history were obtained. Gonadotrophins, steroids, AMH, and inhibin B levels were measured during the follicular phase. The number of pregnancies as well as live births was lower in women with AITD (p < 0.01). No difference was observed in terms of FSH, estradiol, and inhibin B. AMH levels were lower in AITD women than in controls (1.16 + 0.17 versus 1.28 + 0.25 ng/ml, mean + SD, p = 0.001). According to the multiple regression analysis, even after age adjustment, AITD was significantly and independently affected AMH levels (t = 2.674, p = 0.008). Women with AITD seem to have a diminished ovarian follicular reserve and measurement of serum AMH level has the potential to be used to predict this comorbidity.
In conclusion, we found some important differences in the hemostatic parameters between the patients with PHPT and healthy controls. Increased platelet count, F VII and FX activities and D-Dimer levels in patients with PHPT represent a potential hypercoagulable state, which might augment the risk for atherosclerotic and atherothrombotic complications. This condition may contribute to the excess mortality rate due to CVD in patients with PHPT.
Hepatocellular carcinoma (HCC) is one of the more common malignant diseases in the world. Here we have investigated role of hepatic venous outflow obstruction in the development of HCC. During a 10-year period from November 1986 to December 1996, 1,748 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction, or inferior vena cava obstruction without Behçet's disease (BD) and 512 patients with Behçet's disease were examined at Hacettepe University Hospital. The presence of and the effect of hepatic venous obstruction on the subsequent development of HCC was assessed. In each case, hepatic vein thrombosis was assessed by hepatic venography and by digital subtraction angiography (DSA), computed tomography (CT), ultrasonography (US), and liver biopsy. Coagulation factors, including protein C, protein S, anti-thrombin III, and routine laboratory studies assessing the coagulability of blood were also investigated. The role of hepatic venous outflow obstruction on the subsequent development of HCC was determined by periodic laboratory investigations that included alpha-fetoprotein (AFP), ultrasonography, and when indicated liver biopsy. During the same time period all patients diagnosed as having HCC were investigated to identify all potential etiologic factors responsible for the HCC. Fifty-five (10.7%) of the 512 patients with BD were found to have one or more large vein thromboses. Sixteen of these 55 (29%) patients had hepatic vein thrombosis. During the follow-up period HCC developed in 2 of these 16 patients (12.5%), 34 and 21 months after a diagnosis of hepatic vein thrombosis was established. Forty patients from a total of 1,748 patients with clinical evidence of portal hypertension and cirrhosis, but without BD, were found to have evidence of hepatic vein thrombosis. Twenty-one of these 40 patients had an identifiable underlying disorder responsible for their hepatic vein thrombosis. Despite a full clinical and laboratory investigation in the other 19 patients, the etiologic factor responsible for the hepatic vein thrombosis remained obscure. Only one of these 19 patients, who also had portal vein thrombosis, developed HCC during a 9-year follow-up. Thus, a total of three of the 56 (5.36%) of cases of hepatic vein thrombosis developed an HCC. All of the hepatic tumors were of the multicentric, nodular, rapidly growing type. Despite the presence of hepatic vein thrombosis, there was no clear-cut histologic evidence for cirrhosis. Our experience suggests that hepatic vein thrombosis may be a contributing factor responsible for HCC development. Moreover, we advise that individuals with hepatic vein thrombosis should be assessed periodically for the development of HCC.
Polycythemia vera (PV) is a clonal myeloproliferative disorder characterized by predominantly excessive erythrocyte production. During the course of the disease, bleeding or thrombosis may be observed. In PV patients, the influence of antifibrinolytic activities on development of thrombohemorrhagic complications remains to be elucidated. In the present study, alterations in antifibrinolytic activity of PV patients and the effects of treatments on these alterations were investigated. Newly diagnosed and therapy-naive 22 PV patients were included. Thrombomodulin (TM), plasmin-alpha 2-antiplasmin complex (PAP), plasminogen activator inhibitor-1 (PAI-1) and thrombin activable fibrinolysis inhibitor antigen (TAFIa) levels were measured in all individuals and after phlebotomy and 5-hydroxyurea (5-HU) therapy in PV patients. TM, PAP, PAI-1 and TAFIa values of the patient group were higher than those of the controls. After phlebotomy, no changes were detected in TM, PAI-1 and TAFIa values, but PAP values decreased. On the contrary, 5-HU treatment resulted in a marked decrease in TM, PAI-1, PAP and TAFIa levels. These findings suggested that the changes in antifibrinolytic activity and endothelial dysfunction might be contributed to formation of intravascular thrombosis in PV patients, even though not clinically overt. 5-HU in addition to phlebotomy affects antifibrinolytic activity and may have an influence on diminishing predisposition of thrombosis.
Objective: To establish whether there is a relationship between hyperprolactinemia and primary thyroid disorders, focusing on patients with autoimmune features. Materials and methods: The medical records of 100 patients with hyperprolactinemia (HPRL) were retrospectively examined. Records of thyroid ultrasonography (USG), basal serum levels of thyroid stimulating hormone, circulating free thyroxine, free triiodothyronine, antithyroglobulin (anti-Tg), and antithyroperoxidase (anti-TPO) antibodies were analyzed. In 100 control subjects, matched by age and gender with HPRL patients, thyroid USG, thyroid function tests (TFTs), and autoantibody panel were obtained. Results:The median PRL in patients was 93 ng/mL (range: 37-470). Twenty-five patients (25%) and 22 controls (22%) had positive anti-Tg and/or anti-TPO titers (P = 0.739). The median serum PRL was 98 (37-470) ng/mL in patients with positive thyroid autoantibodies, and 92 (40-470) ng/mL in patients who were negative (P = 0.975). Among the individuals with autoantibody positivity TFTs abnormalities were more frequent in HPRL patients (60%, out of 25 patients, 14 with subclinical hypothyroidism and one with hyperthyroidism) than in controls (9.1%, out of 22 patients, 2 with subclinical hyperthyroidism) (P < 0.001). Twenty-seven patients with HPRL and 31 controls had goiter (27 vs. 31%, P = 0.437). Fortysix patients (46%) and 50 (50%) controls had one or more of the features of thyroid disorder, which were goiter, positive thyroid autoantibody, and thyroid function abnormality (P = 0.888). Conclusion:HPRL may be associated with more severe thyroid dysfunction in patients with thyroid autoimmunity.Arq Bras Endocrinol Metab. 2014;58(1):48-52 Keywords Hyperprolactinemia; thyroiditis; autoimmunity; goiter RESUMO Objetivo: Verificar se existe uma relação entre a hiperprolactinemia e distúrbios primários da tireoide, focando em pacientes com características autoimunes. Materiais e métodos: Os prontuários de 100 pacientes com hiperprolactinemia (HPRL) foram examinados retrospectivamente. Foram analisados registros de ultrassonografia da tireoide (USG), níveis séricos basais de hormônio tireoestimulante, tiroxina livre, triiodotironina livre e anticorpos antitireoglobulina (anti-Tg) e antitireoperoxidase (anti-TPO). Foram obtidos de 100 controles, pareados por idade e sexo com pacientes com HPRL, USG, testes de função da tireoide (TFTs) e painel de autoanticorpos. Resultados: A média de PRL em pacientes foi de 93 ng/mL (variação: 37-470). Vinte e cinco pacientes (25%) e 22 controles (22%) foram positivos para títulos de anti-Tg e/ou anti-TPO (P = 0,739). A mediana de PRL sérica foi de 98 (37-470) ng/mL em pacientes positivos para autoanticorpos tiroidianos e 92 (40-470) ng/mL em pacientes negativos (P = 0,975). Entre os indivíduos positivos para autoanticorpos, as anormalidades da TFTs foram mais frequentes em pacientes HPRL (60%; de 25 pacientes, 14 com hipotireoidismo subclínico e um com hipertireoidismo) do que nos controles (9,1%; de 22 pacientes, 2 com hip...
Objective: The purpose of the present study was to investigate the correlation between serum testosterone levels and bone mineral density (BMD) in postmenopausal women. Materials and methods: The study group was made up of postmenopausal women admitted to our tertiary center. Serum calcium, phosphorus, albumin, parathyroid hormone (PTH), thyrotropin (TSH), 25-OH vitamin D, and total testosterone concentrations were measured. Subjects were categorized into three groups regarding bone mineral density (BMD) values: normal (n = 22), osteopenia (n = 21), and osteoporosis (n = 21). Subjects were also categorized into three groups according to serum testosterone levels: low testosterone (n = 10), normal testosterone (n = 42), and high testosterone (n = 12). Results: No significant difference was found for serum testosterone, TSH, calcium, phosphorus, albumin, PTH, and 25-hydroxyvitamin D levels among patients with normal BMD, osteopenia, and osteoporosis (p > 0.05). Lumbar spine, total femur, femoral neck, trochanteric, intertrochanteric, and Ward's triangle BMD values were similar for the different testosterone levels (p > 0.05). Conclusion: There was no correlation between serum testosterone levels and patient age, body-mass index, or any measured BMD values. Given the findings in our study, which failed to demonstrate a statistically significant relationship between testosterone and BMD, adjustment of other risk factors for osteoporosis might have a more distinctive effect in this setting. Arch Endocrinol Metab. 2015;59(4):292-6
The objectives of this study were to assess the nutritional status, daily energy intake, and daily energy expenditure of coal miners in Turkey. A total of 135 healthy coal miners (aged 19-64 years) were evaluated. Heart rates were measured using Polar watches, and the total energy expenditure was calculated using physical activity level formula and Hiilloskorpi equation. The average body mass index of the participants was 25.7 ± 3.98 kg/m, and the average energy intake was 3,973.7 ± 420.85 kcal. According to Dietary Reference Intakes, the energy and nutrient intakes of the miners were adequate, except for the intake of vitamin D. The coal miners were found to be at moderate (43.0%), heavy (41.5%), and very heavy (13.3%) activity levels. Calculations of the energy expenditure at work were found to be 2,189.8 ± 376.19 to 2,788.8 ± 359.89 kcal per day. Further studies have to be conducted for developing national standards for each occupation.
Sheehan's syndrome (SS), which is an important cause of hypopituitarism, is common in developing countries. The most common presentation is the absence of lactation and amenorrhea. Hypothyroidism rather than hyperthyroidism is the usual expected phenomenon in SS. Postpartum hyperthyroidism is also common and Graves' disease (GD) is an important cause of postpartum hyperthyroidism. Here we report a case of a 22-year-old female patient in our clinic presented symptoms of amenorrhea, lack of lactation, palpitations and sweating. Her physical examination revealed goiter, moist skin and proptosis. Her laboratory evaluation showed suppressed thyroid stimulating hormone, elevated levels of free thyroxine and free triiodothyronine. Thyroid antibodies were positive. Tec 99m thyroid scintigraphy results were gland hyperplasia and increased uptake consistent with GD. She gave birth 7 months ago; after delivery she had a history of prolonged bleeding, amenorrhea and inability to lactate. She had hypogonadotropic hypogonadism, hyperprolactinemia and growth hormone deficiency. Serum cortisol and adrenocorticotropic hormone levels were normal. Her magnetic resonance imaging was empty sella. Our diagnosis was GD co-existing with SS. GD with concomitant hypopituitarism is rare but has been described previously, but there are no reports of GD occurring with SS. In this case study, we report a patient with GD associated with SS.
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