Idiopathic hirsutism: Is it really idiopathic or is it misnomer?

Hirsutism, which is characterized by excessive growth of terminal hair in a male pattern, may result from various causes including polycystic ovary syndrome (PCOS), non-classic congenital adrenal hyperplasia, adrenal or ovarian tumors or it may be idiopathic. Idiopathic hirsutism is currently defined as hirsutism associated with normal ovulatory function, normal serum androgen levels and normal ovarian morphology, however, the pathogenesis of idiopathic hirsutism is not clear. The androgens are the main hormones to stimulate growth of body hair, therefore, there should be any form of increased androgen effect irrespective of normal serum androgen levels in any patient with hirsutism. In accordance to this scientific truth, we have previously shown that, although within normal limits, patients with idiopathic hirsutism have relatively higher serum androgen levels (relative hyperandrogenemia) in comparison to healthy subjects which let as to think that is idiopathic hirsutism really idiopathic? In addition to relative hyperandrogenemia, we have previously shown that, in comparison to healthy subjects, women with idiopathic hirsutism demonstrated higher expression of steroid sulphatase and 17-beta hydroxysteroid dehydrogenase mRNA both in the subumbilical region and arm skin, which contributes to local androgen metabolism. Those results support the idea that, in some patients, although the adrenals or ovaries do not secrete increased amount of androgens leading to hyperandrogenemia, pilocebaceous unit locally produce increased amount of androgens leading to hirsutism without ovulatory dysfunction. Upon the demonstration of relative hyperandrogenemia and possible increase in local androgen synthesis in patients with idiopathic hirsutism, we think that idiopathic hirsutism is not idiopathic and it may be named as “normoandrogenic hirsutism”. Furthermore, it may not be a different entity but may be an early stage of hyperandrogenic disorders such as PCOS. Clinically, this can be find out by following-up patients with idiopathic hirsutism prospectively

The evaluation of argyrophilic nucleolar organizing region proteins in fine-needle aspiration samples of thyroid.

Argyrophilic nucleolar organizing region associated proteins (AgNORs) have been shown to be of interest in a variety of different diseases including thyroid disorders. Our aim was to distinguish benign thyroid lesions from papillary thyroid carcinoma (PTC) via AgNOR count and with a new approach, via AgNOR surface area/total nuclear surface area (NORa/TNa) proportions in the nuclei on fine-needle aspiration (FNA) materials. Thirty patients (eight men and 22 women) whose FNA was compatible with benign lesion and 26 patients (eight men and 18 women) whose FNA was compatible with PTC were included in the study. Fine-needle aspiration materials were stained for AgNOR detection according to a specific protocol. One hundred nuclei per individual have been evaluated, and AgNOR number and NORa/TNa proportions of individual cells were measured and calculated by using a computer program. Patients with PTC had significantly (p The evaluation of argyrophilic nucleolar organizing region proteins in fine-needle aspiration samples of thyroid &nbsp; &nbsp; &nbsp; Eroz, R.ae&nbsp;,&nbsp;Cucer, N.b,&nbsp;Karaca, Z.c,&nbsp;Unluhizarci, K.c,&nbsp;Ozturk, F.d View additional authors Retrieving additional authors... a&nbsp; Department of Medical Genetics, Duzce University Medical School, Duzce, Turkey b&nbsp; Department of Medical Biology, Erciyes University Medical School, Kayseri, Turkey c&nbsp; Division of Endocrinology, Department of Internal Medicine, Erciyes University Medical School, Kayseri, Turkey d&nbsp; Department of Pathology, Erciyes University Medical School, Kayseri, Turkey e&nbsp; Department of Genetics, Duzce University Medical School, Duzce 81820, Turkey View additional affiliations Retrieving additional affiliations... View references (28) Abstract Argyrophilic nucleolar organizing region associated proteins (AgNORs) have been shown to be of interest in a variety of different diseases including thyroid disorders. Our aim was to distinguish benign thyroid lesions from papillary thyroid carcinoma (PTC) via AgNOR count and with a new approach, via AgNOR surface area/total nuclear surface area (NORa/TNa) proportions in the nuclei on fine-needle aspiration (FNA) materials. Thirty patients (eight men and 22 women) whose FNA was compatible with benign lesion and 26 patients (eight men and 18 women) whose FNA was compatible with PTC were included in the study. Fine-needle aspiration materials were stained for AgNOR detection according to a specific protocol. One hundred nuclei per individual have been evaluated, and AgNOR number and NORa/TNa proportions of individual cells were measured and calculated by using a computer program. Patients with PTC had significantly (p&lt;0.001) higher AgNOR count (4.6&plusmn;1.2%) than in the patients with benign lesions (2.0&plusmn;0.5%). Additionally, patients with PTC had significantly (p&lt;0.001) higher NORa/TNa (13.4&plusmn;2.4) than in the patients with benign lesion (5.7&plusmn;1.0). Modified method of AgNOR staining is an easy and reliable method for evaluating proliferation activity of cells in malignant and benign thyroid lesions and it may contribute to routine cytopathology in inconclusive situations. &copy; 2011 Springer Science+Business Media, LLC.</p

Primary hyperaldosteronism presenting with rhabdomyolysis in emergency room – Case report

Primary hyperaldosteronism, is a well-known cause of secondary hypertension, mostly idiopathic hypertension or arising from aldosterone-producing adenomas. It is characterized with resistant hypertension, hypokalemia and metabolic alkalosis related with aldosterone production excess and plasma renin activity suppression. Hypokalemic rhabdomyolysis usually presents with muscle pain, cramps, fatigability and generalized weakness. Rhabdomyolysis due to hypokalemia is a rare complication of primary hyperaldosteronism reported within a limited number of cases in medical literature. Diagnosis and treatment of primary hyperaldosteronism is fundamentally important because of the probability of certain cure with accurate surgery. Here, we report a 38-year-old female with hypertension related with primary hyperaldosteronism who presented with rhabdomyolysis most likely due to profound hypokalemia

The coexistence of newly diagnosed acromegaly with primary empty sella: More frequent than expected?

© 2022 Elsevier LtdObjective: We investigated the coexistence of newly diagnosed acromegaly with primary empty sella (ES), which is considered to be a rare association, and the impact of ES on the laboratory, radiological and prognostic status of acromegaly. Design: Acromegaly patients diagnosed and followed-up between 2012 and 2021 were included. Empty sella was defined as the pituitary gland and adenoma filling <50% of the sella turcica on preoperative T1 magnetic resonance imaging (MRI). Results: 102 acromegalic patients (45 male, 57 female, 45.5 ± 12.8 (range: 20–70 years) were included and data of a median 3 years (range: 0.5–9 years) were presented. ES was detected in 19 (18.6%) patients and 4 had complete and 15 had partial ES. Although not significant, adenoma size and residual adenoma on MRI on postoperative 3rd month, and disease remission at last control were lower in acromegaly with ES than in acromegaly without ES, while the rate of female gender and remission on postoperative 3rd month were higher. While preoperative serum prolactin and nadir GH responses to OGTT were significantly lower in patients with ES, there was no difference in terms of other pituitary hormones among both groups. Conclusion: The present study revealed the coexistence of newly diagnosed acromegaly with primary ES at a rate of nearly 20% which is more frequent than expected and this association is not rare. The presence of ES was not associated with any preoperative/postoperative pituitary hormone levels and remission status, except lower preoperative prolactin and nadir GH responses to OGTT

Prediabetes and mild hepatosteatosis are associated with blunted cortisol response to glucagon but not to growth hormone

© 2022 Elsevier Masson SASBackground: Although there is a close relationship between cortisol and growth hormone (GH) levels, glucose intolerance and hepatosteatosis, changes in GH and the hypothalamo-pituitary-adrenal (HPA) axis were not previously studied in prediabetes. The main purpose of the present study was to assess changes in GH and HPA axis and their relationship with hepatosteatosis in prediabetic patients. Methods: Forty prediabetic patients, with body-mass index (BMI) 25–35 kg/m2, and 23 healthy individuals, with normal glucose tolerance and similar age and BMI, were included. The 75 g oral glucose tolerance test and glucagon stimulation test (GST) were used. Results: No significant differences were detected between prediabetic patients and healthy individuals in terms of insulin-like growth factor-1 (IGF-1), insulin-like growth factor-binding protein-3 (IGFBP-3), IGF-1/IGFBP3 ratio or adrenocorticotropic hormone (ACTH). GH responses to GST did not differ between groups. On the other hand, peak cortisol and area under the curve (AUC) (cortisol) response on GST were significantly lower in prediabetic patients. Both peak GH and AUC (GH) response on GST correlated negatively with waist circumference and body weight. The degree of hepatosteatosis correlated negatively with peak cortisol, GH, AUC (cortisol) and AUC (GH) response on GST. Conclusion: Cortisol response to GST is decreased in prediabetic patients, with relatively well conserved GH response. This suggests altered HPA axis responsiveness in prediabetes, as is known in diabetes. Thus, HPA axis changes in patients with diabetes probably start before the development of diabetes as such

Micronucleus evaluation in mitogen-stimulated lymphocytes of patients with acromegaly

Acromegaly is a syndrome characterized by a sustained elevation of circulating growth hormone and insulin-like growth factor-1 (IGF-1). Insulin-like growth factor-1 is a potent mitogen and has a role in the transformation of normal cells to malignant cells. This study aims to evaluate the spontaneous micronucleus (MN) frequency by using the cytokinesis-block MN assay to determine genetic damage in the lymphocytes of patients with acromegaly. The study was carried out in 20 patients who had active acromegaly and in 20 age- and sex-matched healthy controls. The MN values were measured in binucleated cells obtained from mitogen-stimulated lymphocytes of patients and control subjects. The distribution of binucleated cells with 1, 2, 3, or more MNs was also measured. We found significantly higher MN frequency values in the lymphocytes of acromegalic patients than in those of the control subjects (2.23 +/- 0.68 vs 1.03 +/- 0.54, P = .001). The MN frequency increased with increasing IGF-1 levels of acromegalic patients (P = .036, R = 0.47). We observed that the number of binucleated cells with 2 MNs was higher for the majority of patients with acromegaly than for control subjects. Furthermore, the receiver operating characteristic curve (area under the curve = 0.914, P < .0001) was calculated to assess the discriminative power of the MN frequency. Our results indicate that increased MN frequency in the lymphocytes of patients with acromegaly may reflect genomic instability and this increased MN frequency may be associated with elevated levels of circulating growth hormone and IGF-1. (C) 2011 Elsevier Inc. All rights reserved

Dysmetabolic markers predict outcomes in autosomal dominant polycystic kidney disease

Eroglu, Eray/0000-0003-2571-7385; Bayram, Arslan/0000-0002-3682-2140WOS: 000480485400005PubMed: 31134465Background Overweight and obesity were recently associated with a poor prognosis in patients with autosomal dominant polycystic kidney disease (ADPKD). Whether the metabolic consequences of obesity as defined by the metabolic syndrome (MS) are also linked with disease progression remains untested. Methods Eligible ADPKD patients with different stages of CKD (n = 105) and 105 non-diabetic controls matched for CKD stage were enrolled in the study. Groups were evaluated at baseline for presence of MS, blood markers of metabolism, homeostasis model assessment of insulin resistance (HOMA-IR) score, and biochemical markers of inflammation (hs-CRP, IL-1 beta, IL-6, TNF-alpha and PON-1). MS was defined according to the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). Patients were followed for 12 months and progression defined as a decrease in baseline eGFR > 10%. Results MS and hypertension were more prevalent amongst ADPKD patients than in the control group. Meanwhile, markers of inflammation such as hs-CRP (3.63 [3.45-5.17] vs. 4.2 [3.45-8.99] mg/dL; p = 0.014), IL-6 (21.65 [14.1-27.49] vs. 24.9 [16.23-39.4] pg/mL; p = 0.004) and IL-1 beta (21.33 [15.8-26.4] vs. 26.78 [18.22-35] pg/mL; p < 0.001) levels were all more elevated in ADPKD patients than in non-diabetic CKD subjects. in multivariate analysis having a truncating PKD1 mutation predicted (OR 1.25 [1.09-1.43]; p = 0.002) fulfilling the MS criteria. Finally, ADPKD patients fulfilling MS criteria had a significantly more rapid progression during 12 months of follow-up than did those that did not (OR 3.28 [1.09-9.87]; p = 0.035). Conclusions Our data supports the notion that dysmetabolisms part of the ADPKD phenotype and associated with a poor outcome, especially in patients with a truncating PKD1 mutation

Hypoglycemia in a Patient With Metastatic Gastrointestinal Stromal Tumor: Is Chemotherapy a Reasonable Option for Symptom Control?

Tumor induced hypoglycemia is a rare paraneoplastic phenomenon. However, hypoglycemia may also occur in solid tumors of epithelial or mesenchymal origin. Hypoglycemia caused by these types of tumours is referred to as non-islet cell tumour hypoglycemia (NICTH). Sunitinib is a drug that novel, oral, multitargeted tyrosine kinase. The biologic bases of the activity of sunitinib in patients with GISTs that are target multiple signaling pathways in tumor, stromal, and endothelial compartments. In this report, we describe a case of metastatic gastrointestinal stromal tumor (GIST) presented with loss of consciousness due to hypoglycemia caused or worsened by sunitinib. In our opinion, who the patients with imatinib mesylate and sunitinib malate intolerant GIST, combination chemotherapy consisting of cisplatin and etoposid can be useful in the palliative setting, like our case

Hypoglycemia in a Patient With Metastatic Gastrointestinal Stromal Tumor: Is Chemotherapy a Reasonable Option for Symptom Control?

Tumor induced hypoglycemia is a rare paraneoplastic phenomenon. However, hypoglycemia may also occur in solid tumors of epithelial or mesenchymal origin. Hypoglycemia caused by these types of tumours is referred to as non-islet cell tumour hypoglycemia (NICTH). Sunitinib is a drug that novel, oral, multitargeted tyrosine kinase. The biologic bases of the activity of sunitinib in patients with GISTs that are target multiple signaling pathways in tumor, stromal, and endothelial compartments. In this report, we describe a case of metastatic gastrointestinal stromal tumor (GIST) presented with loss of consciousness due to hypoglycemia caused or worsened by sunitinib. In our opinion, who the patients with imatinib mesylate and sunitinib malate intolerant GIST, combination chemotherapy consisting of cisplatin and etoposid can be useful in the palliative setting, like our case