scholarly journals CUSHING DISEASE MASQUERADING AS GLAUCOMA

2019 ◽  
Vol 5 (5) ◽  
pp. e290-e293
Author(s):  
Yumiko Tsushima ◽  
Lubna Bashir Munshi ◽  
Charit Taneja ◽  
Se-min Kim
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Case Reports ◽  
Elevated Serum ◽  
Serum Cortisol ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Hormone ◽  
Cushing Disease ◽  
Corticosteroid Administration ◽  
Late Night ◽  
Stimulating Hormone

Objective: Glaucoma is a well-recognized side effect of corticosteroids. However, steroid-induced glaucoma typically refers to that caused by exogenous corticosteroid administration. Glaucoma secondary to endogenous overproduction of corticosteroids has only been reported in a few case reports. We aim to bring attention to glaucoma as a rare but important manifestation of endogenous hypercortisolism. Methods: Patient history, physical exam, laboratory results, and imaging studies were reviewed. Results: We report a case of glaucoma as the initial presentation of Cushing disease (CD). The patient was diagnosed with glaucoma 16 months prior to his endocrinology evaluation. At our initial encounter, the patient had a cushingoid appearance. Levels of 24-hour urinary cortisol and late-night salivary cortisol were elevated. Serum cortisol was not suppressed by 1 mg of dexamethasone overnight, but it was suppressed by 8 mg of dexamethasone. Adrenocorticotropic hormone was also elevated. All other pituitary hormone axes were unremarkable (thyroid-stimulating hormone, free thyroxine, follicle-stimulating hormone, luteinizing hormone, growth hormone, prolactin, and insulin-like growth factor). Pituitary magnetic resonance imaging suggested a small adenoma (2 to 3 mm); therefore, the patient underwent inferior petrosal sinus sampling. The results were consistent with CD. Transsphenoidal resection was performed and final pathology confirmed an adrenocorticotropic hormone-positive adenoma. Hypercortisolism and intraocular pressures improved after the surgery. Conclusion: Glaucoma can lead to irreversible blindness if left untreated or uncontrolled. However, endogenous hypercortisolism-induced glaucoma can be reversed with treatment of the underlying CD. Thus, heightened awareness of extraocular manifestations of secondary causes of glaucoma such as endogenous hypercortisolism is necessary in order to promote prompt evaluation and treatment.

Influence of Hormones on Sjögren’s Syndrome

2019 ◽  
Vol 24 (35) ◽  
pp. 4167-4176 ◽  
Author(s):  
Liu Yang ◽  
Wei Wei ◽  
Xi He ◽  
Yu Xie ◽  
Mohammad A. Kamal ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Adrenocorticotropic Hormone ◽  
Sjögren's Syndrome ◽  
Follicle Stimulating Hormone ◽  
Hormone Treatment ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Thyroid Stimulating Hormone ◽  
Sjögren‘S Syndrome ◽  
Stimulating Hormone

Sjögren’s syndrome (SS) is an immune system oral disorder that is characterized generally by dry mouth and eyes. In this review, SS classification, presentation and pathogenesis are briefly discussed. Moreover, the epidemiology of SS regarding sex, age and association with other complications are also presented. This review also addresses the interactions between endocrine axes and SS, and the important findings up to regarding hormone treatment of this syndrome. The main hormones discussed in this review includes Adrenocorticotropic hormone (ACTH), Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), Thyroid-stimulating hormone (TSH), and prolactin.

scholarly journals Approach to Subclinical Thyroid Diseas

1970 ◽  
Vol 26 (2) ◽  
pp. 91-96
Author(s):  
Satya Ranjan Sutradhar
Keyword(s):  
Subclinical Hypothyroidism ◽  
Thyroid Dysfunction ◽  
Hormone Level ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Good Evidence ◽  
Reference Ranges ◽  
Mineral Density ◽  
Asymptomatic Patients ◽  
Stimulating Hormone

Subclinical thyroid dysfunction is defined as an abnormal serum thyroid-stimulating hormone level and free thyroxine and triiodothyronine levels within their reference ranges. The prevalence of subclinical hyperthyroidism is about 2 percent. Subclinical hypothyroidism is found in approximately 4 to 8.5 percent of the population. Most national organizations recommend against routine screening of asymptomatic patients, but screening is recommended for high risk populations. The management of subclinical thyroid dysfunction is controversial. There is good evidence that subclinical hypothyroidism is associated with progression to overt disease. Patients with a serum thyroid-stimulating hormone level greater than 10 mIU/L have a higher incidence of elevated serum low density lipoprotein cholesterol concentrations; however, evidence is lacking for other associations. There is insufficient evidence that treatment of subclinical hypothyroidism is beneficial. A serum thyroid stimulating hormone level of less than 0.1 mIU/L is associated with progression to overt hyperthyroidism, atrial fibrillation, reduced bone mineral density, and cardiac dysfunction. There is little evidence that early treatment alters the clinical course. DOI: 10.3329/jbcps.v26i2.4187 J Bangladesh Coll Phys Surg 2008; 26: 91-96

scholarly journals Evaluation of pituitary function in cases with the diagnosis of pediatric mild traumatic brain injury: Cross-sectional study

2016 ◽  
Vol 7 (04) ◽  
pp. 537-543 ◽  
Author(s):  
Hakan Aylanç ◽  
Filiz Tütüncüler ◽  
Necdet Süt
Keyword(s):  
Head Trauma ◽  
Early Period ◽  
Serum Cortisol ◽  
Cross Sectional Study ◽  
Thyroid Stimulating Hormone ◽  
Cross Sectional ◽  
Pituitary Dysfunction ◽  
Duration Time ◽  
Basal Cortisol Level ◽  
Stimulating Hormone

ABSTRACT Background: This study was to determine whether pituitary dysfunction occurs after head trauma in children or not and which axis is affected more; to define the association of pituitary dysfunction with the severity of head trauma and duration time after the diagnosis of head trauma. Materials and Methods: In this study, 24 children who were diagnosed with head trauma were evaluated regarding pituitary dysfunction. In all cases, after 12 h fasting, serum cortisol, fT3, fT4, thyroid-stimulating hormone, prolactin, insulin-like growth factor-1, serum sodium, urine density, follicle-stimulating hormone, luteinizing hormone, in female cases E2, in male cases, TT levels were determined. Results: Mean age of children was 9.5 ± 3.1 years, 14 children (58.3%) had mild, 9 children (37.5%) had moderate, and 1 children (4.2%) had severe head trauma according to the Glasgow coma scale. Mean duration time after head trauma was 29.4 ± 9.8 months. In all cases, no pathologic condition was determined in the pituitary hormonal axis. In one children (4.2%), low basal cortisol level was found. There were no children with hormonal deficiency in this study. Conclusion: Although pituitary dysfunction after head trauma may develop in the early period, some may present in the late period; therefore, all cases should be followed up at outpatient clinics for a longer period.

scholarly journals Wrong Biochemistry Results: Two Case Reports and Observational Study in 5310 Patients on Potentially Misleading Thyroid-stimulating Hormone and Gonadotropin Immunoassay Results

2002 ◽  
Vol 48 (11) ◽  
pp. 2023-2029 ◽  
Author(s):  
Adel AA Ismail ◽  
Paul L Walker ◽  
Julian H Barth ◽  
Kryzsztof C Lewandowski ◽  
Rick Jones ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Observational Study ◽  
Early Identification ◽  
Prospective Observational Study ◽  
Case Reports ◽  
Clinical Care ◽  
Thyroid Stimulating Hormone ◽  
The Common ◽  
Almost All ◽  
Stimulating Hormone

Abstract Background: Immunoassays are used in almost all medical and surgical specialties, but they suffer from interference from proteins such as antibodies in some patients’ sera. Such interferences are usually reported in the literature only as case reports after the introduction of a new assay. Methods: We undertook a prospective observational study on 5310 patients for whom the common immunoassay tests for thyroid-stimulating hormone (TSH) and/or gonadotropins were requested. All TSH and gonadotropin results were critically assessed for a mismatch between the clinical details and analytical results to identify samples suspected of analytical unreliability. These were tested further by three approaches to screen for interference. Results: From the 5310 sets of results, 59 patients’ samples were identified as suspect and were tested further. Analytically incorrect results were found in 28 (0.53% of the total studied). The magnitude of interference varied, but in 23 of 28 patients (82%), it was considered large enough to have a potentially adverse effect on cost and/or the clinical care of these patients. Two cases, described in detail, illustrate the adverse effect of error on patient care and cost, and the second highlights the difficulties and limitations of current approaches for identifying interference and inaccuracy in immunoassays. Conclusions: Because millions of TSH/gonadotropin tests are carried out in UK hospital laboratories alone, our data suggest that thousands of patients could be adversely affected by errors from interferences. Early identification of interference in cases with unusual results could be valuable.

Reactivation of Pituitary Hormone Release and Metabolic Improvement by Infusion of Growth Hormone-Releasing Peptide and Thyrotropin-Releasing Hormone in Patients with Protracted Critical Illness1

1999 ◽  
Vol 84 (4) ◽  
pp. 1311-1323 ◽  
Author(s):  
Greet Van den Berghe ◽  
Pieter Wouters ◽  
Frank Weekers ◽  
Subburaman Mohan ◽  
Robert C. Baxter ◽  
...  
Keyword(s):  
Critical Illness ◽  
Protein Degradation ◽  
Biochemical Markers ◽  
Feedback Inhibition ◽  
Elevated Serum ◽  
Random Order ◽  
Serum Cortisol ◽  
Pituitary Hormone ◽  
Metabolic Markers ◽  
Deconvolution Analysis

Protracted critical illness is marked by protein wasting resistant to feeding, by accumulation of fat stores, and by suppressed pulsatile release of GH and TSH. We previously showed that the latter can be reactivated by brief infusion of GH-releasing peptide (GHRP-2) and TRH. Here, we studied combined GHRP-2 and TRH infusion for 5 days, which allowed a limited evaluation of the metabolic effectiveness of this novel trophic endocrine strategy. Fourteen patients (mean ± sd age, 68 ± 11 yr), critically ill for 40 ± 28 days, were compared to a matched group of community-living control subjects at baseline and subsequently received 5 days of placebo and 5 days of GHRP-2 plus TRH (1+1μ g/kg·h) infusion in random order. At baseline, impaired anabolism, as indicated by biochemical markers (osteocalcin and leptin), was linked to hyposomatotropism [reduced pulsatile GH secretion, as determined by deconvolution analysis, and low GH-dependent insulin-like growth factor and binding protein (IGFBP) levels]. Biochemical markers of accelerated catabolism (increased protein degradation and bone resorption) were related to tertiary hypothyroidism and the serum concentration of IGFBP-1, but not to hyposomatotropism. Metabolic markers were independent of elevated serum cortisol. After 5 days of GHRP-2 plus TRH infusion, osteocalcin concentrations increased 19% vs. −6% with placebo, and leptin had rose 32% vs. -15% with placebo. These anabolic effects were linked to increased IGF-I and GH-dependent IGFBP, which reached near-normal levels from day 2 onward. In addition, protein degradation was reduced, as indicated by a drop in the urea/creatinine ratio, an effect that was related to the correction of tertiary hypothyroidism, with near-normal thyroid hormone levels reached and maintained from day 2 onward. Concomitantly, a spontaneous tendency of IGFBP-1 to rise and of insulin to decrease was reversed. Cortisol concentrations were not detectably altered. In conclusion, 5-day infusion of GHRP-2 plus TRH in protracted critical illness reactivates blunted GH and TSH secretion, with preserved pulsatility, peripheral responsiveness, and feedback inhibition and without affecting serum cortisol, and induces a shift toward anabolic metabolism. This provides the first evidence of the metabolic effectiveness of short term GHRP-2 plus TRH agonism in this particular wasting condition.

Syndrome of'inappropriate secretion of thyroid-stimulating hormone' by partial target organ resistance to thyroid hormones

1981 ◽  
Vol 97 (3) ◽  
pp. 361-368 ◽  
Author(s):  
J. Salmerón De Diego ◽  
C. Alonso Rodriguez ◽  
A. Salazar Orlando ◽  
P. Sanchez Garcia Cervigon ◽  
E. Caviola Mutazzi ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Elevated Serum ◽  
Pituitary Tumour ◽  
Thyroid Stimulating Hormone ◽  
Target Organ ◽  
Resistance To Thyroid Hormones ◽  
Serum Thyroid Hormone ◽  
Serum Tsh ◽  
Tsh Levels ◽  
Stimulating Hormone

Abstract. A 74 year old woman was found to have elevated serum thyroid-stimulating hormone (TSH) levels and elevated serum thyroid hormone levels, with clinical euthyroidism. There was no evidence of a pituitary tumour. TSH levels increased substantially during methimazole therapy. Administration of dexamethasone was followed by a prompt fall in serum TSH levels. Triiodothyronine (T3) was administered over a period of 20 days in doses from 25 μg to as much as 100 μg daily causing a rise in serum T3 above 700 ng/100 ml, a decline of T4 and a blunting of the response to thyrotrophinreleasing hormone (TRH), with normal metabolic responses (pulse rate, photomotogram, cholesterol). These results suggest that the patient's disorder is due to partial target organ resistance to thyroid hormones.

Cervical sympathectomy affects adrenocorticotropic hormone and thyroid-stimulating hormone in rats

1996 ◽  
Vol 10 (3) ◽  
pp. 181-184 ◽  
Author(s):  
Hiroshi Iwama ◽  
Mamoru Adachi ◽  
Choichiro Tase ◽  
Yoichi Akama
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Thyroid Stimulating Hormone ◽  
Cervical Sympathectomy ◽  
Stimulating Hormone

scholarly journals Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaolei Wang ◽  
Jinbao Mao ◽  
Xinli Zhou ◽  
Qiu Li ◽  
Ling Gao ◽  
...  
Keyword(s):  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Cyclophilin D ◽  
Mitochondrial Stress ◽  
Knockout Mouse Model ◽  
Cellular Reactive Oxygen Species ◽  
Underlying Mechanisms ◽  
And Function ◽  
Stimulating Hormone

Background & Aims. Oxidative stress-related liver diseases were shown to be associated with elevated serum thyroid stimulating hormone (TSH) levels. Mitochondria are the main source of cellular reactive oxygen species. However, the relationship between TSH and hepatic mitochondrial stress/dysfunction and the underlying mechanisms are largely unknown. Here, we focused on exploring the effects and mechanism of TSH on hepatic mitochondrial stress. Methods. As the function of TSH is mediated through the TSH receptor (TSHR), Tshr-/- mice and liver-specific Tshr knockout (LKO) mice were used in our study. The thyroid-specific Tshr knockout mouse model injected with TSH (TKO+TSH) was used as a mimic for subclinical hypothyroidism (SCH) patients. Hepatic mitochondrial stress and function were analyzed in these mouse models, and the expression of key genes involved in mitochondrial stress was measured. Results. A relatively lower degree of mitochondrial stress was observed in the livers of Tshr-/- mice and LKO mice than those of their littermate counterparts. TSH caused concentration- and time-dependent effects on mitochondrial stress and cyclophilin D (CypD) acetylation in hepatocytes in vitro. Microarray and RT-PCR analyses showed that Tshr-/- mice had much higher lncRNA-AK044604 expression than their littermate counterparts. The use of the AK044604 overexpression plasmid and SIRT1 agonist proved that TSH aggravates CypD acetylation and mitochondrial stress via lncRNA-AK044604 and SIRT1. An inhibitor of CypD acetylation, cyclosporine A, suppressed TSH-induced hepatic mitochondrial stress and dysfunction. Conclusions. TSH stimulates hepatic CypD acetylation through the lncRNA-AK044604/SIRT1/SIRT3 signaling pathway, indicating an essential role for TSH in mitochondrial stress in the liver.

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