scholarly journals Congenital Thyrotoxicosis with Congenital Glaucoma: A Case Report

1970 ◽  
Vol 20 (1) ◽  
pp. 64-66
Author(s):  
MI Bari ◽  
ME Hoque ◽  
T Alam ◽  
KM Choudhury
Keyword(s):  
Intraocular Pressure ◽  
Case Report ◽  
Preterm Neonate ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Congenital Glaucoma ◽  
Corneal Oedema ◽  
First Case ◽  
Corneal Diameter ◽  
Stimulating Hormone

A case of preterm neonate with congenital thyrotoxicosis associated with congenital glaucoma is reported. Her mother had undiagnosed thyrotoxicosis. The diagnosis of thyrotoxicosis in the neonate was confirmed by an elevated serum tri-iodothyronine (T3) level of 8.09 nmol/L, thyroxin (T4) level of 3.09 nmol and thyroid stimulating hormone (TSH) level 0.16mu/L. Congenital glaucoma was confirmed by increased intraocular pressure (IOP) which was 42.1 mmHg in right eye and 38.2 mm Hg in left eye. Corneal diameter was increased which was 13 mm in both eyes. Corneal oedema and Haab striae were also present. Probably, this is the first case of congenital thyrotoxicosis associated with congenital glaucoma reported in Bangladesh.   doi: 10.3329/taj.v20i1.3094 TAJ 2007; 20(1): 64-66

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 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.

scholarly journals Neonatal COVID-19 Pneumonia: Report of the First Case in a Preterm Neonate in Mayotte, an Overseas Department of France

Children ◽  
2020 ◽  
Vol 7 (8) ◽  
pp. 87
Author(s):  
Soumeth Abasse ◽  
Laila Essabar ◽  
Tereza Costin ◽  
Voninavoko Mahisatra ◽  
Mohamed Kaci ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Case Report ◽  
Respiratory Distress ◽  
Neonatal Intensive Care ◽  
Preterm Neonate ◽  
Chest Ct ◽  
First Case ◽  
Chest Ct Scan

We report the first case of COVID-19 pneumonia in a preterm neonate in Mayotte, an overseas department of France. The newborn developed an acute respiratory distress by 14 days of life with bilateral ground glass opacities on a chest CT scan and a 6-week-long stay in the neonatal intensive care unit (NICU). This case report emphasizes the need for a cautious and close follow-up period for asymptomatic neonates born to mothers with COVID-19 infection. Vertical transmission cannot be excluded in this case.

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.

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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