scholarly journals A Rare Case of 83-Year-Old Transgender Female: Can Thyroid Hormone Deficiency Be Involved in Transgenderism and Gender Dysphoria?

2020 ◽  
Vol 10 (02) ◽  
pp. 23-40
Author(s):  
Andrey Frolov ◽  
Lauren Polcaro ◽  
Craig Lawson ◽  
Yun Tan ◽  
John R. Martin III
Keyword(s):  
Thyroid Hormone ◽  
Gender Dysphoria ◽  
Rare Case ◽  
Hormone Deficiency ◽  
And Gender

The Co-Occurrence of Autism and Gender Diversity

2020 ◽  
pp. 197-211
Author(s):  
Jill C. Fodstad ◽  
Rebecca Elias ◽  
Shivali Sarawgi
Keyword(s):  
Gender Dysphoria ◽  
Gender Diversity ◽  
Gender Nonconforming ◽  
Medical Interventions ◽  
Gender Diverse ◽  
Nonbinary Gender ◽  
Psychiatric Conditions ◽  
The Common ◽  
And Gender

Gender diversity refers to gender expressions and/or gender identity experiences that vary from the common experiences of gender. Gender-diverse people may be gender nonconforming, gender nonbinary, gender fluid, gender exploring, transgender, and so forth. Some gender-diverse individuals experience gender dysphoria and/or gender incongruence and may require gender-affirming supports, including gender-affirming medical interventions. The co-occurrence of autism and gender diversity has been highlighted in a series of studies internationally as well as through rich community expressions. Studies in gender-referred individuals reveal high rates of autism traits as well as high rates of existing autism diagnoses. Studies in autistic populations reveal greater gender diversity characteristics. The long-term course of gender diversity in autistic individuals is poorly understood. Clinical guidelines have been developed for adolescents with the co-occurrence, but much work remains: No gender-related measures have been developed and tested for use in neurodiverse populations, no programs exist to support gender-diverse neurodiverse adults, and little is known about co-occurring mental health profiles, risks, or protective factors for people with the co-occurrence. The inclusion of this chapter on co-occurring autism and gender diversity within a book on “co-occurring psychiatric conditions” is problematic, because gender diversity is not a “psychiatric condition,” but instead a form of human diversity. The diagnosis of Gender Dysphoria is useful only insomuch as it allows individuals to obtain necessary gender-related supports. The authors’ choice to include this chapter in this book reflects a compromise, motivated by the need for educating both autism and gender specialists in this common co-occurrence.

scholarly journals Very rare case of Graves’ disease with resistance to methimazole: a case report and literature review

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199619
Author(s):  
Yusaku Mori ◽  
Munenori Hiromura ◽  
Michishige Terasaki ◽  
Hideki Kushima ◽  
Makoto Ohara ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Rare Case ◽  
Therapeutic Option ◽  
Lithium Carbonate ◽  
Graves Disease ◽  
High Dose ◽  
Hormone Concentration ◽  
Thyroid Hormone Concentration ◽  
Serum Thyroid Hormone ◽  
Inorganic Iodine

Background Methimazole (MMI) is used to treat hyperthyroidism in Graves’ disease. It is rare to encounter patients in whom hyperthyroidism cannot be controlled using high doses of MMI. Case presentation: A 21-year-old woman was referred to our hospital because of MMI-resistant Graves’ disease. Although her MMI dose had been increased to 120 mg/day, her serum thyroid hormone concentration was too high to be measured. Additional therapy with lithium carbonate, and then with dexamethasone and inorganic iodine, was initiated. After 14 days, the patient’s serum thyroid hormone concentration normalized, while she was taking 150 mg/day MMI, 800 mg/day lithium carbonate, 6 mg/day dexamethasone and 306 mg/day inorganic iodine, and total thyroidectomy was then performed. The patient was discharged 8 days after the thyroidectomy and experienced no major complications. Conclusions We have presented a rare case of Graves’ disease that was resistant to high-dose MMI. Combination therapy of MMI with lithium carbonate, dexamethasone and inorganic iodine may represent a therapeutic option for the preoperative preparation of patients with MMI-resistant Graves’ disease.

Effects of postnatal thyroid hormone deficiency on neurogenesis in the juvenile and adult rat

2009 ◽  
Vol 34 (2) ◽  
pp. 366-374 ◽  
Author(s):  
Liqun Zhang ◽  
Klas Blomgren ◽  
H. Georg Kuhn ◽  
Christi M. Cooper-Kuhn
Keyword(s):  
Thyroid Hormone ◽  
Hormone Deficiency ◽  
Adult Rat

Thyroid hormone is required for the phenotype transitions induced by the pharmacological inhibition of calcineurin in adult soleus muscle of rats

2008 ◽  
Vol 294 (1) ◽  
pp. E69-E77 ◽  
Author(s):  
Nathalie Koulmann ◽  
Lahoucine Bahi ◽  
Florence Ribera ◽  
Hervé Sanchez ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Soleus Muscle ◽  
Hormone Deficiency ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Peroxisome Proliferator Activated Receptor ◽  
Thyroid State ◽  
Novel Approach ◽  
A Subunit ◽  
Calcineurin Inhibition

The present experiment was designed to examine the effects of hypothyroidism and calcineurin inhibition induced by cyclosporin A (CsA) administration on both contractile and metabolic soleus muscle phenotypes, with a novel approach to the signaling pathway controlling mitochondrial biogenesis. Twenty-eight rats were randomly assigned to four groups, normothyroid, hypothyroid, and orally treated with either CsA (25 mg/kg, N-CsA and H-CsA) or vehicle (N-Vh and H-Vh), for 3 wk. Muscle phenotype was estimated by the MHC profile and activities of oxidative and glycolytic enzymes. We measured mRNA levels of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), the major regulator of mitochondrial content. We also studied the expression of the catalytic A-subunit of calcineurin (CnA) both at protein and transcript levels and mRNA levels of modulatory calcineurin inhibitor proteins (MCIP)-1 and -2, which are differentially regulated by calcineurin activity and thyroid hormone, respectively. CsA-administration induced a slow-to-fast MHC transition limited to the type IIA isoform, which is associated with increased oxidative capacities. Hypothyroidism strongly decreased both the expression of fast MHC isoforms and oxidative capacities. Effects of CsA administration on muscle phenotype were blocked in conditions of thyroid hormone deficiency. Changes in the oxidative profile were strongly related to PGC-1α changes and associated with phosphorylation of p38 MAPK. Calcineurin and MCIPs mRNA levels were decreased by both hypothyroidism and CsA without additive effects. Taken together, these results suggest that adult muscle phenotype is primarily under the control of thyroid state. Physiological levels of thyroid hormone are required for the effects of calcineurin inhibition on slow oxidative muscle phenotype.

Thyroid hormone deficiency changes the distribution of oligodendrocyte/myelin markers during oligodendroglial differentiation in vitro

2006 ◽  
Vol 24 (7) ◽  
pp. 445-453 ◽  
Author(s):  
V. Younes‐Rapozo ◽  
J. Berendonk ◽  
T. Savignon ◽  
A.C. Manhães ◽  
P.C. Barradas
Keyword(s):  
Thyroid Hormone ◽  
Hormone Deficiency

Consequences of thyroid hormone deficiency induced by the specific ablation of thyroid follicle cells in adult transgenic mice

1994 ◽  
Vol 143 (1) ◽  
pp. 107-120 ◽  
Author(s):  
H Wallace ◽  
K McLaren ◽  
R Al-Shawi ◽  
J O Bishop
Keyword(s):  
Body Weight ◽  
Thyroid Hormone ◽  
Transgenic Mice ◽  
Follicle Cells ◽  
Hormone Deficiency ◽  
Mrna Levels ◽  
Thyroid Follicle ◽  
Receptor Mrna ◽  
The Many ◽  
Tsh Levels

Abstract The herpes simplex type 1 virus thymidine kinase (HSV1-TK) reporter gene was coupled to a bovine thyroglobulin promoter (TG-tk construct). Within the thyroid glands of transgenic mice expression was confined to thyroid follicle cells. Infusion of Ganciclovir (9-[(1,3-dihydroxy-2-propoxy)methyl]guanine) to 8 to 12 week transgenic females led to the complete loss of thyroid HSV1-TK activity (at 3 to 4 days) and thyroid follicles (between 7 and 14 days). During the first 5 days of treatment a single reciprocal oscillation in circulating thyroxine (T4) and TSH levels occurred. By 14 days the circulating triiodothyronine (T3) and T4 levels of all treated animals were below the detection limits of the assays, while TSH levels were elevated ten-fold and continued to increase thereafter. During 14 days of treatment the thyroids regressed, protein content fell by 80–90% and the C cells, normally dispersed within the central region of each gland, came together in aggregates. Pituitary GH levels in females rose and fell back to normal within 14 days and between 14 and 28 days fell to a level comparable with that of GH-deficient lit/lit mice. The levels of hepatic GH receptor mRNA and the predominant 6·6 kb T3 receptor mRNA were unaffected by thyrocyte ablation. Thyrocyte ablation had no effect on the level of prolactin (Prl) receptor mRNA in females, but increased Prl receptor mRNA levels in males and eliminated group 1 major urinary protein (MUP) mRNA in females. T4 replacement reversed the effects of thyrocyte ablation on MUP mRNA in females and on Prl receptor mRNA in males. Despite the many physiological changes induced by thyrocyte ablation, ablated mice have been maintained for up to 1 year without thyroid hormone supplementation. T4-deficient females were normally fertile and carried pups to term. Although transgenic males expressed HSV1-TK ectopically in spermatids and spermatozoa at levels similar to thyrocyte levels, a rate of Ganciclovir infusion which successfully ablated the thyrocytes did not affect the testis. As an alternative to infusion by minipump, thyrocyte ablation could be achieved by 6 twice-daily injections of Ganciclovir, at a level of 112 μg Ganciclovir/g body weight per day, and fetuses in utero could be thyrocyte ablated by administering 50 or 15 μg/g body weight per day to pregnant females between days 14 and 18 of gestation. These data demonstrate the potential value of transgenic thyrocyte ablation in the study of the effects of thyroid hormone deprivation. Journal of Endocrinology (1994) 143, 107–120

scholarly journals The effect of thyroid hormone deficiency on erythropoiesis in dogs

2019 ◽  
Vol 88 (3) ◽  
pp. 257-264 ◽  
Author(s):  
Olga Aniołek
Keyword(s):  
Thyroid Hormone ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Clinical Symptoms ◽  
Cell System ◽  
Hormone Deficiency ◽  
Control Group ◽  
Average Mass ◽  
Packed Red Blood Cells ◽  
Experimental Group

This research aimed to evaluate the effect of thyroid hormone deficiency on the erythrocytic system in dogs. Dogs with clinical symptoms of hypothyreosis such as obesity, hyperpigmentation, and lethargy were selected. The dogs demonstrating breed predisposition to hypothyreosis were incorporated in the analysis: Dachshunds, Retrievers, and mixed-breed dogs. A detailed history was taken and clinical, hormonal, biochemical and haematological blood tests were performed. Peripheral blood samples were taken from 53 dogs. Finally, the dogs with the initial T4 (thyroxine) concentration < 1.3 µg/dl and animals demonstrating clinical improvement after a 2-month therapy with levothyroxine at a dose of 10 µg/kg administeredper ostwo times a day were qualified. The animals between 10 months to 13 years of age were divided into two groups: clinically healthy (control group, n = 35) and dogs presenting clinical symptoms of hypothyreosis (experimental group, n = 18). In this research, the broadly described normocytic normochromic non-regenerative anaemia was not diagnosed in dogs with hypothyreosis. However, a positive correlation between T4 and red blood cell indices such as the average mass of haemoglobin per red blood cell, concentration of haemoglobin in a given volume of packed red blood cells as well as a negative correlation with haematocrit value was discovered in the experimental group after the 2-month therapy with levothyroxine. These results point to the influence of thyroid hormones on erythropoiesis. This observation is partially consistent with other studies, which noted the casual link between the changes in red blood cell system and the function of thyroid in dogs and humans.

scholarly journals Hypothyroidism Therapy

2021 ◽  
Author(s):  
Wissal Abassi ◽  
Nejmeddine Ouerghi ◽  
Anissa Bouassida
Keyword(s):  
Coronary Artery Disease ◽  
Thyroid Hormone ◽  
Hormone Deficiency ◽  
Deficiency Anemia ◽  
Low Doses ◽  
Successful Therapy ◽  
Sympathetic Hyperactivity ◽  
Thyroxine Therapy ◽  
The Common ◽  
Artery Disease

Hypothyroidism refers to the common pathological disorder of thyroid hormone deficiency. The successful therapy for hypothyroidism is levothyroxine (LT4) administration, which is the same as thyroxine but produced synthetically. Serum thyrotropin (TSH) normalization with LT4 replacement therapy in hypothyroidism is generally needed to restore a euthyroid state. The daily dose of thyroxine therapy depends on various factors, such as body weight, age, and severity. It also differs from hypothyroidism during pregnancy to congenital hypothyroidism. The presence of various comorbidities may exist such as myxoedema coma, coronary artery disease, obesity, anemia and COVID-19 which necessitate individualized treatment. LT4 intolerance manifested with sympathetic hyperactivity may appear during the first hours after the LT4 administration. It requires starting with very low doses of LT4 that should be increased gradually, and reaching normal TSH may take several months. The sympathetic hyperactivity may be attributable to the presence of uncorrected iron-deficiency anemia that worsens by the use of thyroid hormone.

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