A case of myxedema coma caused by isolated thyrotropin stimulating hormone deficiency and Hashimoto's thyroiditis

Iida, Keiji; Hino, Yasuhisa; Ohara, Takeshi; Chihara, Kazuo

doi:10.1507/endocrj.k10e-329

Cited by 12 publications

(4 citation statements)

References 18 publications

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“…To examine whether low TSH results in osteoporosis in the human, several groups determined bone mineral density (BMD) in patients with isolated TSH deficiency (ITSHD). Iida et al (15) reported that BMD of a patient with ITSHD (56-yr-old woman) was markedly diminished, with a value of Ϫ4.8 standard deviations, compared with a young adult's mean. However, Papadimitriou et al (24) reported that chronic extremely low TSH levels in children with ITSHD, in the face of normal thyroid hormone levels, are not related to osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

Excess TSH causes abnormal skeletal development in young mice with hypothyroidism via suppressive effects on the growth plate

Endo

Kobayashi

2013

American Journal of Physiology-Endocrinology and Metabolism

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Hypothyroidism in the young leads to irreversible growth failure. hyt/hyt Mice have a nonfunctional TSH receptor (TSHR) and are severely hypothyroid, but growth retardation was not observed in adult mice. We found that epiphysial cartilage as well as cultured chondrocytes expressed functional TSHR at levels comparable to that seen in the thyroid, and that addition of TSH to cultured chondrocytes suppressed expression of chondrocyte differentiation marker genes such as Sox-9 and type IIa collagen. Next, we compared the long bone phenotypes of two distinct mouse models of hypothyroidism: thyroidectomized (THYx) mice and hyt/hyt mice. Although both THYx and hyt/hyt mice were severely hypothyroid and had similar serum Ca(2+) and growth hormone levels, the tibia was shorter and the proliferating and hypertrophic zones in the growth plate was significantly narrower in THYx mice than in hyt/hyt mice. Supplementation of hyt/hyt mice thyroid hormone resulted in a wider growth plate compared with that of wild-type mice. Expressions of chondrocyte differentiation marker genes Sox-9 and type IIa collagen in growth plate from THYx mice were 52 and 60% lower than those of hyt/hyt mice, respectively. High serum TSH causes abnormal skeletal development in young mice with hypothyroidism via suppressive effects on the growth plate.

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Section: Discussionmentioning

confidence: 99%

Excess TSH causes abnormal skeletal development in young mice with hypothyroidism via suppressive effects on the growth plate

Endo

Kobayashi

2013

American Journal of Physiology-Endocrinology and Metabolism

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“…Subsequent rodent and clinical studies have since pointed to a role for TSHRs in normal physiology, as well as in the pathophysiology of bone loss in the hyperthyroid state (5)(6)(7)(8)(9). A recent study, in which a woman with isolated TSH deficiency developed not only myxedema coma, but also severe osteoporosis, is more evidence for a fundamental role for TSH in skeletal homeostasis (10). Less compelling, but nonetheless important, is that individuals with activating TSHR polymorphisms but with normal thyroid function have a higher bone mass than matched controls (11).…”

mentioning

confidence: 99%

Thyroid-stimulating hormone induces a Wnt-dependent, feed-forward loop for osteoblastogenesis in embryonic stem cell cultures

Baliram

Latif

Berkowitz

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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We have shown that the anterior pituitary hormone, thyroidstimulating hormone (TSH), can bypass the thyroid to exert a direct protective effect on the skeleton. Thus, we have suggested that a low TSH level may contribute to the bone loss of hyperthyroidism that has been attributed traditionally to high thyroid hormone levels. Earlier mouse genetic, cell-based, and clinical studies together have established that TSH inhibits osteoclastic bone resorption. However, the direct influence of TSH on the osteoblast has remained unclear. Here, we have used a model system developed from murine ES cells, induced to form mature mineralizing osteoblasts, and show that TSH stimulates osteoblast differentiation primarily through the activation of protein kinase Cδ and the up-regulation of the noncanonical Wnt components frizzled and Wnt5a. We predict that a TSH-induced, fast-forward short loop in bone marrow permits Wnt5a production, which, in addition to enhancing osteoblast differentiation, also stimulates osteoprotegerin secretion to attenuate bone resorption by neighboring osteoclasts. We surmise that this loop should uncouple bone formation from bone resorption with a net increase in bone mass, which is what has been observed upon injecting TSH.

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“…Several well-documented cases of MC associated with hypopituitarism have been reported in PubMed over the past 60 years [ 9 – 16 ]. A case with both Hashimoto thyroiditis and Sheehan syndrome leading to MC has also been reported [ 17 ], as has a case with Hashimoto thyroiditis and TSH deficiency [ 18 ]. In pediatric medicine, Thompson and Henry reported a rare case of MC due to central hypothyroidism in a 7-year-old boy with a chromosome 1q deletion [ 19 ].…”

Section: Discussion and Literature Reviewmentioning

confidence: 99%

Myxedema Coma Associated with Macroprolactinoma: Case Report and Review of the Literature

Omoniyi

Robbins

2022

Case Reports in Endocrinology

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Myxedema coma is a rare life-threatening presentation of severe hypothyroidism associated with a high mortality rate. Although most cases are due to primary thyroid failure, a minority have central hypothyroidism as the underlying cause. We report the case of a 69-year-old man who presented with obtundation, hypoglycemia, and hyponatremia. The patient’s initial thyroid-stimulating hormone (TSH) was within normal limits. Subsequent evaluation revealed critical anterior pituitary insufficiency due to a macroprolactinoma and a diagnosis of myxedema coma after appropriate workup The finding of a normal serum TSH should not eliminate the possibility of myxedema coma.

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A case of myxedema coma caused by isolated thyrotropin stimulating hormone deficiency and Hashimoto's thyroiditis

Cited by 12 publications

References 18 publications

Excess TSH causes abnormal skeletal development in young mice with hypothyroidism via suppressive effects on the growth plate

Excess TSH causes abnormal skeletal development in young mice with hypothyroidism via suppressive effects on the growth plate

Thyroid-stimulating hormone induces a Wnt-dependent, feed-forward loop for osteoblastogenesis in embryonic stem cell cultures

Myxedema Coma Associated with Macroprolactinoma: Case Report and Review of the Literature

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