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      Central hypothyroidism

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          Abstract

          Central hypothyroidism is defined as hypothyroidism due to insufficient stimulation by thyroid stimulating hormone (TSH) of an otherwise normal thyroid gland. It has an estimated prevalence of approximately 1 in 80,000 to 1 in 120,000. It can be secondary hypothyroidism (pituitary) or tertiary hypothyroidism (hypothalamus) in origin. In children, it is usually caused by craniopharyngiomas or previous cranial irradiation for brain tumors or hematological malignancies. In adults, it is usually due to pituitary macroadenomas, pituitary surgeries or post-irradiation. Fatigue and peripheral edema are the most specific clinical features. Diagnosis is established by the presence of normal to low-normal TSH on the background of low-normal thyroid hormones, confirmed by the thyrotropin releasing hormone stimulation test. Therapy includes use of levothyroxine titrated to improvement in symptomology and keeping free T4 in the upper limit of normal reference range.

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          The Colorado thyroid disease prevalence study.

          G Mayor, N Manowitz, Gay Canaris … (2000)
          The prevalence of abnormal thyroid function in the United States and the significance of thyroid dysfunction remain controversial. Systemic effects of abnormal thyroid function have not been fully delineated, particularly in cases of mild thyroid failure. Also, the relationship between traditional hypothyroid symptoms and biochemical thyroid function is unclear. To determine the prevalence of abnormal thyroid function and the relationship between (1) abnormal thyroid function and lipid levels and (2) abnormal thyroid function and symptoms using modern and sensitive thyroid tests. Cross-sectional study. Participants in a statewide health fair in Colorado, 1995 (N = 25 862). Serum thyrotropin (thyroid-stimulating hormone [TSH]) and total thyroxine (T4) concentrations, serum lipid levels, and responses to a hypothyroid symptoms questionnaire. The prevalence of elevated TSH levels (normal range, 0.3-5.1 mIU/L) in this population was 9.5%, and the prevalence of decreased TSH levels was 2.2%. Forty percent of patients taking thyroid medications had abnormal TSH levels. Lipid levels increased in a graded fashion as thyroid function declined. Also, the mean total cholesterol and low-density lipoprotein cholesterol levels of subjects with TSH values between 5.1 and 10 mIU/L were significantly greater than the corresponding mean lipid levels in euthyroid subjects. Symptoms were reported more often in hypothyroid vs euthyroid individuals, but individual symptom sensitivities were low. The prevalence of abnormal biochemical thyroid function reported here is substantial and confirms previous reports in smaller populations. Among patients taking thyroid medication, only 60% were within the normal range of TSH. Modest elevations of TSH corresponded to changes in lipid levels that may affect cardiovascular health. Individual symptoms were not very sensitive, but patients who report multiple thyroid symptoms warrant serum thyroid testing. These results confirm that thyroid dysfunction is common, may often go undetected, and may be associated with adverse health outcomes that can be avoided by serum TSH measurement.
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            Laboratory medicine practice guidelines. Laboratory support for the diagnosis and monitoring of thyroid disease.

            Zubair Baloch, Pierre Carayon, Bernard Conte-Devolx … (2003)
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              Risk for fracture in women with low serum levels of thyroid-stimulating hormone.

              Alan Ettinger, Joshua Stone, … (2001)
              Biochemical evidence of hyperthyroidism may be associated with low bone mass, particularly in older postmenopausal women, but no prospective studies of thyroid function and subsequent fracture risk have been done. To examine the association between low levels of thyroid-stimulating hormone (TSH) and fracture in older women. Prospective cohort study with case-cohort sampling. Four clinical centers in the United States. 686 women older than 65 years of age from a cohort of 9704 women recruited from population-based listings between 1986 and 1988. Baseline assessment of calcaneal bone mass, spine radiography, and history of thyroid disease. Spine radiography was repeated after a mean follow-up of 3.7 years; nonspine fractures were centrally adjudicated. Thyroid-stimulating hormone was measured in sera obtained at baseline from 148 women with new hip fractures, 149 women with new vertebral fractures, and a subsample of 398 women randomly selected from the cohort. After adjustment for age, history of previous hyperthyroidism, self-rated health, and use of estrogen and thyroid hormone, women with a low TSH level (0.1 mU/L) had a threefold increased risk for hip fracture (relative hazard, 3.6 [95% CI, 1.0 to 12.9]) and a fourfold increased risk for vertebral fracture (odds ratio, 4.5 [CI, 1.3 to 15.6]) compared with women who had normal TSH levels (0.5 to 5.5 mU/L). After adjustment for TSH level, a history of hyperthyroidism was associated with a twofold increase in hip fracture (relative hazard, 2.2 [CI, 1.0 to 4.4]), but use of thyroid hormone itself was not associated with increased risk for hip fracture (relative hazard, 0.5 [CI, 0.2 to 1.3]). Women older than 65 years of age who have low serum TSH levels, indicating physiologic hyperthyroidism, are at increased risk for new hip and vertebral fractures. Use of thyroid hormone itself does not increase risk for fracture if TSH levels are normal.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Endocrinol Metab
                Journal ID (publisher-id): IJEM
                Title: Indian Journal of Endocrinology and Metabolism
                Publisher: Medknow Publications (India )
                ISSN (Print): 2230-8210
                ISSN (Electronic): 2230-9500
                Publication date (Print): July 2011
                Volume: 15
                Issue: Suppl2
                Pages: S99-S106
                Affiliations
                [1] Department of Endocrinology, Jaslok Hospital and Research Centre, 15-Deshmukh Marg, Mumbai - 400 026, India
                [1 ] Department of General Medicine/Endocrinology, Khoo Teck Puat Hospital, Singapore
                Author notes
                Corresponding Author: Dr. Vishal Gupta, Department of Endocrinology, Jaslok Hospital and Research Centre, 15-Deshmukh Marg, Mumbai - 400 026, India. E-mail: enquiry@ 123456drvishalgupta.com
                Article
                Publisher ID: IJEM-15-99
                DOI: 10.4103/2230-8210.83337
                PMC ID: 3169862
                PubMed ID: 21966662
                SO-VID: b101c4b6-e9d1-4c14-a7a0-15d547832247
                Copyright © Copyright: © Indian Journal of Endocrinology and Metabolism
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: hypothyroidism,tertiary hypothyroidism,secondary hypothyroidism,levothyroxine,central hypothyroidism,hypopituitarism,thyroid stimulating hormone,thyrotropin releasing hormone,panhypopituitarism
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: hypothyroidism, tertiary hypothyroidism, secondary hypothyroidism, levothyroxine, central hypothyroidism, hypopituitarism, thyroid stimulating hormone, thyrotropin releasing hormone, panhypopituitarism

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