Endocrinology and Metabolism

Case Reports

Secondary Pituitary Hyperplasia Induced by Hashimoto's Thyroiditis Related Hypothyroidism: A Case Report.: Kwang Joon Kim, Hyun min Kim, Obin Kwon, Eun Young Park, Yong ho Lee, Jae Won Hong, Jin Wi, Eun Jig Lee; J Korean Endocr Soc. 2010;25(1):72-77. Published online March 1, 2010; DOI: https://doi.org/10.3803/jkes.2010.25.1.72

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Pituitary hyperplasia associated with untreated primary hypothyroidism in children is a rare condition. There are only a few reports on this condition in children, and especially when pituitary hyperplasia is accompanied with Hashimoto thyroiditis and growth arrest. Here, we describe an unusual association of pituitary hyperplasia with hypothyroidism and growth retardation, and this was all caused by Hashimoto thyroiditis. Hormonal testing showed a low thyroxine level and a high thyroid stimulating hormone level, elevated anti-thyroglobulin, low growth hormone levels and prepubertal levels of gonadotropins. A large intrasellar mass expanding beyond the sella turcica was detected on magnetic resonance imaging (MRI). Homogeneous contrast enhancement of mass highly suggested that it was a pituitary hyperplasia rather than a pituitary tumor. Therapy with L-thyroxine resulted in rapid improvement of the clinical signs, including renewed growth, normalization of the hormone levels and resolution of the pituitary hyperplasia on MRI within 90 days. In children, prolonged unrecognized primary hypothyroidism might be accompanied by growth deficiency and pubertal disharmony. Physicians must be aware of pituitary hyperplasia in these cases.

Citations

Citations to this article as recorded by

Pituitary macroadenoma secondary to Hashimoto’s thyroiditis: inadvertent diagnosis in a pre-pubertal girl
Deepanjan Bhattacharya, Rakesh Kumar, Jaivinder Yadav
Tropical Doctor.2020; 50(3): 240. CrossRef
Pituitary Hyperplasia Secondary to Hypothyroidism Caused by Hashimoto's Thyroiditis in a Female Adolescent
Jeoung Suk Kim, Min Sun Kim, Sun Jun Kim, Gyung Ho Chung, Pyoung Han Hwang, Dae-Yeol Lee
Journal of Korean Society of Pediatric Endocrinology.2011; 16(3): 185. CrossRef

A Case of Piouitary Hyperplasia with Retardation due to Primary Hypothyroidism.: Hong Seung Kim, Choon Hee Chung, Young Goo Shin, Bong Ki Lee; J Korean Endocr Soc. 1997;12(4):589-595. Published online January 1, 2001

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Abstract PDF: Primary hypothyroidism can result in reactive enlargement of the pituitary gland which is indistinguishable from primary pituitary lesions in clinical presentation and on magnetic resonance imaging. A 17-year-old girl came to the hospital due to short stature, general weakness and galac-torrhea. The magnetic resonance imaging (MRI) study showed pitutary enlargement. The hormone study showed hyperprolactinemia, decreased basal growth hormone level and primary hypothyroi-dism. By thyroid replacement therapy only, mass was successfully regressed on follow up MRI after 4 months, and growth acceleration could be achieved.

A Case of Type Ia Glycogen Storage Disease.: Young II Choi, Young In Choi, Jee Won Park, Yoon Sok Chung, Hyon Ju Kim; J Korean Endocr Soc. 1999;14(4):786-792. Published online January 1, 2001

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Abstract PDF: Glycogen storage diseases are inherited disorders of carbohydrate metabolism caused by a deficiency of enzymes that are involved in degradation of glycogen in the liver. The accumulation of glycogen occurs in the liver and other organs. Type Ia is the most common form and clinically may manifest of glycogen storage disease itself rather than growth hormone deficiency. But in this case the patient showed exceptional extreme growth retardation. Growth hormone stimulation test with clonidine and L-dopa revealed that the patient had growth hormone deficiency. Therefore, we report of a case of glycogen storage disease type Ia with the presence of GH deficiency with review of literature. A 16-year-old male was admitted for the evaluation of hepatomegaly and extreme short stature. The height was 113.5cm, less than third percentile of same age group, and compatible with fiftieth percentile of height of 6 years of age. After laboratory work up including liver biopsy, he was diagnosed with type I glycogen storage disease. The patient was presented with metabolic acidosis, hyperuricemia, and hypoglycemia. Hypoglycemia was managed with frequent feeding with high starch diet and intravenous glucose infusion. Metabolic acidosis was treated with sodium bicarbonate. Secondary hyperuricemia was treated with allopurinol. The patient is being followed at out-patient clinic with clinical improvement after of GH administration.

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