- A Case of Thyroid Amyloidosis Misrecognized as Subacute Thyroiditis.
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Young Sil Lee, Seong Su Moon, Soon Kim, Jong Im Lee
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Endocrinol Metab. 2010;25(4):360-364. Published online December 1, 2010
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DOI: https://doi.org/10.3803/EnM.2010.25.4.360
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- Amyloid deposition in the thyroid is found in about 30-80% of the patients with primary or secondary amyloidosis. In a few patients with amyloidosis, the thyroid is enlarged and so called amyloid goiter occurs. The thyroid function usually remains normal, but occasionally hypothyroidism or thyrotoxicosis occurs in patients with thyroid amyloidosis. We have experienced one case of thyroid amyloidosis due to bronchiectasis and the patient developed painful goiter and transient thyrotoxicosis resembling subacute thyroiditis. Biopsies from the gastric antrum, duodenum, colon, kidney and thyroid were positive for deposition of amyloid. When patients have signs and symptoms of subacute thyroiditis, but they develop an unusual course, then the diagnosis of thyroid amyloidosis should be considered.
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Citations
Citations to this article as recorded by  - Amyloid goiter mimicking subacute thyroiditis on clinical and imaging findings: A case report
Yoo Jin Lee, Soo Jin Jung, Dong Wook Kim, Hwa Jin Cho, Ki Jung Ahn
Journal of Clinical Ultrasound.2018; 46(7): 497. CrossRef
- A Case of Pseudopseudohypoparathyroidism with Normal Stature.
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Sae Rom Kim, Yun Jeong Doh, Hee Kyung Kim, Seong Su Moon, Ju Young Lee, Jae Han Jeon, Soo Won Kim, Bo Wan Kim, In Kyu Lee, Jung Guk Kim
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J Korean Endocr Soc. 2009;24(2):138-143. Published online June 1, 2009
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DOI: https://doi.org/10.3803/jkes.2009.24.2.138
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- Pseudopseudohypoparathyroidism (PPHP) is characterized by the phenotype of Albright hereditary osteodystrophy (AHO) alone without biochemical evidence of multihormone resistance, which is unlike pseudohypoparathyroidism. AHO is associated with characteristic developmental abnormalities that include a short stocky stature, a short neck, brachydactyly, a round face, central obesity, mental retardation and subcutaneous ossifications. AHO is an autosomal dominant disease that's caused by heterozygous inactivating mutations in the Gsalpha gene (GNAS1). Melanocortin-4 receptor (MC4R) is a hypothalamic Gs-coupled receptor that is thought to mediate the central effect of leptin on satiety. MC4R mutations cause morbid obesity starting in infancy, as well as an elevated leptin level. A 62 year old man with a height of 171.5 cm, a round face, a short neck, central obesity and brachydactyly had normal ranges of serum calcium, phosphorus and PTH and a normal Ellsworth-Howard test. GNAS1 gene analysis revealed substitution of alanine to cysteine in the 165 codon of exon 6 and substitution of alanine to cysteine in the 231 codon of exon 9. Two known SNPs (Cyt-1042Thy, Gua-719Ade) in the MC4R were detected in the patient. We report here on a case of PPHP and the patient had normal stature. We propose that MC4R may have contributed to the obesity & normal stature of this patient.
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Citations
Citations to this article as recorded by - Polyglandular Autoimmune Syndrome Type III with Primary Hypoparathyroidism
Sang Jin Kim, Sang-Yoon Kim, Han-Byul Kim, Hyukwon Chang, Ho-Chan Cho
Endocrinology and Metabolism.2013; 28(3): 236. CrossRef
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