Journal of Yeungnam Medical Science

Nephrology
Tumoral calcinosis and calciphylaxis treated with subtotal parathyroidectomy and sodium thiosulphate.: Hyunjeong Cho, Yongjin Yi, Eunjeong Kang, Seokwoo Park, Eun Jin Cho, Sung Tae Cho, Rho Won Chun, Kyu Eun Lee, Kook Hwan Oh; Yeungnam Univ J Med. 2016;33(1):68-71. Published online June 30, 2016; DOI: https://doi.org/10.12701/yujm.2016.33.1.68

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Abstract PDF: Tumoral calcinosis (TC) is a condition resulting from extensive calcium phosphate precipitation, primarily in the periarticular tissues around major joints. Calciphylaxis is a fatal ischemic vasculopathy mainly affecting dermal blood vessels and subcutaneous fat. This syndrome is rare and predominantly occurs in patients with end-stage renal disease. Here, we report on a rare case involving a patient with TC complicated with calciphylaxis. Our patient was a 31-year-old man undergoing hemodialysis who presented with masses on both shoulders and necrotic cutaneous ulcers, which were associated with secondary hyperparathyroidism, on his lower legs. He underwent subtotal parathyroidectomy, and sodium thiosulfate (STS) was administered for 27 weeks. Twenty months after beginning the STS treatment course, he experienced dramatic relief of his TC and calciphylaxis.

Nephrology
Furosemide induced medullary nephrocalcinosis mimicking Bartter syndrome.: Sohee Kim, Chanhee Kyung, Yong Hoon Kim, Jang Ho Cho, Changhyeok Hwang, Jung Eun Lee; Yeungnam Univ J Med. 2014;31(1):21-24. Published online June 30, 2014; DOI: https://doi.org/10.12701/yujm.2014.31.1.21

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Abstract PDF: Clinical presentation of Bartter syndrome is similar to surrepitious vomiting or use of diuretics. Therefore, precise differential diagnosis of Bartter syndrome is crucial. We report a case of medullary nephrocalcinosis (MNC) induced by furosemide mimicking Bartter syndrome. A 55-year-old female patient visited our hospital with renal dysfunction on basis of hypokalemia and metabolic alkalosis. She had no history of hypertension or drug use except allopurinol and atorvastatin. She did not complain of nausea or vomiting on presentation and the serum magnesium level was normal. We performed ultrasonography, that showed MNC. For these reasons, we suspected Bartter syndrome and corrected the electrolyte imbalance. During outpatient follow up, we found that the patient had been taking 400 mg of furosemide daily for 30 years. We could diagnose furosemide induced MNC, and recommended to her to reduce the amount of furosemide.

Endocrinology, Diabetes, and Metabolism
A Case of Parathyroid Carcinoma with Systemic Calcification.: Heui Sik Kim, Chan Woo Lee, Sang Yiup Nam, Jin Chul Park, Ji Sang Yoon, Jae Chun Lee, Kyu Chang Won, Ihn Ho Cho, Tae Nyun Kim, Hyoung Woo Lee, Myung Soo Hyun, Hyun Woo Lee; Yeungnam Univ J Med. 1997;14(2):459-466. Published online December 31, 1997; DOI: https://doi.org/10.12701/yujm.1997.14.2.459

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Abstract PDF

Hyperparathyroidism due to parathyroid cancer is rare. It is difficult to diagnose preoperatively but there should be an increased index of suspicion in those parathyroid Patient with palpable neck masses, profound hypercalcemia(greater than 14mg/dl), made increase of the parathyroid hormone level to greater than twice normal, and significant metabolic complications. In parathyroid cancer, systemic calcinosis is an extremely rare manifestation. The most common metastatic calcification site is lung and the other involved site is stomach, liver, skin and heart. After resection of parathyroid tumor, this systemic calcinosis is self-limiting. We experienced a patient with primary hyperparathyroidsm, presented with metastatic calcification in the lung and stomach disappeared by successful parathyroidectomy.

Citations

Citations to this article as recorded by

A Case of Parathyroid Carcinoma in a Patient with Stage 3 Chronic Kidney Disease
Youn Hee Cho, Moo Yong Park, Soo Jeong Choi, Jin Kuk Kim, Seung Duk Hwang, Jung Mi Park, Jeong Ja Kwak
Korean Journal of Medicine.2012; 83(6): 796. CrossRef

Rheumatology
Subcutaneous tissue calcification in a patient with rheumatoid arthritis.: Dong Hyun Kim, Kyung Jin Kim, Sung Min Kwon, Sung Ouk Cha, Jung Ouk Lee; Yeungnam Univ J Med. 2016;33(2):120-124.; DOI: https://doi.org/10.12701/yujm.2016.33.2.120

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Abstract PDF: Subcutaneous tissue calcification in rheumatic diseases usually occurs in connective tissue diseases, such as systemic lupus erythematosus, scleroderma, and dermatomyositis. Domestic cases of calcification in rheumatoid arthritis have not been reported. The mechanism of subcutaneous tissue calcification may differ depending on the cause and it can develop on all parts of the body. Calcification occurring in rheumatic diseases is a major mechanism of tissue damage caused by chronic inflammation. No standard therapy for calcification has been established; however, many studies have reported on medical and surgical treatment. We report on subcutaneous tissue calcification in a rheumatoid arthritis patient tissue calcification on both sides of the buttocks, the upper limbs, and the lower limbs.

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