A 24‐year‐old woman presented to our emergency department with right fifth‐finger metacarpophalangeal (MCP) pain. She had a history of overt hyperthyroidism and had self‐discontinued her methimazole several years prior to admission, and had been lost to medical follow‐up. One week prior to presentation, the patient had noticed mild swelling around the joint and on the palmar surface. Pain developed 2 days prior to admission. She denied any fevers, chills, or trauma to the joint. On the day of admission, she awoke with severe pain and limited range of motion. Her temperature was 98.4°F. On exam, there were no gross deformities and the finger was held in partial flexion at the MCP joint. There was mild erythema over the volar hand, with swelling and tenderness over the MCP joint. A hand x‐ray demonstrated an amorphous focus of calcifications in the volar soft tissue adjacent to the fifth proximal phalanx. Arthrocentesis of the joint did not yield any drainable fluid. An ultrasound demonstrated moderate soft‐tissue edema and an amorphous echogenic area with shadowing consistent with crystal deposition adjacent to and extending into the fifth MCP joint. No drainable collection was seen. This clinical presentation and radiographic evidence of associated periarticular calcifications was most consistent with a diagnosis of acute calcific periarthritis (ACP). Clindamycin, which had been started empirically, was discontinued. The patient was treated with indomethacin, and she noted significant reduction in pain and improvement in mobility within 24 hours, with resolution of all symptoms within 48 hours. She was discharged home to complete a 14‐day course of indomethacin. Of note, the patient was also found to have a TSH < 0.01, and so was started on propylthiouracil on discharge.
Acute calcific periarthritis (ACP) occurs when hydroxyapatite crystals are deposited adjacent to a joint. It is uncommon, but it can closely mimic acute infections of the involved area. The most common joint involved is the shoulder, followed by the hip, spine, fingers, elbow, wrists, knees, and ankles. Diagnosis is made by the presence of amorphous calcific bodies within the periarticular area. Symptoms generally respond to anti‐inflammatory agents. We found 2 prior case reports of ACP in association with hyperthyroidism,1,2 but in both the patients had hypercalcemia at the time of their flare, whereas our patient was normocalcemic with a calcium of 9.4.
ACP is uncommon but can appear similar to infectious arthritis. Doherty M. Triggering of acute calcific periarthritis by thyrotoxicosis.
1. Doherty M. Triggering of acute calcific periarthritis by thyroxicosis (Letter). Br J Rheumatol. 1984:32:76–77. 2. Goldstein A. Letter. Br J Rheumatol. 1986:25:313–322. To cite this abstract:
1. Doherty M. Triggering of acute calcific periarthritis by thyroxicosis (Letter). Br J Rheumatol. 1984:32:76–77.
2. Goldstein A. Letter. Br J Rheumatol. 1986:25:313–322.
To cite this abstract:Alcorn K, Lee D, Yarchoan M, Caroff D, Hecht T. Acute Calcific Periarthritis Presenting in a Woman with Hyperthyroidism and Normocalcemia. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 263. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/acute-calcific-periarthritis-presenting-in-a-woman-with-hyperthyroidism-and-normocalcemia/. Accessed November 17, 2019.