EP08 Acute calcific epicondylitis associated with primary hypoparathyroidism: a paradox effect or an adverse event
Authors: Awadh Basem , Al-Allaf Abdul-Wahab 
Published: April 2020

Background

Calcific tendonitis is characterised by the accumulation of basic calcium phosphate hydroxyapatite crystals within the tendon. It is mainly affects supraspinatus tendon and it is usually idiopathic, but can be associated with other diseases. We are describing a previously unreported case of calcific epicondylitis in a patient with primary hypoparathyroidism on a high dose of calcium supplement with a highlight on its pathogenesis.

Methods

We describe a previously unreported case of calcific epicondylitis in a patient with primary hypoparathyroidism on a high dose of calcium supplement with literature review highlighting the possible mechanism and pathogenesis.

Results

A 33-year-old male presented with acute left elbow pain and swelling. A several months earlier, presented to the Emergency Department with similar attack. The elbow x-ray showed two hyper-dense calcifications at the lateral epicondyle. His Ultrasound revealed hyperechoic deposits over the lateral epicondyle with increased Doppler activity confirming the diagnosis of lateral calcific epicondylitis. Previously, he was seen a few times because of nonspecific symptoms of irritability, generalised weakness and numbness, found to have hypocalcemia of &lt; 1.5 mmol/l and low PTH 3 pg/ml, and diagnosed with primary hypoparathyroidism. His serum calcium was maintained by a high intake of daily calcium carbonate 1250 mg three tablets three times daily and calcitriol one mcg/day. Just prior to his presentation, he developed a foreign body sensation on swallowing, and the CT neck revealed a tiny hyper-density calcification along the posterior surface of the soft palate. We gave him Celecoxib 200 mg daily for five days with good response. All his previous calcium levels were on the low normal range, 24-hour urine calcium was elevated at 11.8 mmol/24 hours. We referred him to Endocrinologist for consideration for PTH replacement therapy. Two fundamentally different processes for calcific tendonitis have been proposed: degenerative and reactive calcification. Degenerative theory proposes that dystrophic calcification follows a necrotic phase, usually attributed to a wear-and-tear and aging. This theory is supported by an observation that calcific tendonitis seldom affects young people. While the Reactive calcification theory was described to involves four phases: pre-calcific, formative, resorptive and healing. Reactive calcification theory is supported by a variety of imaging studies demonstrating a complete resolution of the calcium deposits. Calcific tendonitis is largely idiopathic or traumatic. Metabolic causes proposed to play a role, but nothing mentioned with regards to the hypoparathyroidism. It is not clear in our case whether the cause of calcific tendonitis is primarily due to hypoparathyroidism or secondary to the high calcium replacement

Conclusion

In young patients with hypoparathyroidism on high dose of calcium replacement therapy, a high index of suspicion is needed to diagnose calcific tendonitis. Better understanding of the pathogenesis may help to prevent the soft tissue calcification in general

Disclosures

B. Awadh None. A. Al-Allaf None.