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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 < 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.

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.

The case history of a 4 year old girl with primary hypoparathyroidism is reported. Treatment with oral 1α-hydroxyvitamin D3 did not result in normal calcium and phosphate levels, whereas treatment with oral 1α,25-dihydroxyvitamin D3 did. During the treatment period, the patient developed signs of severe liver disease and died in a picture of increased intracranial pressure. Post-mortem examination revealed a giant cell hepatitis and severe cirrhosis. The clinical course is consistent with a liver vitamin D3 hydroxylation defect.

The "N-tact" immunoradiometric assay (IRMA) from INCSTAR for parathyrin (PTH) in serum involves a 125I-labeled affinity-purified antiserum to PTH 1-34 and an affinity-purified antiserum to PTH 39-84, the latter bound to a polystyrene bead. The mean detection limit, determined in six consecutive assays, was 4 ng/L. The within-batch CV was less than 7% in the range 15 to 2135 ng/L. The between-batch CV was 11.7% and 5.3% at 30 and 371 ng/L, respectively. Serum PTH in 14 proven cases of primary hyperparathyroidism was 49-808 (median 111) ng/L, undetectable (less than 5 ng/L) in 10 cases of primary hypoparathyroidism and in 10 cases of hypercalcemia associated with malignancy, compared with 7-39 ng/L in 45 normal subjects. PTH was 9 to 19 ng/L in four patients with familial benign hypercalcemia. In 39 patients with renal failure, apparent concentrations were 14 to 857 (median 133) ng/L, but sera from these patients pre-diluted with zero standard did not parallel dilutions of the standard, PTH 1-84. PTH concentrations were not significantly decreased in blood or serum kept at 20 degrees C for up to 6 h. After successful removal of a parathyroid adenoma, the mean half-time for disappearance of PTH in vivo in five hyperparathyroid patients was 3.3 min.

SUMMARY A case of untreated primary hypoparathyroidism with psoriasis vulgaris is reported. On systemic prednisone therapy the patient developed generalized erythroderma, pustular psoriasis of the soles, candidiasis of the mouth, dermatogenic enteropathy and manifest tetany. Correction of the serum calcium improved the severe skin lesions, emphasizing that fluctuations in serum calcixim affect psoriasis.

Twenty eight hypocalcaemic patients were studied, 14 with primary hypoparathyroidism, nine with pseudohypoparathyroidism and two with hypo-hyperparathyroidism, to characterize the essential features of these disorders. Like tetany, which was present in 12 of the patients, epilepsy was a common symptom, occurring in 13, seven of whom had received anticonvulsants for two to eight years before hypocalcaemia was detected. Differentiation between primary and pseudohypoparathyroidism could not be made with certainty on clinical grounds but confident distinction could be made by measurement of endogenous parathyroid hormone concentrations and by testing for renal resistance to exogenous parathyroid hormone. This was achieved by measurement of the plasma and, in some patients, the urinary cyclic AMP response to an intravenous injection of highly purified bovine parathyroid hormone. These investigations were also valuable in the assessment of the other three hypocalcaemic patients in whom a diagnosis of parathyroid dysfunction would otherwise have been made. In 10 of the patients synthetic 1α-hydroxylated forms of vitamin D were used to establish and maintain normocalcaemia, though their use required careful monitoring.