Introduction: Primary and secondary hyperparathyroidism may coexist unrelated to chronic nephropathy. It can occur more often than expected, especially in elderly population with malabsorption syndrome or /and liver diseases.
Case report: A women 60 years of age was admitted to hospital due to long standing ostealgia. The primary hyperparathyroidism was suspected. The medical history presented recently diagnosed coeliac disease and cryptogenic hepatic cirrhosis.
Lab tests during hospitalization: PTH level was surprisingly high 2200 pg/ml (n: 1565 pg/ml), calcium serum level and calcium urine excretion in 24 h collection in the normal range, phosphates 1.8 mg/dl (n: 2.54.8 mg/dl), ALP 660 U/l (n: 36123 U/l), 25(OH)D3 extremely below the normal range: 6.7 ng/ml (n: 3080 ng/ml). The level of creatinine was normal. Osteopenia was confirmed. Scintigraphy, USG and CT revealed of single parathyroid adenoma of diameter 3.0 cm.: Gluten-free diet and oral vitamin D (gtt. calcifediol 75 μg each day) was recommended.
Elimination of ostealgia, PTH reduction (540 pg/ml), slight elevation of calcium level: (11.812.2 mg/dl), normalization of 25(OH)D3 level (47 ng/ml) were obtained. Surgical removal of parathyroid adenoma was successfully performed five months later. Hungry bone syndrome was not observed post operatively. Vitamin D supplementation was maintained. PTH, calcium, phosphates, ALP, 25(OH)D remains in the normal range.
Conclusions: 1. Gastrointestinal diseases especially liver diseases can trigger secondary hyperparathyroidism and enhance primary hyperparathyroidism.
2. High levels of PTH/Ca ratios can be caused by profound deficit of Vitamin D3.
3. Early recognised deficit of D3 followed by preoperative D3 supplementation with strict control of calcium serum levels eliminate post operative severe hungry bones syndrome.
4. Vitamin D3 treatment should lasts at least 3 months considering PTH, D3, Ca receptors regulation.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology