Systemic lupus erythematosus-related hypercalcemia with ectopic calcinosis

Abstract

We report a case of a 39-year-old female with active systemic lupus erythematosus who complained of lethargy and weakness with a moderate renal impairment. Hypercalcemia was confirmed by laboratory examination. Her X-ray revealed significant ectopic calcinosis in subcutaneous tissue of bilateral hands, and Tc-99(m) methylene diphosphonate bone scan revealed a remarkably intense uptake of bilateral lungs. She had no evidence suggestive of other diseases related to hypercalcemia such as hyperparathyroidism and malignancy. She had abnormally high serum parathyroid hormone-related protein (PTHrP) which fell to normal after treatment. Glucocorticoid, cyclophosphamide plus calcitonin and etidronate were administered and the patient improved greatly. Literature review demonstrated that lupus-related hypercalcemia with ectopic calcinosis is a rare complication and increased PTHrP is probably one of the main mechanisms. Lung uptake in bone scan may be a special and reliable clue suggestive of hypercalcemia.

Hypercalcaemia due to immobility, about a case

“…However, in our environment it is not easily accessible, so through the systematic review of the clinical evolution and the paraclinical studies carried out during at 28 months. This possibility was displaced to a less probable cause, as thyrotoxicosis, renal failure, increased calcium intake, hypervitaminosis D, prescription drugs such as lithium, thiazides, calcium carbonate or calcium citrate, and other diseases such as pheochromocytoma and adrenal insufficiency, acute kidney injury and systemic lupus erythematosus 7 , leaving hypercalcemia due to immobility as a probable etiology.…”

Lupus Nephritis With Mild Asymptomatic Hypercalcemia in Children: A Case Report and Literature Review

“…Among 17 cases reported, there were 15 females and 2 males (7, 15); 1 mild hypercalcemia (7) (male), 5 moderate hypercalcemia (2, 8, 12, 15, 16) (1 male and 4 females), 11 severe hypercalcemia (1, 3–6, 9–11, 13, 14, 17) (all females); 2 children (all females) (6, 9), 15 adults; there were 14 cases of hypercalcemia in active stage of SLE, 3 cases of hypercalcemia in remission stage of SLE (3, 6, 12) (all female, 2 of them considered the main cause of non-hypercalcemia in SLE); 15 cases of SLE-related hypercalcemia (1, 2, 4–11, 13–17), and 1 case of hypercalcemia were caused by primary hyperthyroidism (3), The coexistence of SLE and hypercalcemia was considered in only 1 case (3); SLE with PTH elevation in 5 cases [including 3 cases of parathyroid adenoma (1, 6, 12), 1 case of parathyroid cyst (3), 1 case was caused by autoantibody of calcium sensitive receptor (9)], SLE with PTHrP elevation in 3 cases (2, 15, 17); 1 case may be caused by false negative PTHrP (11), 2 cases may be caused by anti-PTHrP (4, 8), 5 cases may be caused by PTH-related protein and autoantibodies (7, 10, 13, 14, 16), 1 case may be related to the decrease of fibroblast growth factor 23 (5); 10 cases had increased serum creatinine or decreased creatinine clearance (2, 4–7, 9–11, 13, 15), 5 cases had LN (7, 9, 10, 13, 15); 7 cases had SLE variants, which were described as hypercalcemia-lymphedema Syndrome, characterized by hypercalcemia and serositis (4, 8, 13–17). Among them, 1 case was positive for PTHrP by lymph node biopsy (15); 6 cases were complicated with ectopic calcification (2–4, 9, 10, 13,…”

“…Among them, 1 case was positive for PTHrP by lymph node biopsy (15); 6 cases were complicated with ectopic calcification (2–4, 9, 10, 13, 17). There were 1 case of SLE complicated with tumors (12); 2 cases died, one died of hypercalcemia crisis (1), the other died of refractory septic shock (9); 11 cases of hypercalcemia were effective by glucocorticoid therapy (2, 4, 5, 7, 8, 10, 11, 13–15, 17), 2 cases were ineffective by glucocorticoid therapy (1, 16); after surgical excision of parathyroid gland, blood calcium returned to normal in 3 cases (3, 6, 12) (Table 1).…”

Primary tumor (tumoral) calcification is a rare disease in the practice of a rheumatologist and orthopedist: experience with the use of an interleukin-1 inhibitor in combination with surgical correction

“…Первичный кальциноз -это заболевание с аутосомно-рецессивным типом наследования, которое связано с мутациями в одном из генов, регулирующих фосфорный гомеостаз, -FGF23, Klotho-1 и GALNT3 [2,[9][10][11]. Вторичный опухолевый кальциноз является следствием нарушенной функции почек (кальциноз при хронической почечной патологии) [12][13][14], развивается при иммунопатологических заболеваниях (дерматомиозит) [15], нарушениях фосфорно-кальциевого обмена [16,17].…”