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PubMed1996

Tumoral calcinosis in the upper cervical spine: a case report.

STUDY DESIGN: An elderly women with tumoral calcinosis between the C1 posterior arch and the C2 lamina is reported. OBJECTIVES: To describe a rare occurrence of tumoral calcinosis in the spine and discuss its pathomechanism. SUMMARY OF BACKGROUND DATA: Tumoral calcinosis is a rare condition occurring predominantly in the juxtaarticular regions of the extremities. Involvement of the spine has been reported in only one case in the lumbar spine. The calcium phosphate crystals that have been identified are those of hydroxyapatite. METHODS: The calcified material was removed, and its crystalline phase was analyzed. RESULTS: Neck pain was relieved by removal of the calcified material. Scanning electron microscopy and energy-dispersive x-ray microanalysis revealed that the material consisted of crystals of calcium pyrophosphate dihydrate. CONCLUSIONS: Tumoral calcinosis should be included among the clinical presentations of calcium pyrophosphate dihydrate crystal deposition disease.

Aged↗
PubMed1993

Calcinosis cutis in juvenile dermatomyositis responsive to aluminum hydroxide treatment.

Calcinosis cutis is a frequent complication of juvenile dermatomyositis; however, its treatment remains unsatisfactory. We report a case of calcinosis cutis in juvenile dermatomyositis which was successfully treated with oral aluminum hydroxide. Almost complete clearing of calcinosis was observed after 8 months of therapy. There were no adverse effects from therapy. Aluminum hydroxide is worth trying in treating calcinosis cutis.

Administration, Oral↗
PubMed1999

Two cases of gigantic dystrophic calcinosis cutis caused by subcutaneous and/or intramuscular injections.

We describe two female patients with gigantic dystrophic calcinosis cutis caused by a large number of subcutaneous and/or intramuscular injections which they received when they were much younger. Laboratory data and physical examinations were generally within normal limits, and we detected no disease which might induce cutaneous calcification. There are many reports of dystrophic calcinosis cutis caused by injection of several kinds of drugs. However, we found no previous report describing a patient with calcinosis cutis induced by local tissue injury from a large number of injections and with extraordinarily widespread calcification at the injection sites. Because we do not know the exact drugs injected, it is difficult to say if a specific ingredient in the injections was related to this condition. We do know that a large number of subcutaneous or intramuscular injections were frequently administered to patients who had difficulty in maintaining venous infusions in the past, so there may be similar cases of dystrophic calcinosis cutis which have not been reported.

Aged↗
PubMed2006

Calcinosis cutis of the fingertip associated with Raynaud's phenomenon.

Cutaneous calcification may be divided into four major categories: (i) dystrophic; (ii) metastatic; (iii) idiopathic; and (iv) iatrogenic. Dystrophic calcification is the most common type of calcinosis cutis and is associated with a variety of diseases. It most notably occurs in connective tissue diseases. Diffuse and limited cutaneous systemic sclerosis is an example of connective tissue diseases that frequently show calcinosis. We experienced a case of fingertip calcinosis cutis associated with Raynaud's phenomenon. The patient had no previous trauma, skin lesion or systemic connective tissue disease. We propose that calcinosis cutis of the fingertip may result from chronic ischemic injury caused by Raynaud's phenomenon.

Adult↗
PubMed2005

Generalized calcinosis cutis associated with probable leptospirosis in a dog.

A 6.5-year-old male German Shepherd acutely developed renal and hepatic disease. Serology revealed high concentrations of antibodies against Leptospira copenhageni, and a presumptive diagnosis of leptospirosis was made. The dog was successfully treated with antibiotics and supportive care over a 12-day period. Sixty-two days after the initial presentation, alopecia predominantly involving the dorsum and perineal areas developed. The skin lesions expanded over a 20-day period. Histology revealed generalized calcinosis cutis with follicular atrophy. An injection of 0.01 mg kg-1 dexamethasone suppressed serum cortisol concentrations. No treatment was given and lesions resolved over the following 30 days. This is the third case of generalized calcinosis cutis that has developed in an adult dog after severe systemic disease. Both previous cases developed calcinosis cutis in association with blastomycosis. To the authors' knowledge, this is the first report of generalized calcinosis cutis in an adult dog in association with a presumptive bacterial infection.

Animals↗
PubMed1997

Calcinosis cutis presenting years before other clinical manifestations of juvenile dermatomyositis: report of two cases.

Calcinosis cutis in dermatomyositis is dystrophic calcification appearing late in the course of the disease. Two cases are reported here of calcinosis cutis that presented years before other clinical manifestations of juvenile dermatomyositis. The first case was a 14-year-old Thai girl who had asymptomatic subcutaneous nodules that spontaneously ruptured, exuding a chalky discharge and healing with an atrophic scar 8 years before the onset of other clinical manifestations of juvenile dermatomyositis; that is, Gottron's papules, proximal muscle weakness grade IV/V with atrophy, slightly elevated serum creatinine phosphokinase level and an abnormal electromyogram compatible with myopathy. The second case was a 15-year-old Thai boy who had calcinosis cutis 3 years before the onset of other clinical manifestations of juvenile dermatomyositis, and the calcinosis cutis was so severe that it interfered with the movement of his extremities. Both cases responded well to aluminium hydroxide therapy.

Adolescent↗
PubMed2006

Calcinosis cutis: a complication of intravenous administration of calcium glucanate.

Calcinosis cutis, the deposition of calcium in the dermis, can be dystrophic, metastatic, iatrogenic, or idiopathic. Here, we describe a case of iatrogenic calcinosis cutis secondary to extravasation of an intravenous calcium-containing solution in a child. We also review the literature regarding the pathogenic mechanisms involved in the development of calcinosis cutis after extravasation injuries. While iatrogenic calcinosis cutis is generally a benign entity, it is important to recognize its unique clinical and histopathologic presentation to avoid complications from misdiagnosis.

Calcinosis↗
PubMed1998

Successful treatment of tumoral calcinosis using CAPD combined with hemodialysis with low-calcium dialysate.

Successful treatment of tumoral calcinosis using continuous ambulatory peritoneal dialysis (CAPD) combined with hemodialysis is described. A 32-year-old male patient with a 2-year history of CAPD rapidly developed multiple metastatic calcification (tumoral calcinosis) adjacent to his fingers, elbows, and knee joints. Tests showed severe hyperphosphatemia, moderate hypercalcemia, and increased Ca-P product without elevation of intact parathyroid hormone. An enlarged parathyroid gland was not found by echography. In order to rapidly lower the excessive Ca and P levels, a combined therapy with CAPD and vigorous transient hemodialysis using a low-Ca dialysate was performed. In parallel, the patient was given calcitonin, bisphosphonate, and short-term Al to ameliorate the metastatic calcifications more effectively. The result was dramatic with disappearance of the tumoral calcinosis as well as improvement in subjective symptoms within a few months. The present case suggests that combined therapy with hemodialysis and CAPD using a low-Ca dialysate, together with Ca-modulating agents, can be effective in ameliorating tumoral calcinosis in patients on CAPD.

Adult↗
PubMed1988

Evaluation of vascular calcinosis risk factors in patients on chronic hemodialysis: lack of influence of calcium carbonate.

UNLABELLED: Linear calcifications of the abdominal aorta and of the iliac and femoral arteries were measured yearly for 3 years on X rays of 24 patients on chronic hemodialysis taking variable amounts of calcium carbonate and Al(OH)3 but no pharmacological doses of vitamin D or 1 alpha-hydroxylated vitamin D derivatives. The speed of their extension appeared exponential and covariant with the male sex, age only for men and, independently of these two factors, with diastolic blood pressure and blood triglycerides. Plasma concentrations of calcium, phosphate and glucose were covariant with the extension of calcinosis only at a borderline level. The doses of calcium carbonate and the levels of plasma alkaline phosphatase were not at all covariant. CONCLUSIONS: (1) The effect of high doses of calcium carbonate is possibly harmful only when supraphysiological levels of plasma calcium are induced, whereas plasma phosphate is not adequately decreased. The doses of calcium carbonate per se have no deleterious effect (2). Since alkaline phosphatase is not covariant with the extension of calcinosis, the degree of hyperparathyroidism per se does not seem to play a causative role in vascular calcinosis (3). The main risk factors of vascular calcinosis are: age, the male sex, diastolic blood pressure and blood triglycerides.

Adult↗
PubMed1992

Clinical appraisal of vinpocetine for the removal of intractable tumoral calcinosis in haemodialysis patients with renal failure.

Previous studies have shown that vinpocetine [14-ethoxycarbonyl-(3 alpha, 16 alpha-ethyl)-14,15-eburnamenine] scavenges minerals and/or metals in the soft tissues of rabbits with artificially induced arteriosclerosis. The present study was carried out to determine whether or not vinpocetine would bring about the removal of intractable tumoral calcinosis in haemodialysis patients with renal failure. After administration of 15 mg/day vinpocetine for 3-12 months in haemodialysis patients with X-ray evidence of tumoral calcinosis, calcinosis was completely eliminated in all eight cases. Serum alkaline phosphatase and bone osteocalcin concentrations tended to decrease after treatment with vinpocetine compared with before treatment. Vinpocetine thus appears to be an effective scavenger of tumoral calcinosis in haemodialysis patients with renal failure without any side-effects during treatment.

Adult↗
PubMed2005

A novel GALNT3 mutation in a pseudoautosomal dominant form of tumoral calcinosis: evidence that the disorder is autosomal recessive.

Familial tumoral calcinosis is a rare metabolic disorder, characterized by ectopic calcification and hyperphosphatemia. Recently biallelic mutations in the GalNAc transferase 3 (GALNT3) gene were identified in two families with tumoral calcinosis. In the present study, we performed mutation analysis of the GALNT3 gene in a multigenerational family, which was originally described to have an autosomal dominant form of tumoral calcinosis. We identified a novel splice site mutation in intron 1 (IVS1-2a-->t), likely leading to skipping of exon 2. The proband was a compound heterozygote for the splice site mutation and the previously reported nonsense mutation (484C-->T; R162X). His affected maternal great uncle was homozygous for the splice site mutation. Biallelic mutations found in two generations demonstrated that the family had pseudoautosomal dominant inheritance, confirming that tumoral calcinosis is in fact an autosomal recessive trait. However, genetic and biochemical findings suggest that carriers of a single mutation may also manifest subtle biochemical abnormalities. Furthermore, coexpression of GALNT3 and fibroblast growth factor 23 (FGF23), a key regulator of phosphate homeostasis, in certain tissues suggests that O-glycosylation of FGF23 by GALNT3 may be necessary for proper function of FGF23.

Calcinosis↗
PubMed1980

Phosphorus excretion in tumoral calcinosis: response to parathyroid hormone and acetazolamide.

The cause of hyperphosphatemia in patients with tumoral calcinosis never been explained. We studied two related patients who had tumoral calcinosis and hyperphosphatemia and two normal controls to determine their renal tubular response to parathyroid hormone (PTH) and acetazolamide (ACZ). During baseline periods, the patients had abnormally low fractional excretion of phosphorus (FEP) despite their hyperphosphatemia. Values for patients were 0.114 and 0.128; for controls, values were 0.193 and 0.165. PTH caused an increase in FEP and urinary cAMP in both patients and controls. ACZ also increased FEP in both groups, and the effects of PTH and ACZ were additive, suggesting that patients with tumoral calcinosis have normal sensitivities to PTH and normal responses to ACZ. Levels of vitamin D metabolites in the patients were normal. We conclude that patients with tumoral calcinosis have a reduced ability to excrete phosphorus. This defect does not seem to be due to impaired PTH secretion, an abnormal phosphaturic response to this hormone, or a disturbance of vitamin D metabolism.

Acetazolamide↗
PubMed1988

Correlations of serum concentrations of 1,25-dihydroxyvitamin D, phosphorus, and parathyroid hormone in tumoral calcinosis.

The inherited metabolic disorder tumoral calcinosis is characterized by elevated serum phosphorus and 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels and paraarticular calcific tumors. The pathogenesis of this disease is obscure, but an elevated renal phosphate reabsorption threshold and increased production of 1,25-(OH)2D are postulated as defects. We studied nine affected patients and found that both serum phosphorus and renal phosphate reabsorption threshold (TmP/GFR) were positively correlated with serum 1,25-(OH)2D levels. Since tumoral calcinosis is a disorder with abnormal renal phosphate transport, we compared the TmP/GFR and serum 1,25-(OH)2D levels to values obtained in patients with two other diseases with renal phosphate transport defects: oncogenic osteomalacia and X-linked hypophosphatemic rickets. We found a significant correlation between TmP/GFR and 1,25-(OH)2D levels in all three diseases, suggesting that in these diseases 1,25-(OH)2D production is regulated in some manner by phosphate transport. Furthermore, previous work indicated that in tumoral calcinosis broad variation exists in serum phosphorus levels. In our patients a negative correlation was found between the serum PTH concentrations and both serum phosphorus levels and TmP/GFR values, respectively. We postulate that although the basic defect in tumoral calcinosis most likely resides in the proximal renal tubular cell, the variation in serum phosphorus levels and possibly disease expression is modulated in part by PTH.

Absorption↗
PubMed2005

Early manifestation of calcinosis cutis in pseudohypoparathyroidism type Ia associated with a novel mutation in the GNAS gene.

OBJECTIVE: To clarify the molecular defect for the clinical finding of congenital hypothyroidism combined with the manifestation of calcinosis cutis in infancy. CASE REPORT: The male patient presented with moderately elevated blood thyrotropin levels at neonatal screening combined with slightly decreased plasma thyroxine and tri-iodothyronine concentrations, necessitating thyroid hormone substitution 2 weeks after birth. At the age of 7 months calcinosis cutis was seen and the patient underwent further investigation. Typical features of Albright's hereditary osteodystrophy (AHO), including round face, obesity and delayed psychomotor development, were found. METHODS AND RESULTS: Laboratory investigation revealed a resistance to parathyroid hormone (PTH) with highly elevated PTH levels and a reduction in adenylyl cyclase-stimulating protein (Gsalpha) activity leading to the diagnosis of pseudohypoparathyroidism type Ia (PHP Ia). A novel heterozygous mutation (c364T > G in exon 5, leading to the amino acid substitution Ile-106 --> Ser) was detected in the GNAS gene of the patient. This mutation was not found in the patient's parents, both of whom showed normal Gsalpha protein activity in erythrocytes and no features of AHO. A de novo mutation is therefore likely. CONCLUSIONS: Subcutaneous calcifications in infancy should prompt the clinician to a thorough search for an underlying disease. The possibility of AHO and PHP Ia should be considered in children with hypothyroidism and calcinosis cutis. Systematic reviews regarding the frequency of calcinosis in AHO are warranted.

Calcinosis↗
PubMed2001

Tumoral calcinosis in the upper cervical spine causing progressive radiculomyelopathy--case report.

A 54-year-old woman with chronic renal failure presented with tumoral calcinosis manifesting as progressive radiculomyelopathy. Magnetic resonance imaging revealed a spinal epidural mass in the C-2 to C-4 levels. The clinical and radiological findings suggested malignant tumor. Resection of the lesion was performed with total C-2 laminectomy and C-3 and C-4 laminoplasty. The symptoms totally disappeared after surgery. The histological diagnosis was tumoral calcinosis. Tumoral calcinosis is a rare tumoral calcium pyrophosphate dihydrate crystal deposition disease which presents as periarticular soft tissue calcification. Tumoral calcinosis should be considered in patients with a mass lesion involving the upper cervical spine and associated with metabolic abnormalities. Surgical excision is the treatment of choice, because this is completely curative without known recurrence.

Calcinosis↗
PubMed1981

Calcinosis in dermatomyositis treated with probenecid.

Childhood dermatomyositis is frequently complicated by deposition of calcium salts in the soft tissues. This calcinosis represents a major problem, as severe disability may result. Various drugs have been tried to dissolve the calcinosis, but the results of these trials are disappointing. In this article we present a case report of a 9-year-old girl treated with probenecid. This treatment led to a dramatic decrease in subcutaneous and intermuscular calcinosis. The authors call for controlled studies of probenecid treatment in calcinosis.

Calcinosis↗
PubMedDate not supplied

Ulcerated dystrophic calcinosis cutis secondary to localised linear scleroderma.

Dystrophic calcinosis is a more common form of calcinosis cutis; calcium salts are deposited secondary to local inflammation, tissue damage and degeneration. Various conditions can cause dystrophic calcinosis, including connective tissue disease, infection, inflammatory processes, chronic venous stasis, cutaneous neoplasm and trauma. We report a case of ulcerated cutaneous calcinosis associated with a localised linear scleroderma or morphea. Healing of the ulcerations took place after four months of treatment with colchicine 1 mg per day.

Aged↗
PubMed1975

Ultrastructure of a mixed form of calcinosis.

An unusual form of calcinosis is described presenting a joint occurrence of calcinosis circumscripta and calcinosis universalis. Ultrastructurally, the mineral constituent is of much higher crystallinity than that of normal bone, and includes a rare kind of carbonate apatite. The crystals of the specimen were needle-like and hexagonal, in juxtaposition to normal collagen fibrils. Supposedly, the development of the calcifiable matrix is different in calcinosis and bone tissue.

Apatites↗