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PubMed2006

Glomerular and tubular basement membrane calcinosis: case report and literature review.

Nephrocalcinosis most commonly manifests as renal calculi or deposition within the tubulointerstitial compartment. Conversely, calcium deposition within glomeruli is extremely rare. We present the case of a 50-year-old man with multiple medical problems, including hepatitis C, diabetes, hypertension, proteinuria, and chronic renal failure. Renal biopsy showed impressive calcium deposits along glomerular basement membranes and tubular basement membranes, within intracellular organelles, and in the interstitium in the setting of a normal serum calcium level. Seven months after biopsy, the patient is on hemodialysis therapy. Although serological and medical examination failed to show a treatable cause for this patient's glomerular calcinosis, individual case reports in the literature have described resolution of calcinosis-associated nephrotic syndrome with treatment of the primary cause of hypercalcemia.

Basement Membrane↗
PubMed1981

Tumoral calcinosis in an infant.

Tumoral calcinosis is a disease characterized by large, calcified, painless masses, usually near joints, in otherwise healthy children and young adults. Biochemical findings are normal except for an association with hyperphosphatemia. A familial and racial predisposition is seen, with most cases affecting blacks. This disease is believed to represent an unknown inherited abnormality in phosphate metabolism. Because of the tendency of the masses to recur after incomplete excision, the recommended treatment is early and complete excision. Phosphate binders may be useful in certain cases.

Adolescent↗
PubMed1990

New insights into idiopathic infantile arterial calcinosis. Three patient reports.

We describe the occurrence of idiopathic infantile arterial calcinosis in three newborn siblings. Unusual features in this disease include ultrasonographic prenatal diagnosis in the second two siblings and ultrastructural studies of the third patient that might shed light on the pathophysiologic characteristics of this disease. Ruthenium-red staining for proteoglycans showed a clearly abnormal structure for the granules in areas of calcification. The granules appeared disorganized, with loss of their normal honeycomb interconnections. They also varied in size and density. In addition, matrix vesicles that might serve as nucleation sites for crystalline calcium phosphate were observed in zones of calcification.

Adult↗
PubMed1993

Tumoral calcinosis. Controversies in the etiology and alternatives in the treatment.

OBJECTIVE: To examine our experience and review the literature concerning the diagnosis, origin, and treatment of tumoral calcinosis (TC). DESIGN/SETTING: Case series based on patients with TC treated in University of California-San Francisco hospitals from 1981 to 1992 and the review of the patients described in the English-language literature. PATIENTS: The study included a total of 17 patients: 10 women and seven men. MAIN OUTCOME MEASURES: Sex, age, origin, symptoms, localization, treatment, and morbidity. RESULTS: Seven men and six women, from 32 to 62 years of age, had known disorders of calcium metabolism, and four women, from 37 to 84 years of age, did not. The main causes of the calcium metabolic disorder were secondary hyperparathyroidism in 11 patients (85%) and primary hyperparathyroidism in two patients. In three patients there was a history of trauma at the involved site and in one patient the origin was unknown. Swelling and pain are the most common presenting complaints. Generalized pruritus was observed in 54% of the patients with metabolic disorders (P < .001) but not in patients without metabolic disorders. Among our patients with metabolic disorders, TC occurred most frequently at the shoulder (46%) and elbow (31%). Eleven patients with secondary hyperparathyroidism had received calcium carbonate to bind phosphate, a high level of calcium in the dialysate, and calcitriol (1,25-vitamin D) either orally, intravenously, or both, and three received epoetin alfa (Epogen). Following parathyroidectomy, the patients with hyperparathyroidism improved symptomatically, although calcifications did not change in size. One patient had the calcifications resected and did well, whereas another was treated by subtotal resection and had a recurrence 3 years later. All four of our patients without a metabolic disorder had complete resection of TC with no recurrence. CONCLUSION: We believe TC is becoming more common in uremic patients with secondary hyperparathyroidism because of recent changes in the medical treatment of these patients. The increased use of calcium carbonate to bind phosphate as well as calcitriol and calcium to suppress parathyroid function and possibly epoetin alfa are causing more patients to develop TC.

Adult↗
PubMed1982

Gamma-carboxyglutamate excretion and calcinosis in juvenile dermatomyositis.

Proteins containing gamma-carboxyglutamic acid (Gla) are present in subcutaneous calcifications of adults with dermatomyositis or scleroderma. Sixteen children with juvenile dermatomyositis, including 7 with subcutaneous calcifications, were studied to determine if abnormal synthesis or turnover of Gla-containing proteins occurred. All study children had increased excretion of the amino acid that was greater than that of age- and sex-matched controls. Patients who had juvenile dermatomyositis with calcifications had a 3-fold increase in Gla excretion, and those without calcinosis had a 2-fold increase. Five other children with various connective tissue disorders and subcutaneous calcification had 2-fold increased Gla excretion. Decreased excretion of this amino acid was associated with salicylate therapy (80 mg/kg/24 hours). The data suggest an abnormal turnover of Gla-containing proteins in juvenile dermatomyositis. Metabolism of these proteins may be involved in the pathophysiology of soft-tissue calcification in children.

1-Carboxyglutamic Acid↗
PubMed1987

Tumoral calcinosis presenting as adhesive capsulitis: case report and literature review.

Tumoral calcinosis (TC) is an uncommon disorder characterized by large calcific soft tissue deposits, usually adjacent to large joints. In the past, the etiology was unclear, but recently, TC has been considered to be an inherited metabolic disorder, characterized by elevated serum phosphorus and 1,25-dihydroxyvitamin D levels, normocalcemia, and calcific deposits. However, these features have been shown to vary widely, with formes frustes of TC now being recognized. We report an unusual case of TC, which presented as an adhesive capsulitis, in an elderly North American black woman. The patient's nationality, late age of presentation, and multiple sites of involvement are uncommon features of TC. The clinicopathologic features and possible etiologies of this rare condition are briefly reviewed.

Age Factors↗
PubMed1983

Tumoral calcinosis.

Tumoral calcinosis is an uncommon, usually solitary, tumour-like mass characterized by soft tissue calcification for no apparent reason. Nearly all cases have occurred in negroes, including 2 previously recorded in this country. We report 7 cases seen over a period of 3 years in English caucasian patients and suggest that the condition is not rare but goes unrecognized under a variety of guises. Three of these 7 patients, 2 of whom were on haemodialysis for renal failure, had isolated hyperphosphataemia, which is the only aetiological factor detected so far. Surgical excision appears to be the only effective treatment.

Adult↗
PubMed1984

Scrotal calcinosis: calcification of epidermal cysts.

The so-called idiopathic scrotal calcinosis does not appear to be idiopathic, but rather a process of dystrophic calcification of epidermal cysts. We report a case that would be otherwise called "idiopathic" where we found squamous epithelial lining around the calcified masses. Literature is reviewed in support of the view that the calcified scrotal nodules are related to epidermal cysts.

Adult↗
PubMed2001

Bilateral striopallidodentate calcinosis: clinical characteristics of patients seen in a registry.

Clinical features in bilateral striopallidodentate calcinosis (BSPDC), popularly referred to as Fahr's disease (five autosomal dominant families and eight sporadic cases, n = 38), recruited through a registry, are reported. Applying uniform criteria, cases reported in the literature (n = 61) were combined for detailed analysis. The mean (+/- S.D.) age of Registry patients was 43 +/- 21 and that of literature was 38 +/- 17. In combined data set (n = 99), 67 were symptomatic and 32 were asymptomatic. Of the symptomatic, the incidence among men was higher compared with women (45:22). Movement disorders accounted for 55% of the total symptomatic patients. Of the movement disorders, parkinsonism accounted for 57%, chorea 19%, tremor 8%, dystonia 8%, athetosis 5%, and orofacial dyskinesia 3%. Overlap of signs referable to different areas of central nervous system (CNS) was common. Other neurologic manifestations included: cognitive impairment, cerebellar signs, speech disorder, pyramidal signs, psychiatric features, gait disorders, sensory changes, and pain. We measured the total volume of calcification using an Electronic Planimeter and Coordinate Digitizer. Results suggest a significantly greater amount of calcification in symptomatic patients compared to asymptomatic patients. This study suggests that movement disorders are the most common manifestations of BSPDC, and among movement disorders, parkinsonism outnumber others.

Adult↗
PubMed1999

Chromosomal localization of the loci responsible for dystrophic cardiac calcinosis in DBA/2 mice.

Dystrophic cardiac calcinosis (DCC) occurs in certain inbred strains of mice, including DBA/2 and C3H/He, and is generally found as an incidental lesion in adult animals at necropsy. Preliminary genetic studies into the cause of DCC have been performed in DBA/2 mice and suggest that DCC is inherited as an autosomal recessive trait involving three or four unlinked genes. To investigate the genetics of DCC further, we produced myocardial cell death by freeze-thaw injury to induce DCC. Experiments were conducted with three F1 hybrids made using three inbred strains of mice (DBA/2J and C3H/HeJ, DCC-susceptible strains; C57BL/6J, DCC-resistant strain) to compare the genetic factors in the development of DCC. We found that DBA/2 and C3H/He mice share the same gene pattern(s) that is responsible for DCC. We determined by backcross linkage analysis in DBA/2 and C57BL/6 mice that at least one recessive locus is responsible for DCC. A haplotype analysis of the backcross data demonstrated that the recessive locus, designated dyscalc1, is located on Chromosome 7, 20.5 cM distal to the centromere. The likely candidate genes for dyscalc1 are discussed. Further understanding of the structure and function of these mutant genes will be beneficial in explaining the molecular pathogenesis of DCC.

Animals↗
PubMed1995

Tumoral calcinosis.

A patient with tumoral calcinosis involving the buttock and ischial bone is presented. Bone marrow involvement and a pattern of septal enhancement on MR imaging after intravenous administration of Gd-DTPA were very suggestive of a diagnosis of a chondro(sarco) matous musculoskeletal tumor. The absence of an underlying metabolic disorder, the appreciation of fluid-calcium levels within the lesion and knowledge of the macroscopic and microscopic appearance of this disorder have led to the correct diagnosis in this case.

Bone Diseases↗
PubMed1979

Tumoral calcinosis: accumulation of bone-seeking tracers in the calcium deposits.

Rapid and preferential uptake of 47 calcium 87m Strontium by the multinodular calcareous masses was seen in a patient with tumoral calcinosis. Using 87m Strontium, scintigraphic imaging of the tumors was achieved, while the skeleton was barely visible. More intense accumulation of 87m Sr. in one tumor suggested a higher rate of calcium depostion. This was in agreement with the observation that this tumor showed less tendency to decrease in size during calcium and phosphorus deprivation therapy. Quantitative measurements of the uptake of bone seeking tracers by the tumors may be of value in estimating calcium turnover in the calcified masses.

Calcinosis↗
PubMed1984

Crystal-phagocyte interaction in calcinosis interstitialis.

Based on recent findings indicating the stimulation of the respiratory burst in human neutrophils by crystal phagocytosis, ectopic calcified nodules of a patient with calcinosis interstitialis were exposed to autologous granulocytes and monocytes in vitro. The activity of the respiratory burst was determined by luminol-enhanced chemiluminescence. Controls included amorphous monosodium urate, microcrystalline monosodium urate, hydroxyapatite, and zymosan. Microcrystalline monosodium urate elicited a marked stimulation of both granulocytes and monocytes as did hydroxyapatite in granulocytes. Hydroxyapatite caused no stimulation of monocytes, possibly reflecting selective functional modulation. On the other hand, amorphous monosodium urate failed to induce a respiratory burst with granulocytes or monocytes. Likewise, the contents of the nodule evoked only marginal stimulatory activity on the phagocytes. Stimulation by zymosan was normal with both cell types. The finding that material of the excised nodule failed to induce a respiratory burst in phagocytes may explain the lack of inflammatory reaction in vitro around the nodules on histologic examination, particularly since products of stimulated phagocytes have been described as causing tissue destruction.

Adolescent↗
PubMed1984

Calcinosis universalis associated with tuberculosis.

A 12-year-old girl with clinical evidence of abdominal tuberculosis also had a widespread soft tissue calcification termed calcinosis universalis. Despite antituberculous therapy the patient died and autopsy confirmed tuberculous peritonitis. No cause could be found for the soft tissue calcification. The co-existence of the two diseases is probably incidental.

Abdomen↗
PubMed1996

Pulmonary gallium-67 uptake in diffuse pulmonary calcinosis.

Diffuse pulmonary uptake of both technetium-99m- labeled methylene diphosphonate (99(m)Tc-MDP) and gallium (67Ga) citrate was noted in a patient with chronic renal failure and indicated the presence of pulmonary calcinosis. The uptake of 67Ga could be misinterpreted to represent abnormal uptake due to an opportunistic infection.

Adolescent↗
PubMedDate not supplied

Tumoral calcinosis.

Tumoral calcinosis is an interesting clinical entity. It is not uncommon in certain countries. We report our experience with 22 patients with this condition seen over a 7-year period and review in detail the modalities of clinical presentation, theories of etiogenesis, histological appearances, and treatment modalities.

Adult↗
PubMed1991

Calcinosis cutis, osteoma cutis, poikiloderma and skeletal abnormalities (COPS syndrome)--a new entity?

A 4-year-old boy with subcutaneous tumours is described. These tumours were calcified and had secondary osteoma formation. In addition the patient showed poikiloderma on the face and less prominently on arms and legs. X-ray films of the distal metaphyses of the radius, ulna and tibia revealed irregular mineralisation. Repeated laboratory tests revealed no abnormalities of fat, bone and mineral metabolism. This patient showed a unique combination of symptoms. We propose to call this syndrome: COPS-syndrome (Calcinosis cutis, Osteoma cutis, Poikiloderma and Skeletal abnormalities).

Bone Neoplasms↗