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PubMed1986

Colchicine suppression of local inflammation due to calcinosis in dermatomyositis and progressive systemic sclerosis.

Two girls, one with progressive systemic sclerosis and a second with dermatomyositis, developed calcinosis in the skin of the prepatellar area. Calcinosis was accompanied by local inflammation and skin ulceration. Oral colchicine therapy in a dosage of 1 mg per day was followed within two months by significant regression of local inflammation and healing of the skin ulcers.

Administration, Oral↗
PubMed1985

[Post-phlebitis cutaneous calcinosis. Histochemical study].

A case of cutaneous localized calcinosis of the left upper limb is reported and classified as dystrophic calcinosis because the antecedent of superficial phlebitis. This kind of manifestation is rare in relationship with the frequence of superficial inflammatory processus of veins.

Adolescent↗
PubMedDate not supplied

[Calcinosis universalis associated with dermatomyositis. A report on five cases (author's transl)].

Five patients with dermatomyositis developed calcinosis universalis, the calcinosis lesions being diffuse in three cases and localized to a subcutaneous site in the other two. The diffuse lesions developed in young subjects with severe dermatomyositis, and increased progressively during recovery from the muscle disease. Treatment was ineffective. Subcutaneous calcifications can be detected at an early stage by technetium pyrophosphate scintigraphy, while the fluid nature of the swellings due to a local inflammatory reaction is proved by ultrasonography. Good results are obtained after excision of those calcified masses requiring removal because of their size, site, or superinfection.

Adolescent↗
PubMed1983

Tumoral calcinosis in an infant. A case report.

An unusual calcified soft tissue mass in the knee of an 18-month-old black male infant proved to be tumoral calcinosis. A relatively rare disorder of unknown etiology, this is one of the few reported cases of its occurrence in the knee. The diagnosis is one of exclusion. Because of their radiographic similarity, the differential diagnosis includes intracapsular and paraarticular chondroma, traumatic myositis ossificans, and calcinosis circumscripta.

Calcinosis↗
PubMed1984

Tumoral calcinosis. Report of a case in a one-year-old child.

Tumoral calcinosis is a rare disease known as a progressively growing mass of calcific deposit at a periarticular area. The youngest reported case was the occurrence of the disease in a three-year-old child. This report describes tumoral calcinosis in the area of the knee in a one-year-old child and presents a brief review of the literature. As is usually the case, the blood chemistry was normal in the patient.

Calcinosis↗
PubMed1984

[Phosphorus metabolism in a case of tumoral calcinosis].

Hyperphosphataemia with levels of 65 mg/l was found in a black African aged 20 with a 10-year history of tumour calcinosis. Levels of blood calcium, plasma ionised calcium, serum alkaline phosphatase, 24-hour urinary calcium and phosphate were all normal, as was renal function. Tubular phosphate reabsorption (TmP) was greater than 90 mg per litre of glomerular filtrate (N = 22-42). Levels of circulating parathyroid hormone, nephrogenic cAMP and serum vitamin D metabolites [25 OH D3, 24,25 (OH)2 D3 and 1,25 (OH)2 D3] were normal. The TmP fell by 36% on exogenous PTH stimulation (N = 30.25 +/- 6.7), and by 7.9% 120 min. after injection of acetazolamide. Our results confirm the conclusions of recent studies: patients with tumour calcinosis have disordered renal phosphate excretion with normal PTH secretion, normal PTH action on the renal tubule and normal vitamin D metabolism. In fact in these hyperphosphataemic patients, circulating 1,25 (OH)2 D3 levels would be expected to be low, whereas they were normal in our patient. An attempt at treatment with acetazolamide and phosphate chelating agents gave no significant results.

Acetazolamide↗
PubMed1995

[Tumoral calcinosis--a rare benign calcification of soft tissue].

Tumoral calcinosis is a distinct entity, which is rarely seen in Europe and North America but much more common in black Africans. Typical symptoms are calcified nodules, which grow while remaining asymptomatic and are found in the tissues adjacent to the large joints of the body. Histologically there is collagen necrobiosis initially, which results in aggregates of densely calcified material. The aetiology is unknown, but the condition is probably a form of dystrophic calcification caused by mechanical injury. The patient is suffering from tumoral calcinosis is presented by the authors and they are describing the clinical and histological findings.

Amputation, Surgical↗
PubMed1993

Familial tumoral calcinosis. A clinical, histopathologic, and ultrastructural study with an analysis of its calcifying process and pathogenesis.

We describe histopathologic and ultrastructural changes in tumoral calcinosis (TC) occurring in seven siblings from a single family. Tumoral calcinosis appears to be triggered by bleeding followed by aggregation of foamy histiocytes. These in turn are transformed, with participation of collagenolysis, into cystic cavities lined by osteoclast-like giant cells and histiocytes--the lesion resembling adventitious bursae. Movement and friction, forces generated from the periarticular location of the TC lesions, putatively are key to this transformation. Concomitantly, two calcifying events develop, possibly driven by concurrent hyperphosphatemia or endogenous hypervitaminosis D. One occurs on membranous fragments in antiprotease-containing large cytoplasmic vesicles within osteoclast-like giant cells and mononuclear cells lining the TC cavities; the second, in the TC locules on membranous and cellular debris derived from cavity-lining cells and erythrocytes. The TC cavities ultimately fill with calcified material, losing their synovial-like lining, become encapsulated by fibrous tissue, and ossify. Hydroxyapatite may gain entrance to capillary lumens and embolize to the lung. We conclude that TC represents a disordered reparative process that often is exaggerated because episodes of bleeding, caused by TC-induced vascular injury, provoke development of new lesions. The capricious response of TC to treatment is correlated with its morphologic features.

Adult↗
PubMed1993

Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients.

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.

Aluminum↗
PubMed1993

Combined modality treatment for tumoral calcinosis.

Tumoral calcinosis is a rare syndrome marked by periarticular and intramuscular calcifications. We present the case of a 13-year-old black girl who has received treatment since age 2 for tumoral calcinosis with bilateral shoulder involvement.

Calcinosis↗
PubMed1977

[Age and features of atherosclerosis and primary calcinosis of the tunica media of the major arteries of the pelvis and lower extremities (morphometric study)].

Morphometrical studies were done on 432 longitudinally dissected arteries of the pelvis and lower extremities from 216 fatalities in the age of over 40 years (151 men, 65 women). The atherosclerotic process was found to develop and progress most intensively in the common iliac and popliteal arteries, the third place in the average area of the intima involvement belonging to the femoral artery, while the external iliac and posterior tibial arteries were less affected. In one third of the arteries examined the primary calcinosis of tunica media was found. An inverse relationship between the area of atherosclerotic changes in the intima and the area of primary calcinosis in the media of the vessels was demonstrated. In the lower extremities arteries the fibrinoplastic type of morphogenesis of atherosclerosis was predominant and "complicated" lesions were relatively rare. These data may be the basis for specification of the morphological diagnosis of atherosclerosis and for selection of rational surgical treatment.

Adult↗
PubMed1997

Massive dystrophic calcinosis cutis secondary to chronic needle trauma.

Extensive dystrophic calcinosis cutis of the hips and anterolateral thighs in a woman with insulin-dependent diabetes mellitus is described. Clinical, histologic, and radiographic data are provided to familiarize the reader with this unique and newly described condition. We speculate that repetitive, chronic, needle trauma in susceptible persons can induce massive dystrophic calcinosis cutis.

Aged↗
PubMed1997

[Mitral valve fibrous ring calcinosis in ischemic heart disease].

Calcinosis of the mitral fibrous ring (CMFR) was detected echocardiographically in 11.7% of the examinees with ischemic heart disease (IHD) at the age over 60 years. In CMFR the mitral opening significantly narrows, maximal transmitral diastolic gradient rises, mitral regurgitation becomes more pronounced. In one-third of the patients calcinosis involves the posterior wall disturbing its kinematics. Narrowing of the mitral opening in IHD patients accompanying CMFR is considered to be moderate nonvalvular mitral stenosis.

Aged↗
PubMed1976

Tumoral calcinosis and Engelmann disease.

Four cases of Engelmann disease were observed in a dominant inheritance pattern in a family of St. Landry Mulattoes. In the youngest sibship, one of the cases also had tumoral calcinosis. Another sib had only tumoral calcinosis, though some findings suggested that this sib may also have had Engelmann disease. All 3 of the younger sibs had snow-capped teeth. It is suggested by this family that snow-capped teeth may be part of the syndrome of Engelmann disease.

Bone Diseases, Developmental↗
PubMed1998

Regression of massive tumoral calcinosis of the ischium in a dialysis patient after treatment with reduced calcium dialysate and i.v. administration.

BACKGROUND: Tumoral calcinosis, an inherited metabolic disorder, has been described with increasing frequency over the last 20 years [Drueke 1966]. It is characterized by massive calcium phosphate deposits in periarticular tissues, usually around large joints, especially the hips, knees and elbows (editorial in Lancet 1987). PATIENT AND METHOD: We describe a 58-year-old male patient with tumoral calcinosis of the ischium and severe hyperparathyroid bone disease, successfully treated with reduced calcium dialysate and vitamin D. CONCLUSION: We believe that in cases of tumoral calcification with histologically proven hyperparathyroid bone disease, lowering the calcium dialysate concentration together with careful administration of vitamin analogs and monitoring of serum calcium, phosphate and parathyroid hormone levels, may be the ideal therapeutic approach. Control of hyperphosphatemia would be best achieved with measures other than administration of aluminium phosphate binders if one wishes to avoid the induction of adynamic bone.

Calcinosis↗
PubMedDate not supplied

Diffuse pulmonary calcinosis and multiple soft tissue calcification in renal failure patient with pathological femoral fracture.

The rare occurrence of diffuse pulmonary calcinosis is described with case illustration of a patient who presented with a pathological femoral fracture during end-stage renal failure. Associated metastatic soft tissue calcification with parathyroid hyperplasia requiring parathyroidectomy was observed. Roentgenologic evidence of hyperparathyroidism with osteitis fibrosa cystica and a high product of the calcium and phosphate values were indications for the parathyroidectomy. Recent literature review of pulmonary calcinosis and multiple soft tissue calcification is also presented.

Calcinosis↗
PubMed1995

Tumoral Calcinosis in Infancy. A light and electron microscopic study with X-ray microanalysis.

The most frequent form of idiopathic calcinosis is tumoral calcinosis (TC) which rarely occurs at young ages. We describe here a TC case of a young boy with its light microscopy completed with electron microscopic examinations. X-ray microanalysis revealed in the intracellular crystals CaCl2 besides the previously described hydroxyapatite. The significance of this finding is unknown at the moment.

Journal Article↗