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PubMed1992

Calcinosis and the anticentromere antibody: its clinical, radiological and immunogenetic aspects.

The relationship between calcinosis and the anticentromere antibody (ACA) was studied from a clinical, radiological and immunogenetic standpoint. Ten ACA-positive scleroderma patients, 34 ACA-negative scleroderma patients, 31 ACA-positive patients without sclerodermatous skin changes and 140 ACA-negative patients with various rheumatic diseases were compared with regard to the incidence of calcinosis as measured by radiographs of hand and/or foot. Calcinosis was found in 10 (100%), 12 (35%), 13 (42%) and eight (6%) patients in each group respectively. Frequent sites for calcinosis in the ACA-positive patients were foot (24%), hand (21%) and leg (19%). The forearm was not usually involved (6%). During the follow-up term (1.0-9.5 years; mean 4.5 years) of 11 ACA-positive patients without calcinosis, four (36%) developed new calcinosis and this incidence was significantly higher (P less than 0.02) than that in the ACA-negative control group (2/42; 4.8%). As a whole, 23 (59%) of 39 patients with ACA showed calcinosis. In the ACA-positive patients with calcinosis, sclerodactyly (P less than 0.005) and CREST syndrome (P less than 0.001) were found more frequently than in ACA-positive patients without calcinosis. HLA-A2 was found more frequently (67%) in the ACA-positive patients with calcinosis when compared to normal subjects (41%) (P less than 0.02). We concluded that calcinosis seems closely related to scleroderma, especially those with ACA, and that the development of calcinosis requires a certain genetic background.

Antibodies↗
PubMed1996

Proposal for a pathogenesis-based classification of tumoral calcinosis.

BACKGROUND: Deposition of calcium in skin is currently categorized into a group of disorders referred to as calcinosis cutis. Divisions between types and subtypes within this confusing classification are predominantly based on morphologic differences in the calcification and serve to obscure pathogenesis. This is especially evident in a subtype of calcinosis cutis, known as tumoral calcinosis. Calcifications in cases of tumoral calcinosis share the following characteristics, but without evidence of a common pathogenesis: large size, juxtaarticular location, progressive enlargement over time, a tendency to recur after surgical removal, and an ability to encase adjacent normal structures. The goal of this study was to formulate a pathogenesis-based classification for cases of tumoral calcinosis. METHODS: In a literature review 121 cases of tumoral calcinosis were identified. These cases, along with a case evaluated in our clinic, were reviewed retrospectively, and their features compared. RESULTS: Analysis suggests three pathogenetically distinct subtypes of tumoral calcinosis: (1) Primary normophosphatemic tumoral calcinosis: patients have normal serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; (2) primary hyperphosphatemic tumoral calcinosis: patents have elevated serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; and (3) secondary tumoral calcinosis: patients have a concurrent disease capable of causing soft tissue calcification. Justification for this classification is based on the presence or absence of disorders known to promote soft tissue calcification and statistically significant differences in family history, mean calcification number, mean serum phosphate level, and calcification recurrence after excision. CONCLUSIONS: A classification for tumoral calcinosis is devised that outlines potential pathogenetic mechanisms and predicts response to therapy and prognosis. Analysis of other forms of calcinosis cutis may reveal definable pathogenetic differences that suggest a coherent classification for all cutaneous calcinoses.

Adolescent↗
PubMed1992

Staphylococcal infections in childhood dermatomyositis--association with the development of calcinosis, raised IgE concentrations and granulocyte chemotactic defect.

There is a high incidence of staphylococcal infection in children with dermatomyositis, which is limited to those children who either already have or subsequently develop calcinosis. Of 15 children followed up for 3-10 years after diagnosis, all nine who developed calcinosis had infections with Staphylococcus aureus compared with none of six without calcinosis. Of these nine, the occurrence of staphylococcal infections before calcinosis was observed in four, suggested by history in two, and unclear in three children. Granulocyte chemotaxis to Staphylococcus aureus was more severely depressed in those children with calcinosis, whereas those without calcinosis did not differ significantly from controls. The chemotactic defect was due to a serum factor (patients' serum depressed control chemotaxis and control serum corrected the patients' chemotaxis). The nine children with calcinosis also had significantly higher serum IgE concentrations than non-atopic age matched controls; the six without calcinosis did not differ from controls. The increased IgE concentrations appeared to develop after staphylococcal infection and before calcinosis. Two of five patients with calcinosis had increased antistaphylococcal IgE antibodies; neither of the two patients without calcinosis had such increased antibodies. This suggests preceding immunological differences in patients with dermatomyositis who do and do not subsequently develop calcinosis, either increasing susceptibility to Staphylococcus aureus infection or potentially resulting from such infections.

Antibodies, Bacterial↗
PubMed1998

[A case of idiopathic multiple calcinosis cutis].

A case of calcinosis cutis, appeared since childhood in a woman 73-years-old, affected by diabetes mellitus with complications, is described. This uncommon disorder is discussed on the basis of data from recent literature. Calcinosis cutis is a condition characterized by the deposition of crystals of calcium phosphate (hydroxyapatite) in the skin. Calcinosis cutis may be idiopathic or secondary. The idiopathic calcinosis cutis is uncommon, may be solitary or multiple, sporadic or associated with Down syndrome (MICC or "milialike idiopathic calcinosis cutis") and appears more often in childhood or adolescence. Secondary calcinosis cutis may appear in the course of juvenile dermatomyositis or in the form of systemic scleroderma named CREST syndrome (calcinosis cutis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly and telangectasia). Calcinosis cutis may also be seen later in the course of renal failure, associated with hyperphosphatemia and secondary hyperparathyroidism. In this case report, calcinosis cutis appeared early in life and the laboratory data showed normal erythrocyte sedimentation rate and leukocyte count, negative LE test and absence of rheumatoid factor and non-organ-specific auto-antibodies, and multiple localizations. On these grounds, the diagnosis of idiopathic multiple calcinosis cutis was made. This is a rare and benign syndrome, which does not cause any late complication and whose prognosis is therefore favourable.

Aged↗
PubMed2003

[Multi-center analysis of calcinosis in children with juvenile dermatomyositis].

OBJECTIVES: To reveal the frequency and the clinical characteristics of dystrophic calcification that occurs in children with juvenile dermatomyositis, multi-center analysis was constructed. METHOD: Fifty children with JDM were enrolled, and 14 of them (28.0%) were complicated with calcinosis. Clinical symptoms and laboratory tests at onset, initial therapy and disease course were compared in children with and without calcinosis. RESULTS: The mean age of the onset of calcinosis was 4.78 +/- 3.33 years, and it was younger than those of children without calcinosis (8.66 +/- 3.85 years) (P = 0.0017). No differences of clinical manifestation except Gower's sign were observed. The frequency of positive anti-nuclear antibody was 7.1% in children with calcinosis and 52.9% without calcinosis (P = 0.0112). The initial therapy of methylprednisolon pulses gave no effects on prognosis of calcium deposition. The calcinosis appeared in 1.56 +/- 1.91 year after the onset of the disease. The various types of calcium deposition including large tumorous clumps, subcutaneous plaques or nodules, sheet-type calcification were deserved. They appeared over knee joints (64.3%), elbow joint (64.3%), and hip processes (50.0%). Calcinosis affecting the subcutaneous tissues frequently resulted in painful superficial ulceration of the overlying skin (42.9%), local infection (50.0%), and limitation of joint movement (14.3%). Although aluminum phosphate was effective in 2 children among 7, no other effective treatment was recommended. In 5 cases, surgical removal of tumorous clumps was operated. Thus, juvenile dermatomyositis is frequently complicated with calcinosis. This type of calcinosis was found to be unlikely to resolve completely, and resulted in severe disability in children.

Age of Onset↗
PubMed1995

Tumoral calcinosis: radiologic-pathologic correlation.

OBJECTIVE: Tumoral calcinosis is a frequently misdiagnosed disorder. This study details the radiologic and pathologic characteristics of tumoral calcinosis that distinguish it from most other entities. DESIGN: Radiologic and pathologic findings, and medical records of 12 patients with tumoral calcinosis were reviewed and compared with equivalent information about 5 patients with other calcified lesions. PATIENTS: The 12 patients ranged in age from 15 months to 62 years. Six had idiopathic tumoral calcinosis and 6 had secondary tumoral calcinosis. RESULTS AND CONCLUSIONS: A consistent radiologic finding for tumoral calcinosis was a dense calcified mass that was homogeneous except for a "chicken wire" pattern of lucencies, which correlated histologically with thin fibrous septae. Other characteristics of tumoral calcinosis included fluid-calcium levels, demonstrated in four patients, and smooth osseous erosions adjacent to the mass, demonstrated in three patients. Five cases of tumoral calcinosis were originally confused with other calcified lesions; however, the radiologic findings were characteristic of tumoral calcinosis in retrospect.

Adolescent↗
PubMed2001

Tumoral calcinosis of the spine: a study of 21 cases.

STUDY DESIGN: A retrospective study was conducted to investigate 21 patients found during spinal surgery to have paraspinal masses of dystrophic calcification (tumoral calcinosis). OBJECTIVES: To determine the magnetic resonance imaging characteristics of this disorder, and to document the associated spinal pathology. SUMMARY OF BACKGROUND DATA: Tumoral calcinosis usually is associated with hereditary disorders of calcium metabolism or renal dialysis. It also occurs in degenerated tissues in the absence of systemic disorders. Characteristically, calcific masses in the appendicular skeleton are visible on plain radiographs. Tumoral calcinosis has only rarely been reported in the spine. Documented patients have had an obvious calcific mass, and almost always the disorder has existed in other locations as well. Careful histologic study of specimens removed during spinal surgery suggests that tumoral calcinosis is common in the spine and usually is secondary to preexisting pathology. METHODS: This study involved 21 patients with lesions of tumoral calcinosis identified by histopathologic analysis of specimens removed during spinal surgery. The magnetic resonance images and the plain radiographs of the patients were reviewed and correlated with their clinical histories. RESULTS: In all the patients, the lesion of tumoral calcinosis was associated with a mass lesion seen on magnetic resonance imaging. Calcific masses were not apparent on plain films. In no case was the mass diagnosed before surgery as tumoral calcinosis. The magnetic resonance imaging changes were variously misinterpreted as neoplasms, infections, extruded disc material, or cysts. The observed features of tumoral calcinosis were those of an extradural mass showing a heterogeneous mixed-signal lesion that was identical on T1- and T2-weighted images. Characteristically, gadolinium did not enhance the lesions. CONCLUSIONS: Awareness of tumoral calcinosis of the spine may prevent unwarranted diagnoses of a more serious lesion in patients with characteristic magnetic resonance imaging changes. Also, this awareness may prevent pathologists from interpreting lesional tissue as nondiagnostic when other diagnoses are suspected clinically. This process may be a manifestation of degenerative spinal disease that has become so dominant that the underlying processes are obscured.

Adult↗
PubMedDate not supplied

Tumoral calcinosis: pearls, polemics, and alternative possibilities.

Massive periarticular calcinosis of the soft tissues is a unique but not rare radiographic finding. On the contrary, tumoral calcinosis is a rare familial disease. Unfortunately, the term tumoral calcinosis has been liberally and imprecisely used to describe any massive collection of periarticular calcification, although this term actually refers to a hereditary condition associated with massive periarticular calcification. The inconsistent use of this term has created confusion throughout the literature. More important, if the radiologist is unfamiliar with tumoral calcinosis or disease processes that mimic this condition, then diagnosis could be impeded, treatment could be delayed, and undue alarm could be raised, possibly leading to unwarranted surgical procedures. The soft-tissue lesions of tumoral calcinosis are typically lobulated, well-demarcated calcifications that are most often distributed along the extensor surfaces of large joints. There are many conditions with similar appearances, including the calcinosis of chronic renal failure, calcinosis universalis, calcinosis circumscripta, calcific tendonitis, synovial osteochondromatosis, synovial sarcoma, osteosarcoma, myositis ossificans, tophaceous gout, and calcific myonecrosis. The radiologist plays a critical role in avoiding unnecessary invasive procedures and in guiding the selection of appropriate tests that can result in a conclusive diagnosis of tumoral calcinosis.

Calcinosis↗
PubMed2005

Calcinosis in rheumatic diseases.

BACKGROUND: Calcinosis, or dystrophic soft-tissue calcification, occurs in damaged or devitalized tissues in the presence of normal calcium/phosphorus metabolism. It is often noted in the subcutaneous tissues of connective tissues diseases--primarily systemic lupus erythematosus, scleroderma, or dermatomyositis--and may involve a relatively localized area or be widespread. The calcinotic accumulations may lead secondarily to muscle atrophy, joint contractures, and skin ulceration complicated by recurrent episodes of local inflammation and infection. OBJECTIVES: To review the classification, pathogenesis, clinical features, and treatment of calcinosis in rheumatic diseases. METHOD: A MEDLINE search of articles from 1972 to 2004 was conducted utilizing the index word "calcinosis" with the coindexing terms "scleroderma," "lupus," "dermatomyositis," and "dystrophic calcification." RESULTS: Calcinosis may be the source of both pain and disability in connective tissue disease patients. Illustrative cases of patients with severe calcinosis are described. The literature available was critically reviewed. While warfarin, colchicine, probenecid, bisphosphonates, diltiazem, minocycline, aluminum hydroxide, salicylate, surgical extirpation, and carbon dioxide laser therapies have been used, no treatment has convincingly prevented or reduced calcinosis. CONCLUSIONS: Calcinosis is common in the conditions reviewed and a number of agents have been used for treatment. However, the approach to calcinosis management is disorganized, beginning with the lack of a generally accepted classification and continuing with a lack of systematic study and clinical therapeutic trials.

Adult↗
PubMed2002

Aggressive management of juvenile dermatomyositis results in improved outcome and decreased incidence of calcinosis.

BACKGROUND: Long-term consequences of juvenile dermatomyositis (JDM) include onset of calcinosis and subsequent functional impairment. Historic incidence of calcinosis has been reported between approximately 23% and 70%. Recent reports note improved outcome with high-dose steroids, yet the incidence of calcinosis has remained above 30%. OBJECTIVE: We attempted to determine whether rapid, aggressive disease management can prevent calcinosis and improve functional outcome. METHODS: Medical records of children with JDM managed at a pediatric medical center during a 10-year period were reviewed to determine (1) interval between onset of symptoms and diagnosis, (2) treatment modality, and (3) functional outcome and presence of calcinosis. RESULTS: A total of 21 female and 14 male subjects diagnosed with JDM met inclusion criteria, with a mean age of diagnosis of 7.6 +/- 3.9 years. Mean time from onset of symptoms to treatment was 6.6 +/- 8.2 months. Pulse intravenous methylprednisone (30 mg/kg daily) or high-dose prednisone was used in 31 of 35 patients. Patients who failed to respond within 6 weeks were started on a regimen of methotrexate (23/35). At follow-up, 5 patients had mild calcinosis (14%). Onset of calcinosis was associated with a longer time to diagnosis and treatment (30.6 vs 6 months, P =.003), a longer duration of elevated muscle enzymes (34 vs 12.6 months, P =.03), and longer disease duration (42.8 vs 22.2 months, P =.05). CONCLUSION: Stepwise, aggressive treatment directed at achieving rapid and complete control of muscle inflammation is highly successful in minimizing the long range sequelae of JDM, including calcinosis.

Calcinosis↗
PubMed1984

Parathyroid hormone and calcium metabolism in generalized scleroderma. Increased PTH level and secondary hyperparathyroidism in patients with aberrant calcifications. Prophylactic treatment of calcinosis.

Parathyroid hormone (PTH) in serum and biochemical parameters of calcium metabolism were analysed in 45 patients with systemic sclerosis. Calcification of the skin and subcutaneous tissue was assessed by X-ray examination of the hands. Analyses disclosed secondary hyperparathyroidism (increased PTH in serum, low calcium 'ion' in serum, decreased urinary excretion of calcium and phosphate), in particular in patients with calcinosis (P less than 0.05) as compared to those with no calcinosis. The duration of systemic sclerosis was longer in patients with calcinosis (P less than 0.05). The calcinosis type of systemic sclerosis is characterized by secondary hyperparathyroidism developed during the progression of the disease. A hypothesis is made regarding calcium metabolism in the early no-calcinosis (with increased synthesis of Vitamin D) and late calcinosis types. PTH may stimulate aberrant calcification. The hypothesis implicates that prophylactic treatment with Vitamin D in low dose may prevent calcinosis.

Adult↗