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Calcified aortic valves were detected in 109 patients studied in hospital by an echocardiographic method (2D- and M-scanning). It was found that, unlike rheumatism, calcification starting in the aortic annulus and semilunar bases might result in formation of degenerative (non-inflammatory) calcific aortic stenosis. The latter differs from rheumatic aortic stenosis in commissural fusions. The authors defined clinical and echocardiographic differentially diagnostic criteria for degenerative (non-inflammatory) and rheumatic (inflammatory) calcific aortic stenosis. They also discussed pathogenetic aspects of aortic valve calcification and problems of terminology.
In 2 female patients suffering from chronic renal insufficiency and secondary hyperparathyroidism total parathyroidectomy with autotransplantation was performed, but shortly afterwards tertiary hyperparathyroidism developed. Together with numerous generalized metastatic foci of severe smooth tissue calcification, extensive calcification of the skin occurred. Some of the hard painful areas with papules, nodules and large plaques of calcium deposits were inflamed and ulcerated, and the histological picture was that of severe disseminated calcification of the middle and deep reticular dermis, spreading over into the subcutaneous adipose tissue. Conventional X-ray examinations and computer tomography revealed large asymmetrical areas of bone-dense calcification of the soft tissue. After total excision of the autografts the severe calcifications of the skin diminished or disappeared completely.
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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.
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.
As of the year 1991 there were 358 leprosy patients in National Leprosarium Matsuoka Hoyo-En, including 223 patients (62.3%) who had received the injections of chaulmoogra oil before. Calcinosis cutis caused probably from the injections was noted on 73 patients (32.7%): 67 lepromatous and 6 tuberculosis cases. It has never been reported before that the T type patient suffering from calcinosis cutis was observed in the cases of the chaulmoogra oil injection in Japan. The detectable positions of calcinosis cutis were mostly at the injected sites, that is, outside the right brachium followed by bilateral-branchia and crura. In the group of patients with calcinosis cutis, the anti-PGL antibody was negative for the most part. Urinalyses, peripheral blood figure analyses, histopathological tissue examinations of calcium deposition, X-ray diffraction patterns, differential thermal and gravitational analyses, and chemical analyses were performed on all patients with this disease. Further, as the result of this study six patients with calcinosis cutis caused by sulpyrine was also found. The major component of the deposit by the drug was calcium phosphate. These calcinosis cutis were considered to be of trophopathic calcinosis based on the disorder of subcutaneous tissue due to the injections of respective drugs: chaulmoogra oil and sulpyrine.
In patients who had died due to various diseases and also in practically healthy individuals aged from 10 to 79 years calcinosis of the coronary arteries was studied morphometrically and histologically. The incidence and the extend of calcinosis implicating the coronary arteries increased with growing age and were more pronounced in males than in females. In analysis of observations uncovered, irrespective of the cause responsible for death, a direct relationship between the area of calcinosis and that of atherosclerosis in grosso modo (correlation factor of 0.46) was noted; the diseased in consequence of diverse affections demonstrated considerable variations in the development of arterial calcinosis. More often than not calcinosis of the coronary arteries was definable in atherosclerotic plaques carrying an important fibrotic component, in cases of necrosis and in those marked by a low lipids content and poor vasculalarization of an altered wall of the coronary artery. Calcinosis of the coronary arteries occurred more often than did their stenosis on 50% or more of the lumen. There has been established a direct relation between the frequency of the coronary artery stenosis and the area of calcinosis. The latter usually appears as a sign of disseminated atherosclerosis rather than as that of a progressive atherosclerotic process.
We have followed up a large family in which seven members have tumoral calcinosis. One girl had the skin lesions of localized calcinosis cutis apart from the typical subcutaneous deposits of calcium. Like most persons with tumoral calcinosis, our patient had normal serum calcium concentrations; however, the serum phosphorus levels were greatly elevated. The familial occurrence and elevated serum phosphorus levels suggest the possibility of some as yet undefined, heritable metabolic defect as the underlying cause. The occurrence of tumoral calcinosis with localized calcinosis cutis is a rare association, and there has been only one other reported case to our knowledge. This report describes our patient and offers a brief discussion of tumoral calcinosis. The therapeutic response to the phosphate depletion regimen and topical steroids was disappointing in our case.
We describe a patient with a 23-year history of progressive calcinosis and features of the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) who was treated with diltiazem, 240 mg/day, for 5 years. No clinical exacerbation of calcinosis occurred during treatment. Radiographs showed no new lesions, and there was reduction in the size of the existing lesions. Bone scans revealed a progressive decrease in the uptake of the radionuclide by soft tissue foci. We propose that diltiazem may stop the progression of calcinosis by reducing the cellular calcium influx in affected tissues.
An unusual finding of systemic calcinosis in a patient with a nonparathyroid malignant neoplasm stimulated us to do a sclinicopathologic review of similar cases at our institution in the past seven years. Of 3,268 autopsies performed from 1968 to 1975, a total of 17 cases of calcinosis were found, 11 with solid tumors and 6 with hematopoietic neoplasms. Calcinosis was most prominent in the lung, kidney, heart, and stomach and was rarely discovered prior to death. Eighty-two percent of the patients had hypercalcemia and 53% had associated bony metastatic disease. Corticosteroid or phosphate treatment for the hypercalcemia may have contributed to the tissue deposition of calcium. Significant hepatic, renal, metabolic, and pulmonary dysfunctions were also associated with this disorder. Thirty-six percent of the patients had hypercalcemia without skeletal involvement; tumor-produced parathormone-like substances may be responsible for these calcium abnormalities. Calcinosis was a significant complication of neoplastic disease in these patients and contributed to morbidity and mortality.
The evolution of the mineral constituents of subcutaneous calcinosis induced in rats by topical calciphylaxis was studied by the method of quantitative chemical analysis, and after treatment with excited gases by electron spin resonance (ESR) analysis. Chemical data show that the genesis of the subcutaneous calcinosis does not significantly alter the concentration of Ca, P, F, CO3, Mg, and Fe in the mineral phase of the femoral bone of calciphylactic rats. In the calcinosis an important increase of the fluoride concentration is noticed in function of the time after challenging. There is also a high concentration of Mg2+ ions in the early stages of the experimental calcification. Iron injected for the challenging is continuously present in the calciphylactic tissue after this treatment. This suggests that subcutaneous calcinosis might be a means of fixing certain heavy metal ions. After treatment with excited gases, the proportions of the trapped CO33- and O3- radicals are of the same order of magnitude in calciphylactic tissue after 12 days and observations in bone mineral. These suggest that after 12 days the mineral of the calciphylactic tissue has a crystalline state close to that of bone.