[Cattle calcinosis in Austria. VII. The significance of growth stages and harvesting (silage, hay) of golden oats (Trisetum flavescens) for development of calcinosis].
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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.
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.
Mice of five inbred strains (BALB/c, C3H, C3Hf, DBA/2, and C57BL/6) of both sexes, mated and virginal, were examined for the incidence, severity, and location of dystrophic cardiac calcinosis (DCC) at various ages. Three hybrids, B6C3F1, C3B6F1, and CC3F1 of both sexes, all mated, were likewise studied. Excepting DBA/2, females of the inbred strains acquired the lesion at a much earlier age than males; DCC appeared in young DBA/s mice of both sexes. DCC in BALB/c mice was almost exclusively epicardial and occurred with equal frequency and severity in mated males and females, with higher incidence but lesser extent in virginal females. The occurrence was highest, the degree most severe, and the location exclusively myocardial in C3H and C3Hf mated females, irrespective of parity, whereas virginal females of these strains were entirely free of disease even after administration of exogenous progesterone. Involvement of males, also myocardial, was relatively minimal, especially in C3Hf mice. Over half the DBA/2 mice were affected, regardless of sex or mating; calcinosis appeared in the epicardium and/or myocardium, predominantly in the myocardium. Strain C57BL/6 was completely devoid of the lesion, as were the two hybrids thereof, B6C3F1 and C3B6F1. The hybrid of BALB/c and C3H showed a high incidence of minimal involvement, exclusively myocardial and limited to breeding females, indicating dominance of the C3H gene(s). Renal calcinosis was uncommon among BALB/c mice but was frequently found in C3H, C3Hf, and DBA/2 strains. Pulmonary calcinosis was rare and limited to C3H and C3Hf female breeders. Mated C3H females fed increasing amounts of fat showed a concomitant rise in incidence and severity of the cardiac lesions. Progression of the lesion from necrotic myocardial fibers to fibrocalcific masses is illustrated, as is formation of the renal deposits.
Recent surgical experience with 11 cases of calcinosis cutis has given the authors an opportunity to define the role of surgery in the management of this condition. In scleroderma associated with dermatomyositis, when complications or disability arise from one or more areas of calcinosis, surgery may give significant palliation. Wound healing, although a potential problem, does not constitute a contraindication to operative treatment. Damage to deep structures usually is avoidable, but in some instances is a reasonable trade-off for the benefits obtained. Follow-up has confirmed that surgery is beneficial to patient comfort and function, even in the few patients in whom some calcinosis recurred.
A 49-year-old female patient with a history of fever episodes, muscular weakness, Raynaud's phenomenon, cardiac insufficiency and increasing cutaneous calcinosis over a period of 4 years is reported. Based upon clinical as well as histological and immunological findings, the disease is diagnosed as mixed connective tissue disease with generalized cutaneous calcinosis in an extent yet unpublished, to our knowledge, in this 'overlap syndrome'. The pathogenesis of cutaneous calcinosis is discussed with particular reference to the phenomenon of calciphylaxis, and some therapeutic implications are considered.
Recently, tumoral calcinosis was found in a patient who had been undergoing haemodialysis in this hospital. The tumor was partially removed and subsequently regressed. The tumoral calcinosis of hemodialysis patients seems to be different from classical tumoral calcinosis.
A review is given of the literature concerning the so-called plant induced calcinosis in animals (tabel I), i.e. diseases which in their patological-anatomical appearance show great similarities with vit. D-intoxication. The etiology of the diseases are discussed in view of the last 5--10 years rapid development of knowledge concerning vit. D3 metabolism. It is pointed out that the most recent results indicate that enzootic calcinosis is caused by a 1,25-dihydrocholecalciferol-glycoside, which is hydrolysed in the intestinal tract. By this reaction 1.25 (OH) 2 cholecalciferol--the biological active metabolite of vit. D3 -- is set free, and thus able to act directly on the intestinal absorption mechanism. By this reaction the point of calcium metabolism regulation is essentially by-passed and calcium and phosphate absorption proceeds essentially out of control, causing hypercalcaemia, hyperphosphataemia, hypersecretion of calcitonin and calcinosis.
Mineralized plaques, which develop at the site of repeated subcutaneous injections of 100 mug KMnO4/0.2 H2O in rats, were investigated by electron microscopy. The newly formed, delineated, white plaque tissue at the injection site consisted of numerous, mostly unaltered fibroblasts and collagen fibers, without participation of inflammatory cells. Some signs of cell injury were found in the center of the lesions. Numerous, irregularly distributed, small, mineralized foci were seen near the fibroblasts. These were formed by aggregation of small needle-like units (50 A in diameter and 0.05-2.0 mum long). These needle-shaped units were found either in vesicular, cell derived structures, considered to be shed cell fragments, or on collagen fibers. Intramitochondrial deposits of such needle like units were seen frequently. Fusion of smaller mineralized foci to larger plaques occured and then needle-shaped units were seen at the periphery of the electron-dense lesions. Hypotheses concerning the mechanism of experimental cutaneous calcinosis (soft tissue mineralization) are discussed and related to the findings of this study. Probable intracellular crystal deposition and mineralization in cell-derived structures were shown for the first time in topical cutaneous calcinosis.
A forty-three-year-old man complained of painless, firm scrotal nodules which had first appeared at age sixteen. These were diagnosed clinically as multiple epidermoid inclusion cysts and were excised. Histologically they were composed of calcified, amorphous, granular material, characteristic of idiopathic calcinosis of the scrotum. This is a rare, benign condition without any recognized underlying metabolic abnormalities. The cause of idiopathic calcinosis of the scrotum is unknown, but we believe it is due to dystrophic calcification of dartoic muscles.
The case studies of four patients with post-transplantation calcinosis are presented. Three of the four patients died of inanition and sepsis secondary to infection of extensive soft tissue ulcers and diffuse cutaneous vascular calcification with gangrene. The fourth patient survived following removal of all four parathyroid glands and autografting of approximately one-half of one gland. Common to the patients was secondary hyperparathyroidism, elevated mean serum calcium levels after transplantation, and radiographic evidence of small and medium vessel calcification. No other differences could be found between these patients and other patients with post-transplantation hyperparathyroidism without calcinosis. In the face of apparently minor complaints of lower extremity discomfort, elevated parathyroid hormone levels (PTH) and positive xerography may indicate subtotal parathyroidectomy regardless of the serum calcium level.
A case of tumoral calcinosis with tumoral deposits about the knee is reported. Radiographs demonstrate juxta-articular calcific deposits about the right second and fifth distal interphalangeal joints and the left first distal tuft, both hips, both shoulders, first distal phalanx of the left foot and right knee. Radionuclide images clearly demonstrate all areas of tumoral calcinosis.