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Calcinosis cutis may be associated with metastatic calcification, dystrophic calcification, tumoral calcinosis, or may be deemed idiopathic. The association of cutaneous calcification with metastatic or tumoral calcinosis is quite rare. A case of metastatic calcinosis cutis in a woman with chronic renal failure and secondary hyperparathyroidism is presented. Other causes of calcinosis cutis are discussed briefly.
Juvenile dermatomyositis (JDM) is a multisystem disease characterized by acute and chronic nonsuppurative inflammation of striated muscle and skin. JDM is classified into an independent entity in the classification of dermatomyositis, and it is marked by the development of calcinosis late in the course of the disease. Since an appropriate steroid therapy for the disease was established, the prognosis of the JDM has been improved except for a fulminant case. Frequency of calcinosis in JDM also has been decreasing because of the adequate steroid therapy. However, once calcinosis universalis occurs, this is the most troublesome and debilitating complication in JDM. Treatment of calcinosis universalis in JDM, so far, remains unsatisfactory. We report here a case of JDM, who suffered from at the age of 3 years, with calcinosis universalis that showed remarkable improvement to orally administrated aluminum hydroxide.
We report the first case of calcinosis cutis following electromyographic examination. All previously reported cases of iatrogenic calcinosis cutis occurred following electroencephalographic examination using calcium-containing electrode compounds or following the extravasation of calcium-containing solutions along infiltrated intravenous lines. We also review the literature on calcinosis cutis due to iatrogenic and occupational exposure to calcium salts. The clinical presentation of calcinosis cutis is variable, but the histologic appearance is diagnostic. This entity may be underreported because of its benign, self-limited course and lack of recognition by physicians. Calcinosis cutis should be recognized by family practitioners, dermatologists, and subspecialists who encounter patients who have undergone prolonged monitoring studies that involve the use of electrodes.
INTRODUCTION: Calcinosis cutis is classically described in patients presenting chronic renal failure with secondary hyperparathyroidism. There are three clinical types described in the literature: cutaneous necrosis (secondary to vascular calcification), panniculitis with calcification of the adipose tissue and necrosis of the skin and dermo-hypodermic calcinosis without necrosis usually called metastatic calcinosis. The latter can affect all tissues but skin involvement is rare. CASE REPORT: A case of calcinosis cutis is presented in a 50 years old woman with moderate secondary hyperparathyroidism and chronic renal failure caused by renal amyloidosis. She was referred by the renal unit to our service for erythematous, woody-hard, infiltrated plaques with petechial purpura satellite lesions, involving the flexural areas, that appeared within a few weeks. DISCUSSION: This observation is original by the topography of the cutaneous lesions the involvement of the fexural areas is unusual and by the histologic aspect of pseudoxanthome elastic-like. We must notice that the hyperparathyroidism had always been very moderate (normal parathormonemia) compared to the rapid development of an important dermic calcinosis.
Tumoral calcinosis has up to date been considered as an independent disease. The survey of the literature shows that only its clinical and radiological appearance are generally accepted while its epidemiology and etiology are still under discussion. A genetical disorder, recurrent soft tissue microtrauma or terminal renal failure are blamed to cause tumoral calcinosis. All these causes may lead to localized or generalized disturbance of the calcium-phosphate-metabolism which in turn causes tumoral calcinosis. Therefore tumoral calcinosis should be regarded as a rare symptom of a metabolic disorder rather than an independent disease. Clinical appearance and treatment of two cases of tumoral calcinosis are reported followed by a review of the literature.
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.
OBJECTIVE: To test the hypothesis that the calcium antagonist diltiazem is effective in the treatment of calcinosis. METHODS: Diltiazem, 240-480 mg/day, was given to 4 patients with idiopathic or CREST-related (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) calcinosis for 1-12 years. Serial radiographs of the affected areas, using identical technique, and clinical evaluations were obtained. A fifth patient, who did not tolerate diltiazem, received verapamil, 120 mg/day for 18 months. RESULTS: All patients taking diltiazem had a reduction or disappearance of the calcific lesions, with striking clinical improvement. One patient's case was followed for 12 years. The response to diltiazem during the first 5 years of treatment has been previously reported in detail; however, over 7 years of additional treatment, there was further reduction of the lesions. One patient developed a large calcific lesion while receiving verapamil for hypertension, and after verapamil was replaced with diltiazem, there was a dramatic response. Verapamil was ineffective in the fifth patient, who did not tolerate diltiazem. CONCLUSION: Long-term treatment with diltiazem, but not verapamil, is effective in calcinosis.
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.
Repeated renal transplant calcinosis is a rare event. We report a young woman in whom repeated calcinosis was observed in two consecutive renal transplants. Persistent secondary hyperparathyoidism and hyperphosphatemia due to impaired renal function were assumed as the pathogenic factors for calcinosis. Sub-total parathyroidectomy performed shortly after the third transplantation and good function of the renal graft have prevented calcinosis in the third graft for more than five years.
Bilateral striopallidodentate calcinosis, also known as Fahr's disease, is characterized by symmetric calcifications of the basal ganglia, thalami, dentate nuclei of the cerebellum and white matter of the cerebral hemispheres. Besides the common idiopathic etiology of bilateral intracerebral calcinosis, alterations of calcium metabolism are present in rare cases, which are especially caused by hormonal dysfunction of the parathyroids. Advanced imaging techniques, such as CT and MRI, demonstrate increasing relevance regarding diagnosis of bilateral striopallidodentate calcinosis. Intracranial calcifications are routinely observed with high sensitivity by CT. On MR images calcifications exhibit different signal intensities, which depend on the stage of the disease, differences in calcium metabolism and the compound of these calcifications. Application of a new high-resolution, susceptibility-weighted MR sequence allows detailed visualization of the intracerebral calcifications in Fahr's disease. Further diagnostic methods and important aspects regarding clinical manifestation of bilateral striopallidodentate calcinosis are also discussed.
Massive medial calcific deposits (Mönckeberg's calcinosis) are described in the peripheral and visceral arteries, and similar but small-sized deposits in the coronary arteries of a 41 year old woman with diabetes mellitus. Although observed by roentgenogram fairly commonly during life in the muscular arteries of the legs in middle-aged men, medial calcinosis infrequently involves the visceral arteries and has never, to our knowledge, been documented in the coronary arteries. Although it may be associated with intimal atherosclerosis, medial calcinosis, per se, does not obstruct the lumens of the arteries and, therefore, does not lead to symptoms or signs of limb or organ ischemia. The cause of medial calcinosis remains a mystery, but it appears to affect people with diabetes more frequently than those without.
The calcinogenic plants are among the most noxious plants to animals in the world. The pathological and biochemical effects of calcinogenic plants in cattle, sheep, goats, pigs, horses, buffalo and laboratory animals have been determined. The chemical nature of the toxic agents and the precise mechanism by with the calcinogenic plants induces calcinosis have been defined. Most of the active principle present as steroidal glycoside is hydrolyzed in intestine, rumen and other tissues or by the bacterial flora releasing the steroidal fragment, in most cases 1,25(OH)(2)D(3). The excess of vitamin D stimulates CaBP synthesis and calcium and phosphate absorption, producing hypercalcemia and/or hyperphosphatemia. The excessively absorbed mineral cannot be physiologically accommodated, and the deposition in soft tissues results in calcinosis. The different means of treatment of calcinosis and control of calcinogenic plants are discussed with regards to their effectiveness. A number of potential uses of calcinogenic plants have been suggested but none has been exploited on a large scale. The understanding of the mechanisms involved with calcinosis contributed enormously to the compression of vitamin D mechanism. Research methods were developed and improved but a lot is to be done in this fascinating subject.
Pulmonary calcinosis is a recognized complication of renal failure. The resulting pulmonary compromise may be severe or even fatal. The potential contribution of hypercalcemia, hyperphosphatemia, and increased calcium-phosphorus product to the development of pulmonary calcinosis has been controversial. We describe four patients (ages 2 1/4 to 18 years) who had severe pulmonary calcinosis and respiratory failure within three to five days after renal transplantation. Initial clinical and roentgenographic findings suggested noncardiogenic pulmonary edema. Marked pulmonary hypertension was present in the two patients in whom pulmonary artery pressure data were available. Other clinical features in common included poor allograft function with persistent uremia requiring dialysis and evidence of moderate to severe secondary hyperparathyroidism. In three of the patients, the calcium-phosphorus product increased markedly after transplantation, to peak values of 122 to 147. This increase occurred at the same time as the onset of respiratory failure. Peak serum calcium levels were 10.0 to 11.0 mg/dL and peak serum phosphorus levels were 9.2 to 13.5 mg/dL. All patients died of respiratory failure five to 58 days after transplantation. The posttransplantation period may be a time of increased risk of potentially fatal pulmonary calcinosis in pediatric renal transplant recipients. The diagnosis should be considered in any patient with respiratory failure of unknown cause following renal transplantation.
In vascular smooth muscle, calcium overload is a highly pathogenic event, which increases with advancing age. An increase in the calcium content of arterial wall may be produced in rats by treatment with vitamin D3. The aim of this study was to evaluate the renal clearance of sulfanilamide (a model organic anion, preferentially eliminated by the kidneys) and other parameters of global renal function in rats with arterial calcinosis. Arterial calcinosis was produced in adult rats by means of a single dose of vitamin D3 (300,000 UI/kg bw, i.m.) 5 days before the experiment. Treated rats showed a large increase in calcium content of aortic tissue and an increase in systolic arterial pressure. No modifications were observed in plasma calcium levels and in plasma lipid profiles. Statistically significant decrements were observed in renal clearance of sulfanilamide, in renal blood flow, in fractional excretion of sodium and potassium. A slight decrease, not statistically different, was observed in the glomerular filtration rate. Rats with arterial calcinosis also showed an increment of total calcium levels in renal tissue, in fractional excretion of calcium and in the expression of organic anion transporter 1 (OAT1). Histological studies revealed tubular alterations. In summary, modifications in hemodynamics and tubular parameters are early manifestations of nephropathy in rats with arterial calcinosis, some of which may account for the changes observed in organic anions renal depuration. It is important to mention that the decrease in clearance of organic anions were seen in spite of the increase in expression of OAT1.
OBJECTIVES: Our aim was to perform a pilot study to investigate whether iontophoresis of acetic acid, followed by ultrasound, might be a safe and effective treatment for systemic sclerosis (SSc)-related calcinosis. This combination treatment has been used in other calcifying disorders. METHODS: Three female patients (ages 51, 62 and 59 yr) were studied. Each underwent treatment nine times over a 3-week period. Iontophoresis was with 2-5% acetic acid at 100 microA for 20 min, followed by ultrasound at 1.5 W/cm(2) for 8 min at each visit. The primary endpoint was the degree of radiographic calcinosis as quantified by image analysis after adjusting for soft tissue change. RESULTS: There were no side-effects from treatment. Mean radiographic intensity fell in all patients (by 18.0, 8.9 and 8.5%), although the maximum density and the area of calcinosis fell in only one patient. However, none of the patients reported any benefits from the treatment. CONCLUSIONS: In this small pilot study none of the patients experienced clinical improvement, despite an intensive treatment schedule over 3 weeks. However, there may have been some radiographic improvement. Given that there is currently no effective treatment for SSc-related calcinosis a larger study incorporating higher 'doses' of iontophoresis is indicated.
OBJECTIVES: Our aim was to evaluate (i) whether the bone matrix proteins osteonectin and matrix gamma-carboxyglutamic acid protein (MGP) are up-regulated in skin biopsies from patients with systemic sclerosis (SSc) and (ii) whether there is differential expression between patients with and without dermal calcinosis, a distressing and debilitating complication of SSc. METHODS: Skin punch biopsies were taken from the forearms of 38 SSc patients with the limited cutaneous subtype of SSc [17 without calcinosis (lcSSc) and 21 with calcinosis (lcSScCal)] and from 11 healthy control subjects. Immunohistochemistry was performed with antibodies to osteonectin and MGP. Staining was assessed semiquantitatively in the microvascular endothelium and in dermal fibroblasts. The Kruskal-Wallis one-way ANOVA was used to compare the data between patient groups. RESULTS: Both lcSSc and lcSScCal groups showed a statistically significant increase in the percentage of microvessels with osteonectin-positive endothelial cells (EC) (especially the lcSScCal group), whereas lcSScCal alone showed an increase in the percentage of microvessels with MGP-positive EC when compared with controls. In both SSc groups, the percentage of osteonectin and MGP-stained fibroblasts was increased in the reticular dermis (for osteonectin this was more marked in the lcSScCal group). In the papillary dermis, the percentage of osteonectin-stained fibroblasts was increased in both SSc groups but the lcSScCal group alone had a higher percentage of MGP-stained fibroblasts. CONCLUSIONS: When compared with controls, protein expression of osteonectin and MGP was greater in SSc patients generally, and osteonectin expression was significantly higher in EC and fibroblasts of the lcSScCal patients than the lcSSc patients without calcinosis.
Pulmonary opacities following orthotopic liver transplantation (OLT) are frequent due to pneumonia, infarction, or pulmonary edema. Metastatic pulmonary calcifications are present as persistent opacities that may mimic these conditions. In a series of 91 patients who underwent OLT, chest radiographs of 77 were reviewed and pulmonary calcinosis was seen in 4 (5.2%). Pulmonary calcinosis may be due to a variety of conditions, including dystrophic calcification in damaged lung and primary or secondary hyperparathyroidism. In this series, patients with pulmonary calcinosis had significantly higher levels of serum phosphate and calcium postoperatively and had received more intraoperative platelets and other blood products containing exogenous calcium than other patients. Pulmonary calcinosis should be considered in patients following OLT when stable, nonspecific pulmonary opacities are present. CT or radionuclide studies will aid in confirming this diagnosis.