Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCINOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2005

Heredofamilial brain calcinosis syndrome.

Brain calcinosis syndrome (BCS) usually is defined as bilateral calcium accumulation in the brain parenchyma, primarily in the basal ganglia. More than 50 reported clinical conditions have been associated with BCS. We reviewed clinical, radiological, and genetic features of heredofamilial BCS accompanying all conditions associated with calcium accumulation in the brain reported in English between 1962 and 2003 in MEDLINE. The location, extent, and degree of calcification in the brain show diversity not only among the various disorders but also among patients sharing the same condition. The pathogenesis of BCS is uncertain. More complicated mechanisms may be Involved when brain calcinosis is present but calcium, phosphorus, and parathyroid hormone metabolism abnormalities are absent. We review conditions associated with heredofamilial BCS in which brain calcinosis is nearly uniformly present because such information may be Important to the clinician pursuing an investigative strategy.

Basal Ganglia Diseases↗
PubMedDate not supplied

Calcinosis cutis with siliconomas complicated by hypercalcemia.

OBJECTIVE: To report a case of extensive calcinosis cutis presumably caused by silicone injections, which was complicated by hypercalcemia. METHODS: A long-standing case of calcinosis cutis with subsequent development of hypercalcemia is presented, and possible mechanisms for the underlying metabolic dysfunction are discussed. RESULTS: A 78-year-old woman presented with severe hypercalcemia and was found to have extensive subcutaneous calcifications on the anterior chest wall and abdomen, likely related to previous silicone injections. The hypercalcemia was treated with intravenously administered pamidronate and aggressive rehydration. Resection of the extensive long-standing calcific deposits was not a viable option. The hypercalcemia resolved with treatment, but the patient died of urinary tract sepsis. CONCLUSION: Extensive calcinosis cutis can result in hypercalcemia, possibly attributable to granulomatous reaction and vitamin D excess.

Aged↗
PubMedDate not supplied

Calcinosis cutis associated with systemic blastomycosis in three dogs.

Three dogs treated for systemic blastomycosis with intravenous amphotericin B (one case) or amphotericin B lipid complex (two cases) developed mild to severe calcinosis cutis two to six weeks after the initiation of treatment. Abnormalities in serum calcium and phosphorus during treatment for blastomycosis or at the time of diagnosis of calcinosis cutis were slight or absent. The calcification was not associated with lesions of cutaneous blastomycosis. Calcification was limited to the skin in two cases and may have also involved the kidneys in one. The calcinosis cutis resolved completely in all three dogs with no (two cases) or only palliative (one case) therapy.

Animals↗
PubMed1982

Hyperphosphatemic tumoral calcinosis: association with elevation of serum 1,25-dihydroxycholecalciferol concentrations.

Seven siblings with hyperphosphatemic tumoral calcinosis were studied using metabolic measures. Serum phosphorus and 1, 25-dihydroxycholecalciferol concentrations were significantly increased and serum parathyroid hormone and 25-hydroxycholecalciferol concentrations were significantly decreased in these subjects. Metabolic balance studies done in three of the siblings showed positive calcium and phosphorus balances, reflected by increased gastrointestinal absorption and decreased renal excretion. These data suggest that a hereditary abnormality of vitamin D metabolism may be present in patients with hyperphosphatemic tumoral calcinosis. Failure of the normal feedback mechanism regulating the 25-hydroxy-1-alpha-hydroxylase enzyme is suggested as the major cause. Although this defect could lead to many of the metabolic abnormalities seen in these patients, the overall contribution of altered vitamin D metabolism to the pathogenesis of tumoral calcinosis is not fully understood.

Adolescent↗
PubMed2000

Calcinosis cutis following the administration of intravenous calcium therapy.

Calcinosis cutis, the cutaneous deposition of calcium salts in the dermis, can occur through a variety of pathogenetic mechanisms, and can be associated with both normal and elevated calcium levels. Iatrogenic causes of calcinosis cutis include extravasation of intravenously administered calcium chloride or calcium gluconate, and traumatic deposition of calcium in the skin, subsequent to electromyography or electroencephalography. We report two cases of calcinosis cutis following intravenous infusion of a calcium-containing salt.

Adult↗
PubMed2002

Idiopathic calcinosis cutis of the vulva in an elderly woman. A case report.

BACKGROUND: Idiopathic calcinosis cutis of the vulva is a rare condition of unknown etiology. Only seven cases have been reported to date, and all of them were in children. We report the first case in an elderly woman. CASE: A 68-year-old woman presented with a labial lesion of unknown etiology. Excisional biopsy was performed, and histopathologic evaluation showed subepidermal calcification. Follow-up biochemical and hormonal analysis and screening tests for collagen vascular diseases revealed normal results. CONCLUSION: After diagnosis of calcinosis cutis, a laboratory workup to rule out abnormalities of calcium and phosphorus metabolism, malignant processes and collagen vascular diseases must be carried out. This approach in the evaluation of calcinosis cutis could lead to diagnosis of the underlying disease at an early stage.

Aged↗
PubMed1976

Enzootic calcinosis in sheep: clinical signs and pathology.

Enzootic calcinosis in Corriedale sheep was characterized by degeneration and mineralization of elastic connective tissue of aorta, arteries, lung, and kidney and by ulceration of cartilage of joints of limbs. Results of serum chemical analysis revealed low Ca X P value and significantly low, but inconsistent magnesium concentration and normal inorganic phosphorus content. The Ca:P ratio in bone was low in affected sheep. Clinicopathologically, calcinosis of sheep at Mattewara, India, appeared to be similar to the disease described as Enteque seco in South America, Naalehu disease in Hawaii, Manchester wasting disease in Jamaica, and calcinosis in central Europe, Israel, and South Africa. The disease might be due to complex mineral imbalance, although the possibility of a plant poisoning has not been ruled out.

Animals↗
PubMed2003

[Enzootic calcinosis in sheep after consumption of golden oat grass (Trisetum flavescens L., P. B.)].

In 12 sheep (Coburger Fuchsschaf; 10 female, 1 male, 1 wether), grazing on a pasture with approximately 20 (to 40)% golden oat grass and fed the respective hay, clinical findings and outcome of Trisetum flavescens induced calcinosis were controlled for 2 1/2 years. Besides lameness typical for calcinosis (slightly bent carpus and relatively stretched position of tarsal and fetlock joints when standing, 'kneeling' on the carpi) the patients showed increasing impairment of the circulatory and respiratory systems (holosystolic endocardial murmur, congestion, exspiratory dyspnoea etc.). 4 of the 12 sheep died (2) or had to be euthanatized (2) because of peracute heart failure; 5 patients showing chronic circulatory insufficiency as well as 1 animal suffering from severe lameness had likewise to be euthanatized (Ubersicht 1-3). One calcinotic ewe (No. 12), still alive at the time of this evaluation (2003), gave birth to 2 healthy lambs and nursed them. The ram (No. 5) had to be eliminated for another disease. The mostly severe calcifications of the cardiac valves, the endocardium and the arterial vessels as observed during the pathomorphological examination are consistent with the clinically diagnosed cardiovascular insufficiency. Furthermore, calcification of several tendons and ligaments, the kidneys and in 3 cases of the pulmonary parenchyma could be found. Clinical observations and post mortem findings showed a remarkable individual variation. Compared to calcinosis in cattle, in sheep the functional disturbance of the circulatory system was striking.

Animal Feed↗
PubMed2004

Extensive calcinosis cutis in relapsed acute lymphoblastic leukaemia.

INTRODUCTION: Hypercalcaemia with calcinosis cutis occurring at relapse of acute lymphoblastic leukaemia (ALL) is rare and unusual. CLINICAL PICTURE: A 19-year-old lady with B precursor ALL presented with extensive waxy, verrucous, tender plaques over the flexures of her arms and legs a week after relapse of leukaemia. She was found to have hypercalcaemia, hyperphosphataemia, hyperuricaemia and acute renal impairment. Skin biopsy was consistent with calcinosis cutis. There was no evidence of metastatic calcification in other organs. TREATMENT: Hypercalcaemia was treated with aggressive hydration and intravenous pamidronate. High doses of analgesics were required for partial pain relief. OUTCOME: Cutaneous lesions proved resistant to early calcium lowering and were a source of constant pain. She succumbed to leukaemia four months later. CONCLUSION: Treatment of calcinosis cutis was unsatisfactory and would have been dependent on the successful treatment of the underlying leukaemia.

Adult↗
PubMed1992

[Tumoral calcinosis. Apropos of a further case in a child].

Tumor-like calcinosis is an infrequent condition whose etiology is poorly understood. Calcifications develop in the subcutaneous tissue neighboring the large joints. All age groups can be affected, although the disease is more common before the age of twenty years. A new case of tumor-like calcinosis in an eight-year-old girl is reported here. A huge mass in the right hip region and a smaller mass around the right elbow were found. Biologic studies revealed increased serum phosphorus levels with normal serum calcium levels. Roentgenograms confirmed the diagnosis of tumor-like calcinosis by showing calcified masses independent from the bones of the neighboring joint. Management consisted in complete removal of both masses. Outcome was favorable. In this patient's family, the disease appears to be inherited according to a dominant pattern, although recessive autosomal transmission is believed to be more common.

Calcinosis↗
PubMedDate not supplied

Spinal cord compression by ectopic calcinosis in scleroderma.

Systemic sclerosis (SS) is a chronic, multisystemic disease, characterized by inflammation associated with fibrosis. Calcinosis is one of the manifestations of this disorder, observed in 10 to 20% of cases. It is usually located on the extensor surface of the phalanges, peri-articular tissue and near the bone prominences. There are only a few cases reported of SS with vertebral column involvement and spinal cord compression by calcinosis causing serious neurological complications. We describe a fatal case of SS who showed tetraplegia secondary to ectopic calcinosis in the cervical medulla and present a review of the literature on the subject.

Calcinosis↗
PubMed2006

Calcinosis cutis in a patient with eosinophilia-myalgia syndrome: case report.

Eosinophilia-myalgia syndrome (EMS) often is a disabling disorder caused by the consumption of contaminated L-tryptophan. Affected patients present with an array of symptoms, including cutaneous manifestations, peripheral eosinophilia, myalgias, and long-term neurocognitive disability. This article is the first reported case of a patient with EMS who developed calcinosis cutis. While many long-term sequelae of EMS are reported in the literature, there are no reports of the development of dystrophic calcification in these patients. The calcinosis cutis in this patient with EMS may represent a new manifestation of EMS that has not been documented to date. If more patients with EMS develop calcinosis cutis, it will present a therapeutic challenge to the physicians managing these patients.

Aged↗
PubMed1991

[Clinicopathological features of metastatic pulmonary calcinosis with malignant neoplasm].

Metastatic pulmonary calcinosis is a rare complication seen in malignancies accompanied by hypercalcemia, or chronic renal failure. We reviewed the clinicopathological findings of 8 cases of metastatic pulmonary calcinosis accompanied malignancy revealed at autopsy. The underlying diseases were malignant lymphoma in 3 cases (adult T cell lymphoma in 2 cases), multiple myeloma in 2, lung cancer in 2, and acute myelocytic leukemia in 1, all cases were complicated by hypercalcemia and renal failure. Chest X-ray revealed almost normal findings in 2 cases, bilateral diffuse infiltrates in 4, bilateral infiltrates in the apex in 1, and right atelectasis in 1. Bone scintigraphy was performed in 4 cases, and revealed warm pulmonary uptake in 1 patient with multiple myeloma and 1 with lung cancer, but normal findings in the 2 other cases. Histopathological examination revealed diffuse alveolar septal edema and fibrosis due to calcium deposition, which were considered to be the cause of respiratory failure. Metastatic pulmonary calcinosis is a rare but a serious complication in malignancies accompanied by hypercalcemia and renal failure, and bone scintigraphy seems to be a useful method for its diagnosis.

Adolescent↗
PubMed1991

[Case report of multiple myeloma associated with diffuse pulmonary calcinosis].

A case of multiple myeloma with diffuse metastatic calcinosis of the lung is presented. The patient was a 60-year-old male with IgA-kappa-myeloma who developed renal failure and hypercalcemia. Multiple small nodular shadows were observed both in plain chest films and CT films. The patient died of progressive respiratory failure. Postmortem examinations showed pulmonary infiltrations and massive pulmonary calcifications. Small nodular shadows were due to diffuse calcium deposits which were observed in and around the alveolar basement membranes of both the bronchioles and the blood vessels. It is generally believed that pulmonary calcinosis may not be detected by routine chest films; however, the nodular shadows observed in our patient seem to be pathognomonic and may indicate the severity of calcinosis.

Calcinosis↗
PubMed1991

Vasculitis and calcinosis in juvenile dermatomyositis.

Dermatomyositis of childhood onset is characterized by vasculitic lesions and often complicated by calcinosis. We describe 32 patients with juvenile dermatomyositis. All suffered from vasculitic skin changes like facial erythema often with edema, Gottron's sign, telangiectasias, erythematous eruptions, different rashes and necrotic ulcerations. Vasculitis appeared also in inner organs as gastrointestinal ulceration, neurologic and cardiac manifestation. 4 children complained of Raynaud's phenomenon. Calcinosis of soft tissues developed in 21 patients within 0.5 to 10 years after onset. In 6 of them we saw regression of calcium deposits after a progressive phase of 1 to 5 years. Functional outcome in juvenile dermatomyositis depends mainly on the degree of calcinosis together with shortening of diseased muscles.

Adolescent↗
PubMed1977

[Enzootic calcinosis and other plant induced calcinoses (author's transl)].

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.

Animals↗
PubMed1991

[Cutaneous calcinosis of the footpads in a cat].

A case of cutaneous calcinosis of the footpads in a cat is described. The animal had developed lameness of one hindleg which was presumably due to infection by an abscess-like lesion of one pad. Histologically the lesion proved to be based on a cutaneous calcinosis. Shortly afterwards the animal died of uremia. Post mortem examination revealed fine granular shrinkage of the kidneys and signs of demineralisation of the skeleton accompanied by calcifications in the pads of all four paws, major arteries, hear, kidneys, lung and gastric mucosa. The clinical and morphological findings suggest a cutaneous calcinosis of the footpads as an additional localisation of extraosseous calcification in osteorenal syndrome.

Animals↗
PubMed1990

[Idiopathic arterial calcinosis in children and pulmonary giant-cell elastolysis].

4 lethal cases of idiopathic arterial calcinosis (IAC) in three girls (1 month 10 days, 2 months and 3 months of age) and one 8-month-old boy are described. The authors' own material and literature data confirm the autosomal recessive character of the disease. The initial step in the IAC morphogenesis belongs to the genetically conditioned elastolysis with the participation of giant multinuclear cells with subsequent arterial calcinosis. Differential diagnosis of IAC with secondary arterial calcinosis is recommended.

Arteries↗