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At least 757 records · Page 42Linked to original sources
PubMed1986

Arthropathy and cutaneous calcinosis in hemodialysis oxalosis.

Recently, calcium oxalate crystals have been identified in the synovial fluid of patients with arthritis and end-stage renal failure. We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin. Clinical manifestations included podagra, tenosynovitis, olecranon bursitis, and acute and chronic synovitis of the large joints that were associated with chondrocalcinosis or subchondral bone erosions. Diffuse involvement of the hand, with chondrocalcinosis of the finger joints, miliary calcified deposits in the skin, and artery calcifications, was observed in 3 patients. The fourth patient had erosive arthropathy. Oxalosis secondary to end-stage renal failure in patients treated with long-term hemodialysis can present with articular manifestations that resemble those of gout, pseudogout, and apatite deposition disease. Other characteristic features of the synovitis associated with oxalosis secondary to end-stage renal disease were: predominant involvement of the hand, mild inflammatory changes in the synovial fluid and synovium, and poor response to administration of nonsteroidal antiinflammatory agents.

Calcinosis↗
PubMed1997

Symptomatic spinal calcinosis in systemic sclerosis (scleroderma).

Two patients with diffuse cutaneous systemic sclerosis and spinal calcification, involving the lumbar spine in one and the cervical spine in the other, are described. Computed tomography-guided aspiration of the calcific masses was performed, and material aspirated from one patient was shown to be apatite, Ca5(PO4)3OH. One patient showed improvement following lumbar laminotomy, hemilaminectomy, and diskectomy.

Calcinosis↗
PubMed1998

Functional improvement in a patient with cerebral calcinosis using a bisphosphonate.

Idiopathic cerebral calcification can be associated with a progressive neurologic disorder for which there is no known treatment. This report describes a patient with a familial form of this disorder presenting in middle age with progressive Parkinson-like features along with spasticity, dystonia, and ataxia. Disodium etidronate, a bisphosphonate, produced a two-fold improvement in the rate of his speech and gait, but did not affect his spasticity, dystonia, or ataxia. Quantitative analysis of cerebral calcification did not reveal any reduction in the amount of calcification, suggesting other possible mechanisms for this clinical improvement.

Basal Ganglia Diseases↗
PubMed1980

Ultrastructural and cytochemical aspects of the initial phases of an experimental cutaneous calcinosis (calcergy) in the rat.

In rats a subcutaneous injection of KMnO4 leads to the calcification of the connective tissue. During mineral deposition, both intra- and extracellular changes are observed in the connective tissue. The intracellular phase is characterized by the formation of intramitochondrial granules and cytoplasmic vesicles, both in fibroblastic and extrinsic cells. In the extracellular phase, numerous heterogeneous matrix vesicles appear in the extracellular matrix. At the same time, globular particles which are resistant to microincineration, are observed between the collagen fibrils. The mineralization of the extracellular matrix takes place in two stages. The first stage comprises the appearance of needle-like structures and round aggregates. The needle-like structures are observed occasionally in the matrix vesicles and often in the extracellular matrix where they appear isolated or diverging from a central point. The round aggregates, composed of dense particles, are seen in the ground substance between the collagen fibrils. The second stage is characterized by a progressive mineralization of the collagen fibrils and the elastic fibers, without formation of extended calcified plaques.

Animals↗
PubMed1985

[Results of a study of a family with aggregated occurrence of bilateral symmetrical basal ganglia calcinosis].

We present a familial study (45 members), in which 31 members have been examined. Seven were afflicted with bilateral symmetrical calcification of the basal ganglia (Fahr's syndrome), as verified by CT scans. The case history and biochemical results for one additional proband, who had died, strongly indicate that this patient also had Fahr's syndrome. The wide range of examinations used in our study were aimed at excluding differential diagnoses of bilateral symmetrical calcification of the basal ganglia, other than when the origin was suspected to be in the parathyroid. The examinations had to be undertaken on an outpatient basis. Some of the variables, such as Fe, Cu, and Mg in the plasma, are connected with results that have been published on the composition of the apatite deposits. Psychiatric, psychological, neurological, and EEG examinations are emphasized. Together with the case reports they are meant to illustrate the neuropsychiatric aspects of this syndrome, the composite view of which has often been previously neglected. Nineteen of 31 probands showed neurological, psychopathological, psychological, and encephalographical deviations. We also noted a high incidence of organic brain syndromes that are phenomenologically similar to affective disorders. We believe these deviations to be directly related to morphological alterations of the basal ganglia, possibly due to errors in phosphorous and calcium metabolism. Although the CT scan has greatly facilitated the diagnosis of intracerebral calcifications, we assume that basal ganglia alterations under the CT-density threshold may also be of clinical importance. Our metabolic results, genetic issues, and neuropsychiatric findings are discussed.

Adolescent↗
PubMed1987

Excessive myocardial calcinosis in a chronic hemodialyzed patient.

Secondary oxalosis in chronic hemodialyzed patients is caused by impaired renal excretion and inadequate removal of oxalic acid during hemodialysis. Ascorbic acid is a precursor of oxalic acid. We report a parathyroidectomized patient with chronic renal failure, on hemodialysis, who received over a period of several months a total dose of 91.0 g ascorbic acid i.v. The plasma oxalic acid level in this patient was 14-fold higher than in healthy persons. Increased oxalic acid synthesis from its precursor ascorbic acid may be responsible for hyperoxalemia, high content of oxalic acid in myocardium, aorta and lung, and calcium oxalate deposition in soft tissues. Application of high doses of ascorbic acid should be avoided in hemodialysed patients with chronic renal failure.

Adult↗