Extensive Metastatic Calcification Research Articles

Extensive intracranial calcification presenting with neurological symptoms due to primary hypoparathyroidism and secondary hyperparathyroidism: Two case reports

Metastatic calcification involving basal ganglion in idiopathic hypoparathyroidism (IHPT) and intracranial vascular calcification in secondary hyperparathtyroidism (SHPT) in end-stage renal disease (ESRD) on hemodialysis are not uncommon. Extensive bilateral symmetrical intracranial calcification involving basal ganglion, cerebellum and white matter presenting with neurological symptoms has been rarely reported in literature. We report 2 such cases. The first case belongs to a 56 year-old lady with IHPT with extensive intracranial calcification who presented with choreoathetotic movements. The second case is concerning a 14 year-old boy with SHPT with ESRD on hemodialysis with extensive intracranial calcification who presented with seizures. The possible pathogenesis of extensive metastatic calcification and treatment was discussed with review of literature.

Tumoral Calcinosis in a Patient on Peritoneal Dialysis

A 23-year-old woman presented with multiple swellings around her shoulders which had developed over many months. She had been on continuous ambulatory peritoneal dialysis treatment for 4 years for renal failure caused by polycystic kidney disease. Her compliance with the dialysis prescription had been very poor. Examination revealed multiple large hard masses related to both shoulders and ankles; the largest was 9.5 × 5 cm. Laboratory results revealed severe hyperparathyroidism and an elevated calcium × phosphate product. A biopsy showed dense fibrous tissue containing large areas of calcification. Radiographs showed extensive metastatic calcification around the right shoulder (Figure 1A). The patient was re-educated and supervised with her peritoneal dialysis. After 6 months there was marked reduction in the size of the mass (Figure 1B). She then had total parathyroidectomy with forearm reimplantation of one gland. A radiograph (Figure 1C) 1 month later showed almost complete resolution. Figure 1. A, Radiograph showing extensive metastatic calcification around the patient's right shoulder. B, Radiograph shows marked reduction in the size of the mass 6 months after peritoneal dialysis and re-education of patient. C, One month after total parathyroidectomy ... In this case, tumoral calcinosis was the result of metastatic calcification related to underdialysis with a chronically raised calcium phosphate product. The condition completely resolved with proper dialysis and parathyroidectomy.

Multiple organ failure associated with extensive metastatic calcification in a patient with an intermediate state of human T lymphotropic virus type I (HTLV‐I) infection: Report of an autopsy case

A patient with an intermediate state of human T lymphotropic virus type I (HTLV-I) infection and in whom autopsy showed multiple organ failure (MOF) associated with extensive metastatic calcification in systemic organs is described. A 56-year-old man presented with signs and symptoms of advanced cardiac insufficiency, respiratory disturbance and renal failure. Serologically, the anti-human T lymphotropic virus type I (HTLV-I) antibody titer and the levels of both calcium and parathyroid hormone-related peptide (PTHrP) were distinctly elevated. These data suggested a diagnosis of adult T cell lymphoma/leukemia (ATLL). However, examination of a peripheral blood sample revealed only a few atypical lymphoid cells (3%) associated with mild leukocytosis (white blood cell count, 13.7 x 10(3)/mm3). Lymph node swelling was systemic but mild, with some nodes up to 10 mm in diameter. The patient died of MOF. Adult T cell leukemia/lymphoma was unable to be diagnosed definitively because of the short duration of laboratory abnormalities and because of the discrepancy between the laboratory data and the magnitude of lymphoproliferation in both the lymph nodes and peripheral blood. At autopsy, the most conspicuous finding was extensive metastatic calcification in the multiple organs, including the heart, lungs, kidneys, tongue, liver, pancreas, spleen and systemic arterial walls. Very small numbers of medium-sized atypical lymphoid cells admixed with small reactive lymphocytes were identified in multiple organs, with no evidence of massive infiltration. Molecular analyses could not detect monoclonal integration of HTLV-I provirus DNA or monoclonality of T cell lineage cells. Parathyroid hormone-related peptide was demonstrated in the cytoplasm of the atypical lymphoid cells on immunohistochemical examination. The bone trabeculae generally showed distinct evidence of resorption associated with marked proliferation of osteoclasts. These findings suggested that the hypercalcemia in the present case was categorized as humoral hypercalcemia of malignancy rather than local osteolytic hypercalcemia.

Tertiary hyperparathyroidism associated with metastatic cardiac calcification in a haemodialyzed patient

A 32-year-old man undergoing haemodialysis treatment for 10 years was referred to our hospital because of intractable heart failure with atrioventricular block. On the 5th hospital day he was found dead in bed. Autopsy revealed extensive metastatic calcification involving the myocardium and the cardiac conduction system, and a parathyroid adenoma with hyperplastic parathyroid glands. Retrospectively, first-degree heart block developed 14 months before death, and was subsequently associated with intraventricular conduction defect and atrioventricular block (Wenckebach type). Throughout the 3 years the patient received 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) and the calcium-phosphorus product (Ca X P) exceeded 70. 1 alpha-OH-D3 should not be prescribed when patients develop an increase in Ca X P and exploration of the parathyroid glands should not be delayed if heart block presents in long-term haemodialyzed patients.

Extensive metastatic calcification of the lung in an azotemic patient

An unusual case of extensive pulmonary metastatic calcification occurring during the course of chronic pyelonephritis is described. The important features of this case are as follows: (1) Metastatic calcification appeared to develop in an early state of chronic renal failure when there was neither hypercalcemia, hyperphosphatemia, hyperparathyroidism nor evidence of bone disease. (2) The calcium and phosphate ion product was normal during the last 3 years when the pulmonary metastatic deposits persisted and progressed with the roentgenologic appearance of pulmonary edema. (3) There was calcium carbonate rather than the anticipated calcium phosphate in the deposited material. A review of the literature offers some theoretic explanation for the sites of calcification but no practical explanation for the presence of calcification.

Pulmonary Calcification in a Patient with Multiple Myeloma

A patient with multiple myeloma and hypercalcemia was treated with intravenous sodium sulfate and prolonged oral sodium phosphate. She subsequently developed extensive metastatic calcification in the lungs, alveolar-capillary block and severe respiratory distress. The probable mechanism of phosphate and sulfate induced soft tissue calcification in hypercalcemia is reviewed and caution is urged in the administration of phosphate as a hypocalcemic agent.

Determination of body composition by neutron activation analysis in patient with renal failure.

Abstract In vivo neutron activation analysis and whole-body counting techniques were used to measure the body composition of patients with chronic renal failure. Levels of total body calcium, phosphorus, sodium, chlorine, nitrogen, and potassium were measured in uremic patients at various times prior to and during maintenance dialysis. The metabolic derangements in individuals with chronic renal failure often result in the development of overt secondary hyperparathyroidism. The action of PTH on bone is associated with osteodystrophy as well as with extensive metastatic calcification. These effects present major problems in the therapeutic management of uremic patients. The most interesting finding is that of normal total body calcium (Ca/height) measured in uremic patients both prior to and during hemodialysis. Presumably, this high total Ca, occurring simultaneously with a condition such as osteoporosis, reflects the translocation of Ca from skeletal tissue to soft-tissue depots. Uremic patients on dialysis usually experience a loss of total body Ca. TBNAA (total body neutron activation analysis) alone does not distinguish between Ca in bone and Ca in the soft tissue; hence data from tracer studies are required for this analysis. However, following parathyroidectomy in uremic patients with extensive metastatic Ca, TBNAA measurements show a decrease in total body Ca concurrent with reduction of metastatic calcification as indicated by roentgenographic evidence. With renal failure, phosphate is released from the skeleton, and hyperphosphatemia ensues. The P/Ca values for patients on hemodialysis are, on the average, slightly higher than those of normal persons and of uremic patients not on dialysis. The total body sodium in uremic patients was, on the average, higher than that observed in a normal contrast population, as well as higher than that of a group of osteoporotic patients. However, no causal relationship was established between the reduction of total body Na during dialysis and the observed improvement in the hypertensive condition. There was little evidence of K depletion in uremic patients maintained on chronic dialysis as determined by whole-body counting. With few exceptions, uremic patients were found to have body K levels grams of K per kilogram of body weight) normal for their age and sex. The mean total-body nitrogen levels of the uremic patients expressed in terms of body K were similar to those of the normal contrast population, but lower than that of osteoporotic patients. The new insights acquired by the application of in vivo neutron activation technique in studying chronic renal disease, particularly with patients on hemodialysis, are to date chiefly suggestive. However, the acquisition of further data appears to be of considerable value for the understanding of chronic renal failure and the managment of patients through hemodialysis, particularly with respect to associated osteodystrophic changes.