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Biomedical subjects

G M Palmieri

Publications and source records attributed to G M Palmieri.

At least 55 records · Page 3Linked to original sources
PubMed1982

The effects of diltiazem in dystrophic hamsters.

Calcium accumulates in muscles of dystrophic hamsters (DH) and patients with Duchenne muscular dystrophy. Various Ca antagonists were beneficial to the cardiomyopathy of DH, but had only minor effects on skeletal muscle. We administered a new Ca antagonist, diltiazem, 25 mg/kg/day orally to normal and dystrophic hamsters from ages 37 to 92 days. We observed a marked reduction in muscle Ca in DH treated with diltiazem: 73% in the heart, 61% in the diaphragm, and 48% in the rectus femoris. Plasma CK was significantly lower (by 37%) in treated DH, while the elevated rate of noncollagen protein synthesis in the diaphragm was not diminished. Histologically, the most important change was a reduction in Ca deposits in the heart. Diltiazem was well-tolerated by all animals and did not modify Ca content in normal hamsters. This study suggests that diltiazem may have therapeutic value in those conditions that are accompanied by excessive accumulation of Ca in tissues, such as muscular dystrophy.

Animals↗
PubMed1982

Muscle calcium and magnesium content in Duchenne muscular dystrophy.

Calcium (Ca) and magnesium (Mg) content were determined in muscle of 27 patients with Duchenne muscular dystrophy, 36 with other neuromuscular diseases, and 22 whose muscle biopsy specimens were histochemically normal. Muscle Ca was significantly elevated in all diseases studied but was about 50% higher in Duchenne dystrophy patients (p less than 0.0001). Mg was decreased by 44% in Duchenne dystrophy, compared with less striking deficits in other diseases (p less than 0.005). In older, nonambulatory Duchenne dystrophy patients, Mg was significantly lower than in younger, ambulatory patients (p less than 0.001); muscle Ca was the same in both groups. On the basis of noncollagen nitrogen concentration, muscle MG depletion could not be attributed solely to reduced muscle mass. These findings strengthen arguments for a role of Ca in the pathogenesis of muscular dystrophy and may implicate Mg depletion as another pathogenetic factor.

Adolescent↗
PubMed1981

The postabsorptive urinary hydroxyproline (spot-HYPRO) in patients with multiple myeloma.

The simple postabsorptive urine hydroxyproline (Spot-HYPRO) with dialyzable and non-dialyzable (ND) fractions was measured in 28 patients with multiple myeloma. Myeloma patients with bone disease had higher total Spot-HYPRO and dialyzable fractions (P less than 0.001) than myeloma patients without bone disease or controls. The ND fraction of the Spot-HYPRO was elevated in myeloma patients with renal disease as compared with myeloma patients without renal disease and controls (P less than 0.01). Follow-up studies of ten myeloma patients demonstrated a close correlation between Spot-HYPRO and the dialyzable fraction and the evolution of bone disease. The Spot-HYPRO and its dialyzable fraction constitute a simple, inexpensive, and accurate test for the diagnosis and follow-up of the skeletal disease in patients with multiple myeloma.

Bone Resorption↗
PubMed1981

Parathyroid ablation in dystrophic hamsters. Effects on Ca content and histology of heart, diaphragm, and rectus femoris.

Cumulative evidence indicates that there is an increased accumulation of calcium in dystrophic muscle and that this may have a pathophysiological role in the progression of the dystrophic process. The accumulation may be related to a defect of the plasma membrane. Because parathyroid hormone (PTH) stimulates calcium influx into the cytosol, the chronic effects of surgical ablation of the parathyroid glands on muscle Ca, Mg, protein synthesis, and histology, as well as plasma creatine phosphokinase (CPK), Ca, and Mg, were studied in normal and dystrophic (BIO 14.6) hamsters. Thyroparathyroidectomized (TPTX) hamsters receiving replacement doses of l-thyroxine were killed at age 90 d, 55 d after TPTX. In intact dystrophic hamsters, the Ca content in the heart was 20 times higher than in normal animals and was reduced by half in TPTX dystrophic hamsters. Similar results were observed in diaphragm and rectus femoris. No abnormalities in Mg content were observed in intact or TPTX dystrophic hamsters. Ether-extractable fat of the heart and diaphragm was reduced in dystrophic hamsters and was not modified by TPTX. Protein synthesis was enhanced in the diaphragm of dystrophic hamsters but was not changed by TPTX. The concentration of CPK in plasma was elevated in dystrophic hamsters and fell significantly after TPTX. In the latter animals, microscopic examination of the heart showed lesser signs of dystrophy, particularly in the degree of fibrosis. To determine the degree of dystrophy at the age when TPTX was performed, identical analyses were made in 35-d-old hamsters. Definitive histological signs of dystrophy were observed, and although the Ca content in heart, diaphragm, and rectus femoris was elevated, the values were lower than in 90-d-old intact and TPTX dystrophic hamsters. This indicates that chronic TPTX in dystrophic hamsters reduces, but does not arrest, the dystrophic process. In normal hamsters, a 50% reduction in plasma Ca concentration was observed 6 h after TPTX; 55 d after TPTX, however, plasma Ca was within normal limits in both normal and dystrophic hamsters. No parathyroid tissue was observed in serial sections of the trachea and adjacent tissues in TPTX animals. This suggests that in chronically TPTX hamsters fed a standard laboratory diet, plasma Ca can be maintained by mechanisms independent of parathyroid function. THE DATA INDICATE THAT IN DYSTROPHIC HAMSTERS TPTX CAUSES A MARKED REDUCTION IN: (a) muscle Ca accumulation, (b) levels of plasma CPK and, (c) intensity of histological changes in the heart. These changes were independent of the levels of plasma Ca and were not observed in normal hamsters. We conclude that PTH accentuates the dystrophic process, probably by enhancing the already increased Ca flux into muscle (apparently caused by defective sarcolemma). We postulate that normal secretion of PTH may have a deleterious effect in congenital or acquired conditions associated with altered plasma membranes.

Adipose Tissue↗
PubMed1981

Increased adenine nucleotide turnover in duchenne muscular dystrophy.

To investigate a possible disorder of adenine nucleotide turnover in Duchenne muscular dystrophy, we evaluated 15 patients with mild Duchenne muscular dystrophy, eight patients with severe muscular dystrophy, seven patients with other neuromuscular disorders, and eight patients with hypogammaglobulinemia but no muscle disease. The serum urate concentration was similar in all four groups. Base line urinary purine excretion was elevated in all patients with neuromuscular disease with values of 1.72 +/- 0.15, 2.37 +/- 0.22, 2.49 +/- 0.35, and 2.60 +/- 0.48 mumoles/100 ml glomerular filtration for control subjects, mild Duchenne muscular dystrophy, severe disease, and other neuromuscular diseases, respectively. Adenine nucleotide pool turnover was measured by labeling with [8-14C]adenine and then 5 days later administering intravenous fructose. Five-day cumulative mean radioactivity excretion was elevated in mild and severe Duchenne muscular dystrophy with excretion values of 11.4 +/- 0.7 and 11.5 +/- 1.1% of administered radioactivity, respectively, as compared to 9.0 +/- 0.9% of administered radioactivity for control subjects. After intravenous fructose infusion, patients with Duchenne muscular dystrophy had a less than normal rise in serum urate concentration, a normal increase of urinary urinary purine excretion, and a greater than normal elevation of urinary radioactivity excretion and urinary purine specific activity. Patients with other neuromuscular diseases had virtually no rise in plasma urate concentration, less than normal increase in urinary total purine excretion, and a greater than normal increase of urinary radioactivity excretion and urinary specific activity. These observations suggest that there is an increased rate of adenine nucleotide turnover in Duchenne muscular dystrophy. In patients with other neuromuscular disease an increased rate of adenine nucleotide turnover resembled the abnormality expected from a diminished adenine nucleotide pool.

Adenine Nucleotides↗
PubMed1981

Postabsorptive urinary hydroxyproline test in patients with metastatic bone disease from breast cancer.

Postabsorptive urine hydroxyproline (HYPRO) excretion ("spot" HYPRO test) was compared with the 24-hour urine excretion of HYPRO in 45 patients with breast cancer and nine normal subjects on a low-gelatin diet. A good correlation was observed between the results of these two tests in both groups. Patients with skeletal metastasis showed a higher spot HYPRO value than those without bone involvement and the number of lesions by bone scanning correlated with the values of spot HYPRO. In 20 of 22 patients with bone metastasis followed up for three to 19 months, spot HYPRO values correlated well with the evolution of bone disease. We conclude that the spot HYPRO test is a simple, inexpensive, and accurate method for the diagnosis and follow-up of patients with skeletal metastasis from breast cancer.

Bone Neoplasms↗
PubMed1980

Parathyroid storm.

Primary hyperparathyroidism frequently has a chronic and relatively benign course. Occasionally, however, it may have a stormy presentation requiring prompt adequate diagnosis and urgent surgical treatment. We describe a 71-year-old woman who had severe hypercalcemia, seizures, and coma refractory to treatment with anticonvulsant drugs, intravenous infusion of normal saline, furosemide, glucocorticoids, calcitonin, and hemodialysis. Bone roentgenograms were normal, but a strikingly positive bone scan that also showed marked soft-tissue uptake prompted the diagnosis of primary hyperparathyroidism and the successful surgical removal of a large parathyroid adenoma. This was followed by a remarkable recovery and marked reduction in soft-tissue radioactive uptake on bone scan. The association of hypercalcemia and seizures and the diagnostic value of bone scanning are discussed. An up-to-date review of the literature is presented. We proposed this condition to be named "parathyroid storm" on the basis of the rapid and lethal course unless surgery is performed without delay.

Acute Disease↗
PubMed1979

Hypercalcemic effect of insulin in the chick.

There are conflicting reports on the effect of insulin on plasma Ca concentration in rats. Low doses appear to decrease and higher doses to increase plasma Ca. Since birds are known to be very sensitive to parathyroid hormone and have resistance to the hypoglycemic effects of insulin, the effect of commercial and highly purified insulin on plasma Ca concentration was studied in 10-day-old chicks 60 min after the administration of the hormone. Both commerical bovine and purified porcine insulin provoked a dose-related elevation of plasma Ca. Although hypophosphatemia was observed with the highest dose of insulin used (0.4U), hypercalcemia was observed with 0.05 U insulin, a dose that did not modify plasma phosphate concentration. The slopes of the dose-response curves of insulin and parathyroid hormone were indistinguishable and different from that of 1 alpha-hydroxyvitamin D3. Neither propranolol nor deprivation of vitamin D altered the hypercalcemic response to insulin. Unexpectedly, propranolol (40 microgram/chick) provoked elevation of plasma Ca. It is concluded that insulin raises plasma Ca concentration in the chick by a mechanism(s) not yet elucidated.

Animals↗
PubMed1974

Immunochemical localization of parathyroid hormone in cancer tissue from patients with ectopic hyperparathyroidism.

Immunoreactive parathyroid hormone (PTH) in nonparathyroid malignant tumors associated with hypercalcemia and hypophosphatemia in the absence of demonstrable bone metastases was determined by radioimmunoassay and immunofluorescent techniques. Six of seven tumors contained material with immunological cross-reactivity to bovine PTH by radioimmunoassay and immunofluorescence. The intensity of the immunofluorescent stain varied considerably in the different tumors. From 15 to 90% of neoplastic cells were stained specifically with fluorescein-labeled anti-PTH. In contrast, normal parathyroid glands and parathyroid adenomas showed uniform distribution of immunofluorescence in all parenchymal cells. In one malignant tumor, PTH was localized also by immunoautoradiography. In every case PTH was detected only in the cytoplasm of parenchymal cells. One patient lacked detectable PTH in his tumor, yet showed regression of the hypercalcemia to normal values after removal of large masses of neoplastic tissue and recurrence of hypercalcemia when new growth occurred.Dilutional radioimmunoassay curves of nonparathyroid malignant tumors were in most cases different from those obtained with extracts of normal parathyroid glands and parathyroid adenomas. Although both nonparathyroid neoplasmas and parathyroid extracts demonstrated immunoheterogeneity by gel filtration, greater heterogeneity was found in nonparathyroid malignant tumors. In those tumors in which immunological cross-reactivity to PTH was detected, the capability of secreting PTH may be restricted to derepressed cell clones amidst other neoplastic cells, whereas the greater heterogeneity of ectopic PTH may reflect hormone cleavage by proteolytic enzymes in the tumor that is less specific than the Pro-PTH cleaving enzyme in the parathyroids.

Adenoma↗