Biomedical subjects

S J Silverberg

Publications and source records attributed to S J Silverberg.

46 records · Page 3Linked to original sources

PubMed1989

Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism.

PURPOSE: The classic neuromuscular abnormalities of primary hyperparathyroidism are based on observations from an earlier time when the disease presented commonly with signs and symptoms. The purpose of the present study was to test for neuromuscular abnormalities among patients currently seen with primary hyperparathyroidism, in whom the vast majority are asymptomatic. PATIENTS, METHODS, AND RESULTS: Forty-two patients (30 women, 12 men) were studied. Serum calcium level was 11.1 +/- 0.1 mg/dL (normal, 8.7 to 10.7 mg/dL); phosphorus level was 2.8 +/- 0.1 mg/dL (normal, 2.5 to 4.5 mg/dL). Parathyroid hormone levels by radioimmunoassay for N-terminal and for mid-molecule regions were 32.6 +/- 2.4 pg/mL (normal, 8 to 24 pg/mL) and 831 +/- 127 pg/mL (normal, 50 to 330 pg/mL), respectively. Although generalized weakness and easy fatigability were common complaints, they were not seen on neurologic examination. No patient showed typical neuromuscular findings such as muscle weakness or atrophy, hyperreflexia, abnormal gait, tongue fasciculations, or objective changes in mental status. On the other hand, paresthesias and muscle cramps were reported by 22 patients (52%). Neurologic examination in 12 patients (29%) demonstrated findings consisting of either stocking-glove loss of pain sensation or loss of vibratory sensation with diminished reflexes. Creatine phosphokinase levels were normal in all patients. Electromyography and nerve conduction studies were performed in nine patients. None showed myopathy or signs of motor unit denervation. Isolated nerve abnormalities (n = 6) and nonspecific sensory neuropathy (n = 2) were observed. CONCLUSION: We conclude that the classic neuromuscular syndrome of primary hyperparathyroidism is rarely seen among a typical modern-day group of patients with primary hyperparathyroidism. The results suggest that the neurologic component of primary hyperparathyroidism should be included among those features of the disease that have changed along with other aspects of the clinical profile of primary hyperparathyroidism.

Aged↗

PubMed1987

Neoplastic hypercalcemia: physiologic response to intravenous etidronate disodium.

Following a four-day control period during which an elevated serum calcium level either stabilized or continued to rise despite maximally tolerated saline diuresis, 12 patients with neoplastic hypercalcemia were treated with intravenous etidronate disodium (etidronate) 7.5 mg/kg/day for up to seven days. Serum calcium reverted to normal levels in all patients, with the mean pretreatment serum calcium level of 12.5 +/- 0.4 mg/dl dropping to 9.2 +/- 0.2 mg/dl (p less than 0.01) by Day 7. Elevated urinary calcium (1,107 +/- 134 mg/g creatinine) and hydroxyproline levels (154 +/- 16 mg/g creatinine) declined to 245 +/- 52 mg/g creatinine and 75 +/- 14 mg/g creatinine, respectively, suggesting a marked reduction in bone resorption following treatment. Serum phosphorus levels were unchanged, but urinary phosphorus levels dropped rapidly from 1,181 +/- 125 mg/g creatinine before treatment to 723 +/- 94 mg/g creatinine after two days. Serum parathyroid hormone levels (mid-molecule assay) were suppressed before treatment (64 +/- 16 pg/ml), but rose rapidly to 223 +/- 68 pg/ml by Day 7 of treatment. The value of serum 1,25-dihydroxyvitamin D was initially below normal (16 +/- 3 pg/ml), but rose rapidly with treatment to 42 +/- 12 pg/ml by Day 7. Symptoms of hypercalcemia and bone pain improved with treatment, and no serious adverse reactions to treatment were encountered. Intravenous etidronate is apparently an effective and safe treatment for neoplastic hypercalcemia.

Adult↗

PubMed1987

Postmenopausal osteoporosis.

Osteoporosis is a major public health problem, particularly for the postmenopausal woman. With the withdrawal of estrogen at menopause, bone resorption begins to exceed formation in remodeling cycles and bone mass is inexorably lost. Clearly, preventing postmenopausal osteoporosis is the aim of management. Individuals with risk factors for developing this condition should have noninvasive bone density determination and should be considered for preventive regimens. Therapeutic options for prevention include calcium, estrogen, and exercise. Once osteoporosis is established, therapeutic options may include those listed previously as well as fluoride and other modalities currently under investigation.

Bone Resorption↗

PubMed1986

The effect of oral phosphate administration on major indices of skeletal metabolism in normal subjects.

The effect of brief periods of phosphate administration on indices of human skeletal metabolism was investigated. Thirteen subjects (8 women, 5 men; 19-36 years old) received 2 g of oral phosphate daily for 5 days. Serum phosphorus rose 26% (3.8 +/- 0.1 mg/dl to 4.8 +/- 0.1 mg/dl; p less than .01) while total calcium fell (9.3 +/- 0.1 mg/dl to 8.9 +/- 0.1 mg/dl; p less than .01). Parathyroid hormone levels increased by 50% (14.1 +/- 2.0 pg/ml to 21.5 +/- 1.7 pg/ml; p less than .05) although values remained within the normal range. A persistent phosphaturia (0.64 +/- 0.10 g/g Cr to 1.8 +/- 0.4 g/g Cr; p less than .05) and a 69% fall in urinary calcium (80.8 +/- 10.0 mg/g Cr to 24.6 +/- 6.0 mg/g Cr; p less than .001) were observed. 1,25-dihydroxyvitamin D3 and urinary hydroxyproline concentrations did not change significantly but the bone gamma-carboxyglutamic acid protein (BGP) concentration rose 41% by day 2 (9.6 +/- 1.3 mg/ml to 13.5 +/- 2.2 mg/ml; p less than .005) and remained elevated throughout the study period. These results support the possibility that brief periods of phosphate administration may be useful in the therapy of disorders associated with low bone turnover, such as osteoporosis.

Administration, Oral↗

PubMed1985

Clinical clues to the cause of Addison's disease.

Tuberculosis and other potentially treatable diseases remain important causes of adrenal insufficiency. Knowledge of the cause of adrenal destruction, although often difficult to ascertain clinically, is necessary for appropriate management. Clinical data are reviewed in eight patients with Addison's disease who underwent computed tomographic scanning and in 31 additional patients with Addison's disease in whom autopsy was performed. Seven of eight patients (87 percent) with tuberculous Addison's disease of no greater than two years' duration had enlarged glands whereas patients with longer duration of disease had smaller or normal-sized glands. Adrenal enlargement was also found in five of six (87 percent) subjects with carcinomatous replacement of the adrenal glands. The adrenal glands were small or undetectable in each of 16 patients with idiopathic Addison's disease. Adrenal calcification was found in nine of 17 (53 percent) tuberculous patients and was not found in any of the 22 other patients. Duration of adrenal disease, adrenal size on computed tomographic scanning, and presence of adrenal calcification were useful clues to the cause of Addison's disease.

Addison Disease↗

PubMed1985

2,3-Dimercaptosuccinic acid as an antidote for lead intoxication.

2,3-Dimercaptosuccinic acid (DMSA) is an orally effective drug more specific and with a wider therapeutic index than currently available drugs for lead intoxication. Eighteen men with elevated blood lead (BPb) concentrations received either 30, 20, or 10 mg/kg DMSA for 5 days in three divided daily doses. The mean BPb level decreased 72.5%, 58.3%, and 35.5% of the pretreatment values, with a simultaneous elevation in urinary Pb excretion. Clinical symptoms and biochemical indices of lead toxicity also improved. Red blood cell d-aminolevulinic acid dehydratase activity increased, while urinary excretion of d-aminolevulinic acid and coproporphyrin fell. DMSA was well tolerated; the only observed adverse drug reaction was a mild, transient elevation of serum SGPT levels in two subjects. DMSA appears promising and may greatly simplify the treatment of lead intoxication.

Administration, Oral↗

PubMed1977

Inhibition of C1s-induced vascular leakage in guinea pigs by substituted benzamidine and pyridinium compounds.

A variety of benzamidine and pyridinium compounds were examined for their ability to inhibit irreversibly C1s-induced vascular leakage in guinea pig skin. Vascular leakage was compared with esterolysis of N-Z-L-Tyr-Np and catalysis of EAC42 formation by C1s. Vascular leakage correlated significantly better with esterolytic activity than with EAC42 formation. The presence of a sulfonyl fluoride moiety in the compounds is important in the inhibition of C1s-induced vascular leakage.

Amidines↗

PubMedDate not supplied

Osteoporosis and low bone mass in premenopausal and perimenopausal women.

OBJECTIVE: To characterize the historical, clinical, and biochemical features of 111 young women (age, <55 years) referred for evaluation of osteoporosis or low bone mass. METHODS: Women with a bone mineral density T score < or = -2.0 (N = 111) at one or more anatomic sites (by dual-energy x-ray absorptiometry) were assessed relative to anthropomorphic and biochemical characteristics and risk factors for osteoporosis. RESULTS: Of 111 women with low bone mass or osteoporosis, 73 (66%) had identifiable causes of bone loss, of which estrogen deficiency (menopause, premenopausal estrogen deficiency) and conditions associated with estrogen deficiency (anorexia nervosa, cancer chemotherapy) were the most common. Prolonged use of glucocorticoids was the most common secondary cause of osteoporosis. Of 38 women with no identifiable cause of bone loss, 21 were premenopausal (mean age, 38 +/- 10 years [standard deviation]) and 17 were perimenopausal (mean age, 50 +/- 3 years). The mean lumbar spine T score was -2.18 +/- 1.0 in the premenopausal and -2.51 +/- 0.6 in the perimenopausal women. Nontraumatic fractures were reported by 42% of the premenopausal women and 18% of the perimenopausal women. A family history of osteoporosis was reported by 71% of the premenopausal and 47% of the perimenopausal women. CONCLUSION: Most young women with osteoporosis or low bone mass had estrogen deficiency or another secondary cause of premature bone loss (or both). A subset of premenopausal and perimenopausal women, however, had no identifiable cause of bone loss. The strong family history of osteoporosis, especially in the premenopausal women, provides further support for current theories of a genetic predisposition to osteoporosis.

Adult↗

PubMedDate not supplied

Primary hyperparathyroidism in women: a tale of two cities--New York and Beijing.

The Western world has been used to describing disease on its terms, as if it is a prototype for the same disease found anywhere else in the world. It is unusual that one can test the hypothesis that a common disease can present in markedly different ways, depending on the country in which it is studied. We have had the opportunity to compare and contrast primary hyperparathyroidism in the United States and in China as seen in New York City and in Beijing. The cohort of subjects in each case was well over 100, and the experience extends to well over a decade of observations. In the United States, primary hyperparathyroidism typically presents as asymptomatic hypercalcemia in women within 10 years of menopause. Most often, it is discovered accidentally in the course of a routine multichannel chemistry screening test. The serum calcium is 10.5 + 0.1 mg/dL, within 1 mg/dL above the upper limit of normal, 10.2; the serum parathyroid hormone level is 118 + 9 pg/mL (within 1.5-2-fold above the normal limit, 65). The average 25-hydroxyvitamin D level is 21 ng/mL, in the lower range of normal. The classical clinical manifestations of primary hyperparathyroidism, stone and bone disease, have become much less common than earlier descriptions of the disease in the United States through the 1950s. Overt radiological bone disease (osteitis fibrosa cystica) is almost never seen, whereas stone disease is reduced in incidence from a high of 60% in the 1940s to current estimates of 15-20% now. Most patients are asymptomatic; skeletal involvement is detected only by measuring skeletal calcium by bone densitometry. Primary hyperparathyroidism in China presents much differently. Patients are younger, with an average age of 37. The serum calcium level is much higher, averaging about 12 mg/dL. PTH is over 20 times the upper limits of normal. The average 25-hydroxyvitamin D concentration is much lower than in the United States population, 8.8 ng/mL. Radiological evidence for osteitis fibrosa cystica is seen in 60% of patients; virtually all patients have osteoporosis. Thirty-five percent of patients suffer pathological fractures, most often of the femur or humerus. Forty-two percent demonstrate kidney stones, with half showing bilateral disease. Constitutional features of weakness and easy fatigability are always present. There are both facile and rather subtle explanations for this dramatically different presentation of the same disease in the United States (New York City) and China (Beijing).

Adult↗

PubMedDate not supplied

Biochemical markers of bone metabolism.

Bone metabolic homeostasis is regulated by a number of hormones and local modulators, and the study of these factors has been of major help in our understanding of bone disease. However, these parameters do not, in a strict sense reflect the metabolic and biochemical changes in the diseased bone tissue. Thus, there is a great interest in the study of biochemical specific "markers" of bone metabolic processes, namely of bone formation and bone resorption. Alkaline phosphatase, osteocalcin, osteonectin, and procollagen type I propeptides are the currently known markers of bone formation, whereas urinary hydroxyproline and hydroxylysine glycosides, plasma tartrate resistant acid phosphatase, and urinary hydroxy-pyridinium crosslinks of collagen are considered markers of bone resorption. In this paper, we review the background work on each of these markers, and subsequently give an overview of the currently available data on their usefulness in metabolic bone diseases, namely in Paget's disease of bone, primary hyperparathyroidism, osteoporosis, and renal osteodystrophy.

Biomarkers↗