PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Hyperparathyroidism, Secondary”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1978

Anemia and secondary hyperparathyroidism.

Anemia has been recognized recently as a possible complication of primary hyperparathyroidism. If the hyperparathyroid state can induce anemia in patients with normal kidney function, the extremely high levels of circulating parathyroid hormone usually observed in hyperparathyroidism secondary to chronic renal failure may have an unfavorable influence on the anemia of uremic patients. We investigated the influence of subtotal parathyroidectomy on the severity of the anemia of 18 uremic subjects undergoing long-term hemodialysis therapy. Subtotal parathyroidectomy resulted in a significant increase of mean hematocrit value. RBC count, and hemoglobin level. Serial bone biopsies suggested a relationship between the amount of marrow fibrosis and the improvement of anemia after surgery, but the precise mechanism of this phenomenon is still unknown.

Adult↗
PubMed1978

[Skeletal manifestations of primary and secondary hyperparathyroiditis. Differential radiological diagnostic problems].

Primary and secondary hyperparathyroidism are both marked by widespread skeletal demineralisation, subperiosteal erosion of the cortex, brown tumours, osteosclerosis, and extraosseous calcification. Differential diagnosis is guided by the different association of these findings. Brown tumours and more extensive erosion are marks of the primary form, whereas osteosclerosis and extra-osseous calcification are a prominent feature of secondary hyperparathyroidism. Radiologists, therefore, should direct their attention to features suggesting the presence of secondary forms in addition to looking for bone alterations associated with hyperparathyroidism.

Bone Diseases↗
PubMed1978

Secondary hyperparathyroidism in chronic renal failure. Pathophysiology and treatment.

The secondary hyperparathyroidism of chronic renal failure is a result of many factors which result in chronic stimulation of parathyroid hormone secretion and secondary hyperplasia of the parathyroid glands. The secretion and metabolism of parathyroid hormone and its fragments in chronic renal failure are complex and only partially understood. Constant elevated levels of PTH contribute to bone disease and other clinical features of chronic renal failure. Calcium supplementation, high calcium dialysis, control of plasma phosphate and judicious use of the vitamin D metabolites can, to a large extent, prevent or control the development of secondary hyperparathyroidism. Subtotal parathyroidectomy or total parathyroidectomy with autotransplantation is indicated in certain cases, sometimes on an emergency basis. Prevention of postoperative hypocalcemia requires careful management. Successful renal transplantation is usually associated with gradual healing of the bone disease and slow, but sometimes incomplete involution of the parathyroid hyperplasia.

Bone and Bones↗
PubMed1992

Clinical and biochemistry findings, and parathyroid hormone concentrations in three horses with secondary hyperparathyroidism.

Three cases of horses with nutritional secondary hyperparathyroidism (NSH) are described. The horses showed typical thickening of the maxillae and mandibular bones with or without lameness. Laboratory findings included elevated concentrations of parathyroid hormone (carboxy-terminal and mid-molecule fractions), alkaline phosphatase and an increase in the fractional excretion rate of serum inorganic phosphorus.

Animals↗
PubMed1976

Secondary hyperparathyroidism in human kidney transplant recipients.

76 kidney transplant recipients who were up to 4 years post transplant, were studied to assess the incidence of secondary hyperparathyroidism. All patients had good renal function with a mean serum creatinine of 1.4 mg/100 ml. Secondary hyperparathyroidism, as evidenced by increased serum parathyroid hormone levels, was present in 53 of the 76 patients (66%) and radiologic bone disease in 26 of the 76 patients (34%), while hypercalcemia (serum calcium greater than 11.0 mg/100 ml) occurred in only 6 patients (8.5%). The incidence of secondary hyperparathyroidism decreased slightly with time following transplantation, but the degree of secondary hyperparathyroidism as indicated by the levels of serum parathyroid hormone at various times following renal transplantation was essentially similar. The causes for the persistence of this condition are not totally known, but it was found that its incidence was related to the duration of dialysis prior to transplantation.

Follow-Up Studies↗
PubMed1992

Thyroid carcinoma in patients with secondary hyperparathyroidism.

There have been few reports of coexistence of secondary hyperparathyroidism (2 degrees HPT) and thyroid carcinoma. Eleven consecutive patients with 2 degrees HPT who underwent parathyroidectomy were analyzed. They consisted of six males and five females, whose age ranged from 34 to 55 years. None of the patients had a history of irradiation of the head or neck. Associated thyroid nodules were also present in seven patients (64%): four patients with benign nodules, and three patients with papillary carcinomas, and one with papillary carcinoma and two follicular adenomas. This incidence of thyroid carcinoma in the patient group with 2 degrees HPT (36%) was significantly higher than that of the autopsy group in the same geographical area (11%). The level of carboxyl-terminal parathyroid hormone in the patients with thyroid carcinoma was higher than that in the patients without thyroid carcinoma (P less than 0.05). The importance of searching for possible thyroid cancer in patients with 2 degrees HPT should be emphasized.

Adult↗
PubMed1992

Secondary hyperparathyroidism and sonographic evaluation of parathyroid gland hyperplasia in dialysis patients.

Ninety-six hemodialysis patients were examined by ultrasonography of the parathyroid glands to study the prevalence of parathyroid gland hyperplasia and to assess the relevance of sonography in the evaluation of secondary hyperparathyroidism. The results were compared with clinical, biochemical and radiological parameters. Thirty-two (33.3%) patients had sonographically enlarged glands. Of them 19 had 1 and 13 had 2 and more enlarged glands. Patients with enlarged glands, compared to those with undetected glands, had a significantly higher frequency of bone and joint pains (65.5% vs 40.6%), radiological features of hyperparathyroid bone disease (in hands 28.1% vs 6.9%, in acromioclavicular joints 37.5% vs 13.6%) and higher levels of intact serum parathyroid hormone (1-84) concentration (52.8 +/- 47.9 pmol/l vs 18.1 +/- 18.0 pmol/l) and serum alkaline phosphatase concentration (260.2 +/- 201.1 U/l vs 129.8 +/- 127.3 U/l). Those with enlarged glands had been on dialysis for a longer period (87.7 +/- 51.0 months vs 62.5 +/- 47.4 months). The severity of secondary hyperparathyroidism increased with the number of enlarged glands. Our study shows that ultrasonography is a useful noninvasive screening method for the evaluation of secondary hyperparathyroidism in patients on hemodialysis and that sonographically enlarged glands may be a measure of the severity of secondary hyperparathyroidism.

Female↗
PubMed1992

[Adequate Ca level for dialysis patient (study on medical therapy for secondary hyperparathyroidism in dialysis patient)].

We evaluated our medical therapy of secondary hyperparathyroidism (2 degrees HPT) in dialysis patients. Ten hemodialysis patients with 2 degrees HPT (PTH-C; higher than 10ng/ml) were treated with vitamin D3, large amounts of phosphate binders and calcitonin and data over three years were examined. Our data showed that 2 degrees HPT is manageable by medical therapy. Furthermore, we suggest that the adequate Ca level for dialysis patients is to maintain the Ca (mEq/1) xP (mg/dl) at less than = 35. When plasma P is less than 6mg/dl. The maintenance of this Ca level successfully treated 2 degrees HPT, and this prevent the appearance of renal osteodystrophy (ROD) in dialysis patients.

Adult↗
PubMed1979

Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure.

Chronic renal failure is accompanied by secondary hyperparathyroidism. Inhibition of parathyroid hormone secretion has been reported to be induced by hypomagnesemia in conditions other than chronic renal failure, since severe hypomagnesemia is rare in chronic renal failure. In the case reported here, the patient had chronic renal failure and malabsorption-induced hypomagnesemia; she exhibited hypoparathyroidism while hypomagnesemic, and hyperparathyroidism after magnesium was replaced. Hypomagnesemia induced parathyroid hormone suppression in this patient with chronic renal failure, despite the presence of chronic hyperfunctioning parathyroid cells.

Female↗
PubMed1975

Neuromuscular disease in secondary hyperparathyroidism.

Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studies had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studies histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.

Adolescent↗
PubMed1976

[Plasma-cAMP in primary and secondary hyperparathyroidism (author's transl)].

3 patients with operatively proven primary hyperparathyroidism showed normal plasma cAMP concentrations. 5 patients in chronic dialysis treatment independent of the level of parathyroid hormone had increased plasma cAMP concentrations. These observations suggest that there is under these circumstances no regulation of plasma cAMP by the parathyroid hormone.

Cyclic AMP↗
PubMed1992

Low-dose intravenous calcitriol treatment of secondary hyperparathyroidism in hemodialysis patients. Italian Group for the Study of Intravenous Calcitriol.

Intravenous calcitriol is known to directly suppress PTH secretion and release. We evaluated the effect of four months of treatment with low-dose intravenous calcitriol on PTH levels in 83 hemodialysis patients. The criteria for including patients in the study were a serum PTH levels at least four times the normal limit, a serum total calcium less than 10 mg/dl and good control of the serum phosphorus level. All patients underwent standard bicarbonate or acetate dialysis; dialysate calcium level was maintained at the usual 3.5 mEq/liter concentration. Initial calcitriol dose was 0.87 +/- 0.02 (SEM) micrograms (0.015 micrograms/kg body wt) thrice weekly at the end of dialysis, and it was reduced in case of hypercalcemia or elevated calcium-phosphate product. Seven out of 83 patients dropped out during treatment. Among the 76 patients who completed the study, 58 (76%) showed a highly significant decrease of intact PTH levels (average reduction 48%) and of alkaline phosphatase levels after four months of therapy. Total serum calcium increased slightly but significantly in the responder group but remained unchanged in the non-responders. No significant changes in ionized calcium levels could be detected, even in responders. Treatment was well tolerated by patients, but 60% of them had transient episodes of hyperphosphatemia. Mean serum phosphate was 4.95 mg/dl at the beginning of the study. It increased significantly after four months of treatment in patients who showed a decrease of PTH levels, although it remained within acceptable limits, below 5.5 mg/dl. Twenty-eight of 76 patients (37%) reduced the dose of calcitriol because their calcium-phosphate products exceeded 60.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗