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Biomedical subjects

M J Favus

Publications and source records attributed to M J Favus.

At least 91 records · Page 5Linked to original sources
PubMed1980

Vitamin D metabolism during recovery from severe osteitis fibrosa cystica of primary hyperparathyroidism.

Serum concentrations of 1,25-dihydroxyvitamin D [1,25-(OH)2D] and immunoreactive parathyroid hormone were measured before and for 7 months after the removal of a 15-g parathyroid adenoma from a 44-yr-old woman with primary hyperparathyroidism and severe osteitis fibrosa cystica. Despite the fall in parathyroid hormone levels from preoperative levels of 20 to 1--2 ng/ml after surgery (normal, up to 1.2 ng/ml), serum 1,25-(OH)2D concentrations remained markedly elevated (156 pg/ml) preoperatively; 124 pg/ml 17 weeks postoperative), approaching the normal range (18--56 pg/ml) only after 5 months (65 pg/ml). Hypocalcemia and hypophosphatemia persisted despite oral 1,25-(OH)2D3 (1 and 2 micrograms/day) and large doses of (oral and iv) calcium gluconate (up to 30 g/day). Healing of the skeletal lesions, reversal of the myopathy, and return of 1,25-(OH)2D circulating levels to normal corresponded to the time when serum phosphate became normal. The stimulus for the persistently elevated serum 1,25-(OH)2D levels may have been hypocalcemia per se, low serum phosphate, or an unidentified signal that paralleled serum phosphate, as serum PTH levels remained in the upper normal range throughout the recovery period.

Adenoma↗
PubMed1980

Clinical characteristics and pathogenetic mechanisms in hyperuricosuric calcium oxalate renal stone disease.

Studies of patients with hyperuricosuria have provided four kinds of evidence linking their hyperuricosuria to calcium stone formation and identifying them as a distinct entity apart from other calcium stone formers. The evidence includes a more virulent natural history of stone disease, in vitro evidence for heterogeneous nucleation of calcium oxalate crystallization by seed crystals for uric acid or sodium hydrogen urate, and a reduction by uric acid or urate of the inhibitory activity which urine normally has upon calcium oxalate crystal growth. The fourth bit of evidence, the dramatic reduction in stone formation rates with allopurinol treatment, will be discussed in detail in a following paper.

Adolescent↗
PubMed1980

The effects of allopurinol treatment on stone formation on hyperuricosuric calcium oxalate stone-formers.

The syndrome of hyperuricosuric calcium oxalate nephrolithiasis, consisting of calcium oxalate stones, hyperuricosuria and the absence of known causes of calcium stones, follows a course of particularly severe stone disease. This course can be dramatically altered by the reduction in new stone formation by the chronic administration of allopurinol. The mechanisms proposed in linking hyperuricosuria to calcium oxalate stones are both dependent upon the presence of oversaturation of the urine with one or both species of uric acid. Allopurinol reduces the saturation of the urine with respect to sodium hydrogen urate and reduces urine concentration of undissociated uric acid, thus directly altering the pathogenetic mechanisms proposed for this disorder.

Allopurinol↗
PubMed1978

Idiopathic hypercalciuria in children: prevalence and metabolic characteristics.

A group of 273 children with minor complaints was screened for idiopathic hypercalciuria by measurement of the urine Ca/Cr. Borderline or definitely high levels were noted in 17 of these children, 11 of whom were boys. More intensive metabolic studies were completed on four of these children and on three children who were noted to have symptomatic renal stones associated with idiopathic hypercalciuria. These studies suggest that IH, well recognized in adults, may have its origins in childhood and that appropriate management, if initiated in childhood, may have significant long-term benefits.

Adolescent↗
PubMed1977

Plasma thyroglobulin in detecting thyroid carcinoma after childhood head and neck irradiation.

The level of thyroglobulin in plasma was measured in 904 subjects with a history of head and neck irradiation during childhood to evaluate its potential value in screening for and differentiating thyroid neoplasms. Mean plasma thyroglobulin level was significantly elevated in subjects with nodular thyroid disease versus those without evidence of nodules (49.8 versus 27.0 ng/ml). However, the overlap with normal subjects does not allow thyroglobulin assays to serve as the only screening procedure. The mean levels in subjects with benign and malignant thyroid nodules were indistinguishable (48.8 versus 53.9 ng/ml). Thirteen percent of otherwise normal-appearing subjects had elevated values that may represent clinically inapparent thyroid disease. It is concluded that in screening large numbers of persons at risk for thyroid neoplasia, thyroglobulin assays are useful in combination with other modes of evaluation. The assay is without value in distinguishing benign from malignant disease.

Adult↗
PubMed1977

Salivary gland neoplasms as a late consequence of head and neck irradiation.

An increased occurrence of salivary tumors was observed in 1922 patients who received radiation to the tonsils and nasopharynx. Twenty-seven tumors, 19 benign and eight malignant, were found in this group as compared with an expected 0.2 malignant and less than 1 benign tumor. The latent period between the initial radiation treatment and diagnosis ranged from 7 to 32 years. After the first 15 years the incidence (77 cases/10(5) subjects/year) has remained constant and shows no indication of declining. Continued observation for salivary gland tumors is therefore indicated for subjects who received childhood irradiation.

Adult↗
PubMed1976

Thyroid cancer occurring as a late consequence of head-and-neck irradiation. Evaluation of 1056 patients.

From January 1 to September 30, 1974, we examined 1056 of 5266 subjects (20.1%) who had received therapeutic irradiation primarily for infections and inflammatory disease of the upper respiratory tract at our institution during the 1940's and 1950's. The tonsillar and nasopharyngeal region was the treatment site in 85% of those examined. Palpable nodular thyroid disease was found in 16.5%, and nonpalpable lesions were detected by 99m Tc pertechnetate thyroid imaging in an additional 10.7%, for a prevalence of nodular disease of 27.2%. Operation on 71% with nodular disease revealed thyroid cancer in 33% (60 of 182). Preliminary analysis for potential risk factors suggests a correlation between radiation exposure and the presence of thyroid nodules (P less than 0.001). These findings indicate that nodular thyroid disease, both benign and malignant, continues as a major health problem for at least 35 years in exposed subjects.

Adolescent↗
PubMed1975

Effects of magnesium deficiency and thyroparathyroidectomy on calcium active transport by rat duodenum.

Mg deficiency was produced in rats by feeding a Mg-free diet. Ten days of dietary Mg depletion led to an increase in active duodenal Ca absorption in sham-operated animals, but this increase was abolished by thyroparathyroidectomy (TPTX). In addition, TPTX reduced Ca absorption in control aminals fed a Mg-containing diet. More prolonged Mg deficiency was produced by feeding sham-operated animals the Mg-free diet for 19 days. This condition resulted in more marked hypomagnesemia and a depression of Ca transport rates to the level observed in the TPTX groups. These results are consistent with the concept that adaptation of duodenal Ca transport in response to Mg deficiency occurs through an increase in parathyroid hormone (PTH) secretion; however, direct blood PTH measurements will be required to prove this point.

Animals↗
PubMed1974

Effects of dietary calcium restriction and chronic thyroparathyroidectomy on the metabolism of (3H)25-hydroxyvitamin D3 and the active transport of calcium by rat intestine.

Previous studies have shown that chronically thyroparathyroidectomized (TPTX) rats, fed a diet with restricted calcium but adequate phosphorus and vitamin D content, have higher levels of intestinal calcium absorption than controls. The results of recent acute experiments have suggested that parathyroid hormone (PTH) may be essential for regulating the renal conversion of 25-hydroxyvitamin D(3) (25-OH-D(3)) to 1,25-dihydroxyvitamin D(3) [1,25-(OH)(2)-D(3)] in response to dietary calcium deprivation. Since 1,25-(OH)(2)-D(3) is the form of the vitamin thought to be active in the intestine, increases in calcium transport mediated by this metabolite would not be expected to occur in the absence of the parathyroid glands if the preceding model is correct. The present study was undertaken to examine the chronic effects of both dietary calcium restriction and the absence of PTH on the metabolism of [(3)H]25-OH-D(3) and duodenal calcium-active transport in rats given thyroid replacement. These relatively long term studies confirm earlier observations which indicated that the adaptation of calcium absorption to a low calcium intake occurs in both sham-operated and TPTX animals. The present studies also demonstrated that despite reduced levels of 1,25-(OH)(2)-D(3) in the plasma of chronically TPTX animals fed a low calcium diet, the accumulation of this metabolite in at least one target tissue, intestinal mucosa, is identical in both the sham-operated and TPTX groups. A reduced, but continued level of 1,25-(OH)(2)-D(3) production, together with its selective accumulation by intestinal mucosa, probably explains the calcium adaptation which is observed inspite of the chronic absence of the parathyroid glands.

Animals↗
PubMed1973

Effects of cortisone administration on the metabolism and localization of 25-hydroxycholecalciferol in the rat.

Glucocorticoid administration is known to decrease calcium absorption in vivo and the vitamin D-dependent active transport of calcium by rat duodenum in vitro. The basis for this antivitamin D-like effect of glucocorticoids is unclear. Previous studies in the rat failed to demonstrate an effect of glucocorticoid treatment on the hepatic conversion of the parent vitamin to 25-hydroxycholecalciferol (25-HCC). Moreover, pharmacologic doses of 25-HCC did not restore intestinal calcium transport to normal. The results of these experiments suggested that if indeed glucocorticoids interfere with the metabolism of vitamin D, the step involved must be subsequent to 25-hydroxylation. The present studies demonstrate that the administration of cortisone to vitamin D-deficient rats does not affect the rate of conversion of a physiologic dose of [(3)H]25-HCC to the biologically important metabolite, 1,25-dihydroxycholecalciferol (1,25-DHCC). Furthermore, pretreatment with glucocorticoids affects neither the tissue distribution nor the subcellular localization on or in intestinal mucosal cell nuclei of 1,25-DHCC. Of note is the fact that 1,25-DHCC is currently considered to be the "tissue-active" form of the vitamin in the intestine. Whereas tissues from cortisone-treated animals had increased concentrations of the biologically less active 24,25-DHCC, the physiologic significance of this observation remains unclear. The results of the present studies strongly support the concept that the antivitamin D-like effects of glucocorticoids in the intestine are due to hormonal influences on the biochemical reactions responsible for calcium transport. While the effects of these hormones are opposite in direction to those of vitamin D, they occur by a mechanism that is independent of a direct interaction with either the vitamin or its biologically active metabolites.

Animals↗
PubMed1973

Effects of 1,25-dihydroxycholecalciferol on intestinal calcium transport in cortisone-treated rats.

The administration of glucocorticoids may decrease intestinal calcium absorption in vivo and the active transport of calcium in rat duodenum in vitro. It has been suggested that this apparent "anti-vitamin D-like" effect of steroid hormones may be related to alterations in vitamin D metabolism. In order to test this hypothesis, vitamin D-deficient control and cortisone-treated rats were given an intraperitoneal injection of 5.5 IU of 1,25-dihydroxycholecalciferol (1,25-DHCC), the probable end-organ active vitamin D metabolite in the intestine, and 16 h later studies of duodenal calcium transport were performed in modified Ussing chambers. In the vitamin D-deficient state, cortisone administration was associated with a diminution in J(MS), J(Net), and the flux ratio (J(MS)/J(SM)). While the magnitude of the increases in J(MS) and J(Net) that resulted from 1,25-DHCC treatment were approximately the same in control and cortisone-treated animals, 1,25-DHCC failed to restore these parameters to "normal levels" in the steroid-treated rats. Furthermore, contrary to the results obtained in the saline-treated controls, 1,25-DHCC failed to reduce J(SM) in the duodenum from cortisone-treated rats. The cortisone-related defect in calcium transport was due to alterations in both unidirectional calcium fluxes (decrease in J(MS) and increase in J(SM)), such that the J(Net) and the flux ratio (J(MS)/J(SM)) were only approximately 50% of the levels achieved in vitamin D-deficient control animals repleted with the same dose of 1,25-DHCC. The administration of 1,25-DHCC was accompanied by a marked increase in the serum calcium levels of control rats, but there was no such response in the cortisone-treated group. The results support the concept that under the conditions of these experiments in the rat the apparent antagonism between glucocorticoids and vitamin D may be due to steroid hormone-related alterations in end organ function that are independent of any direct interaction between the hormone and the vitamin and that cannot be reversed by the vitamin.

Animals↗