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Biomedical subjects

L V Avioli

Publications and source records attributed to L V Avioli.

At least 289 records · Page 16Linked to original sources
PubMed1975

The Jewish Hospital of St. Louis therapeutic grand rounds no. 9. Diagnosis and therapy of acromegaly.

Acromegaly, the clinical expression of chronic hypersecretion of growth hormone, develops insidiously and is too often not recognized until the disease is advanced. However, a useful screening procedure, the measurement of serum growth hormone after an oral glucose load, is available. Though evidence suggesting that acromegaly may be a disorder of defective hypothalamic regulation of pituitary growth hormone secretion has accumulated, the pathogenesis of the diease is not sufficiently understood to permit consistently effective medical therapy. Current therapy, therefore, is directed toward destruction of growth hormone producing pituitary tissue. Patients with major suprasellar extension and chiasmal compression usually require transfrontal surgery. Patients without major suprasellar extension can be treated with external irradiation or with transsphenoidal surgery. It is our current practice to limit the former to young patients withe relatively modest elevation of the serum growth hormone concentration.

Acromegaly↗
PubMed1975

The Jewish Hospital of St. Louis therapeutic grand rounds number 10. Chemoprophylaxis of tuberculosis.

Isoniazid therapy has been proved an effective means of preventing overt clinical tuberculosis in persons with positive tuberculin skin tests, persons who are close contacts of active cases, and persons with inactive tuberculosis that were never treated. The administration of isoniazid in standard dosage for one year in these situations will help greatly to reduce tuberculosis as a community health problem in the future. Studies in recent years, however, point to hepatic dysfunction as a complication of isoniazid therapy in up to 10% of patients. In a few patients, liver disease as a complication of this therapy has been fatal. The likelihood of this complication increases with age. Accordingly, isoniazid chemoprophylaxis should be undertaken with the understanding that the patient has to be followed up closely, especially for evidence of liver disease during the course of therapy. This potentially serious side effect suggests that isoniazid chemoprophylaxis should be used primarily with patients in high risk groups.

Adult↗
PubMed1975

The nature of the collagen cross-links in bone in the chronic uraemic state.

The cross-links from NaB3H4-reduced bone collagen of chronically uraemic rats and pairfed controls were compared. The ratio of the reduced cross-links deltadelta'-dihydroxylysinonorleucine to delta-hydroxylysinonorleucine was significantly increased in the uraemic animals. The observed increment in the dihydroxylysinonorleucine:hydroxylysinonorleucine ratio was accentuated as the uraemic state advanced. The data indicate that osteodystrophy of chronic renal insufficiency is characterized by an alteration of the quantitative relations between cross-links and aldehydic precursors of bone collagen.

Animals↗
PubMed1975

Experimental renal osteodystrophy. The response to 25-hydroxycholecalciferol and dicholomethylene diphosphate therapy.

Bone mineral and matrix maturation in chronically uremic, nonacidotic rats were investigated after 25-hydroxcholecalciferol (25OHD) and/or dichloromethylene diphosphonate (C12MDP) therapy utilizing bromoform-toluene density gradient fractionation and X-ray diffraction analyses. The bromoform-toluene density gradient analyses demonstrated that the progressive accumulation of less dense, more immature bone characteristic of progressive uremia was reversed by 25OHD and/or C12MDP therapy for a 2-wk period, and that after 4 wk of therapy the maturational profile of bones from chronically uremic animals treated with 250HD and/or C12MDP was comparable to that from nonuremic littermates. X-ray diffraction analysis revealed that by the 4th wk of therapy with 25OHD and C12MDP both the degree of crystallinity and the crystal size/perfection parameters in the uremic bones were comparable to those of nonuremic, pair-fed control littermates. Treatment for 4 wk with 25OHD resulted in enlarged and/or more perfect apatite crystallites, while C12MDP alone slightly inhibited crystal growth and/or perfection after 2 wk of treatment. Soft tissue calcification was diminished in uremic animals treated for 4 wk with C12MDP or a combined C2MDP/25OHD regimen, the latter being much more effective in this regard. The accumulated data in this study support the premise that the attendant accelerated bone resorption, soft tissue calcification, and abnormal mineralization and maturation of the skeletal tissue, well documented to characterize experimental ranal insufficiency, may be alleviated with therapeutic dosages of 25OHD and/or C12MDP.

Animals↗
PubMed1975

25-hydroxycholecalciferol-enhanced bone maturation in the parathyroprivic state.

In vitro evidence presently favors a direct osteolytic effect of biologically active vitamin D metabolites. Studies were designed to evaluate the effect of 25-hydroxycholecalciferol (25OHD3) on bone collagen and mineral maturation in vivo and its dependence on parathyroid hormone (PTH). After treatment of sham-operated control and parathyroidectomized (PTX) mature rats with either 25OHD3 or an oil vehicle for 2 wk, tibial bone mineral-collagen maturation was quantitated by bromoform-toluene density gradient fractionation techniques. Intestinal calcium absorption was measured by in vivo 45Ca transport procedures. In contrast to the control group, the response to 25OHD3 of PTX rats was dramatic. Bone mineral and matrix maturation were both accelerated by 25OHD3 treatment without concomitant reduction in total bone mineral or collagen content or changes in the intestinal calcium absorption. These observations support the premise that biologically active vitamin D metabolites stimulate bone tissue maturation, and that PTH is not required in this regard.

Animals↗
PubMed1975

Parathyroid hormone status and renal responsiveness in familial hypophosphatemic rickets.

Basal serum and urinary biochemical parameters and their response to PTH or calcium infusion were examined in 14 untreated patients with familial hypophosphatemic rickets (FHR) from 5 kindreds and 9 normal control subjects after a period of dietary equilibration. FHR subjects exhibited significantly elevated basal serum iPTH levels (FHR: 11.4 +/- 0.8, controls: 5.1 +/- 0.5 ng/ml, P less than 0.001) and urinary cAMP excretion (FHR: 7.83 +/- 0.81, controls: 3.78 +/- 0.46 nmol/mg creatinine P less than 0.001). In response to PTH infusion (6 units/kg over 4 hours) FHR subjects exhibited a mean 34% decrease in TRP and a 22-fold increase in cAMP excretion, both comparable to the control response. Calcium infusion (10 mg/kg over 1 h) rapidly suppressed serum iPTH and urinary cAMP values in FHR subjects. However, TRP remained inappropriately low for the level of serum phosphate. Basal and post-calcium infusion serum iPTH levels correlated positively with urinary cAMP in FHR subjects and controls. Pre- and post-calcium infusion iPTH levels correlated with serum calcium in FHR subjects. Mean Salivary phosphate concentration was significantly reduced in FHR subjects (FHR: 12.68 +/- 0.87, controls: 22.47 +/- 2.16 mg/100 ml, P less than 0.001). However, calculated salivary phosphate clearance rates were similar in FHR and control subjects. PTH or calcium infusion did not significantly alter salivary phosphate concentration or clearance rates in either patients or controls. We concluded that untreated FHR patients exhibit a state of mild secondary hyperparathyroidism and an at least normal renal phosphaturic response to PTH. In addition, there is no evidence for increased salivary phosphate excretion in FHR.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗