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Biomedical subjects

L V Avioli

Publications and source records attributed to L V Avioli.

At least 271 records · Page 15Linked to original sources
PubMed1977

25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol: conversion impaired by systemic metabolic acidosis.

An acute systemic acidosis in vitamin D depleted rats that was induced by ammonium chlroide feeding resulted in defective biological hydroxylation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol. Impaired enzymatic hydroxylation occurred despite the presence of either hypophosphatemia or hypocalcemia. The data suggest that acidosis interfers with the adaptive enzymatic control of 25-hydroxycholecalciferol metabolism in the vitamin D depleted state.

Acidosis↗
PubMed1977

Effect of long-term calcitonin therapy on the clinical course of osteogenesis imperfecta.

10 children with osteogenesis imperfecta, 4 with "tarda" and 6 with "congenita" varieties of the disease, were treated with salmon calcitonin (SCT) for intervals ranging from 14 to 35 months. Responses to SCT therapy in patients with osteogenesis imperfecta tarda were characterized by an apparent decreased fracture incidence in three, a fall in either alkaline or acid phosphatase, and a rate of increase in forearm bone mass which was greater than that observed in an untreated "tarda" population. The chemical response SCT therapy varied in children with osteogenesis imperfecta congenita, only one demonstrating a decrease in both acid phosphatase and urinary hydroxyproline. Three others responded with a rise in acid phosphatase, two of whom also demonstrated a fall in urinary hydroxyproline; in two other "congenita" patients urinary hydroxyproline was actually higher after SCT treatment and acid phosphatase relatively unchanged. Alkaline phosphatase was normal in all "congenita" patients before and following the SCT treatment interval. These varied biochemical responses were associated with temporary increments in bone mass early in the treatment course, although in bone mass early in the treatment course, although one "congenita" patient with the largest calciuric response to SCT and an increase in hydroxyproline excretion demonstrated progressive increments in skeletal mineral content during a 14-month treatment interval. In both "tarda" and "congenita" subjects, parathyroid hormone was unchanged by chronic SCT treatment; SCT-antibodies were detectable although biological responsivity to SCT persisted.

Acid Phosphatase↗
PubMed1977

Hypercalcemic hyperparathyroidism in hypophosphatemic rickets.

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.

Adolescent↗
PubMed1977

Grand rounds: autoimmune hemolytic anemia.

Autoimmune hemolytic anemia (AHA) may be either primary (ie, "idiopathic," one third of all patients) or secondary (ie, associated with underlying illness, two thirds of all patients). A positive Coombs antiglobulin test is the most important criterion for diagnosis of AHA, and characterization of RBC coating (as to whether it is by IgG alone, by IgG plus complement, or by complement alone) may be valuable in ruling out certain underlying illnesses as causative in selected patients. Many limitations to the antiglobulin test must be kept in mind. As routinely performed, a positive result requires greater than 500 molecules of IgG per RBC. Red blood cells from normal subjects have less than 35 molecules of IgG per RBC. Up to 2% to 5% of patients with AHA will have RBC coating in the 50 to 500 molecules per cell range and may therefore have "false"-negative antiglobulin tests. Apparent failures of strength of antiglobulin reactions to correlate with severity of in vivo RBC destruction may result from technical factors or may reflect intrinsic differences among autoantibodies (eg, IgG subclass, affinity). A likely mechanism of in vivo RBC destruction in AHA has been demonstrated in immune-mediated in vitro RBC "rosette" formation about macrophages and lymphocytes bearing specific receptors for subclasses of IgG and for subcomponents of complement. Increased avidity of macrophages for coated RBCs in response to such stimulus as infection may play an additional role. Treatment involves control of underlying disease and the judicious use of adrenal steroids, splenectomy, and immunosuppressive agents. Transfusions, while life-saving in life-threatening anemia, carry substantially increased risks in AHA patients. Their use should be strictly limited.

Aged↗
PubMed1976

Effects of diabetes mellitus on bone mass in juvenile and adult-onset diabetes.

To assess the influence of diabetes mellitus on bone metabolism, we measured skeletal mass in the forearms of 35 patients with juvenile diabetes on insulin and 101 stable patients with adult-onset diabetes, on diet alone, insulin, or oral hypoglycemic agents. There was a significant loss of bone mass in both juvenile and adult-onset diabetes (P less than 0.01) as compared to controls matched for age and sex. The decrease was already present in patients with diabetes of less than five years' duration. Bone loss and duration of the diabetes did not correlate; the greatest decrease in bone mass was observed in the patients receiving oral agents. These data are consistent with the hypothesis that the loss of skeletal tissue in diabetes reflects the underlying disease since it occurs early and is not related to severity as evidenced by the need for insulin, to duration, or to treatment with insulin or diet alone.

Adult↗
PubMed1976

Calcifediol in chronic renal insufficiency. Skeletal response.

Quantitative histology of thin, nondecalcified sections was performed on sequential bone biopsy specimens from five patients undergoing long-term hemodialysis and treated with calcifediol (25-hydroxycholecalciferol) for periods of three to nine months. With increase of intestinal absorption of calcium and decline of circulating immunoreactive parathyroid hormone and alkaline phosphatase, the bones of each patient exhibited striking histological improvement. The group as a whole showed statistically significant decreases in osteoclast number and in the percentages of osteoid surface covered by active osteoblasts. Marrow fibrosis was either eliminated or strikingly decreased in each patient. Osteoid volume significantly declined in four of five patients. In patients with osteitis fibrosa as the predominant histological lesion, calcifediol therapy resulted in decreased calcification front activity. Increased activity was the result when osteomalacia predominated.

Adult↗
PubMed1976

The Jewish Hospital of St. Louis therapeutic grand rounds no. 13. Cushing disease.

Although several effective therapies for Cushing disease have been demonstrated, associated complications, side-effects, and production of adrenal insufficiency indicate the continuing need for a completely satisfactory treatment. Of the surgical approaches to the adrenal gland, total adrenalectomy offers the most predictable amelioration, but is necessitates lifelong replacement and augmentation therapy and can be followed by progressive sella enlargement and hyperpigmentation. Drugs can inhibit adrenal steroid biosynthesis or selectively destroy the zona fasciculata. Inhibitors can be overwhelmed by endogenous ACTH increases, and cause variable electrolyte changes and side-effects. The adrenocorticolytic drug (o,pDDD) is slow in onset, irreversibly destroys adrenocortical reserve, and is poorly tolerated in the gastrointestinal tract. Conventional pituitary irradiation is unpredictably effective in only half of the cases, but is not often followed by the serious neurologic sequelae and hypopitiutarism observed after implantation and heavy particle therapy. Selective hypophysectomy via modern techniques is relatively new, but apparently offers a direct, and possibly, definitive therapeutic option in this disorder.

Adult↗
PubMed1976

The Jewish Hospital of St Louis Therapeutic Grand Rounds No. 14. Hypersensitivity pneumonitis.

Two examples of immunologically mediated diseases of the lung have been discussed. The first, extrinsic allergic alveolitis, is caused by sensitivity to inhalation of an organic dust. It is largely a restrictive type of lung disease and is probably caused by a combination of type 3 and type 4 allergic reactions. The second disease, allergic bronchopulmonary aspergillosis, is caused by a type 1 and type 3 allergic response to Aspergillus antigen in a basically atopic, generally asthmatic individual. It is vital to keep the diagnostic index of suspicion high so as to recognize these diseases early enough to prevent irreparable tissue damage. Extrinsic allergic alveolitis may masquerade as idopathic pulmonary fibrosis or Hamman-Rich syndrome. Allergic aspergillosis may be called Loeffler pneumonia or PIE syndrome (pulmonary infiltrates with eosiniphilia). Failure to diagnose properly may result in extensive pulmonary fibrosis or bronchiectasis and condemn the patient to a lifetime as a pulmonary cripple.

Antigens↗
PubMed1976

Histological studies of bone from normocalcemic post-menopausal osteoporotic patients with increased circulating parathyroid hormone.

Quantitative histological evaluations were made of nondecalcified iliac crest needle biopsies were obtained from 16 untreated, normocalcemic, normophosphatemic postmenopausal osteopenic females. Six of the patients had elevated circulating immunoreactive parathyroid hormone. Morphometric parameters, which were significantly increased in the hyperparathyroid group compared with the euparathyroid patients were the cortical osteoclast count and the percentage of trabecular surface covered by active or inactive osteoid. In addition, in all patients, the cortical osteoclast count, and the per cent of trabecular surface covered by osteoid and inactive osteoid were directly related to levels of immunoreactive parathyroid hormone. These data suggest that progressive osteopenia in some patients with crush fracture, or postmenopausal or senile osteoporosis, may be conditioned by an osteoclastosis, elevations in circulating parathyroid hormone, and a relative increase in poorly mineralized osteoid tissue. As such they emphasize the heterogeneity of a so-called "osteoporotic population" and stress the need for specific histological morphometric evaluation of bone before initiating long-term therapeutic modalities.

Aged↗
PubMed1976

The effects of phosphate and vitamin D therapy on osteopenic, hypophosphatemic osteomalacia of childhood.

Two severely osteopenic adolescent males with clinical manifestations of adult onset hypophosphatemic osteomalacia were resistant respectively to physiological and pharmacological doses of vitamin D. Clinical improvement ensued following initiation of pharmacological doses of vitamin D and phosphate. Non-decalcified bone biopsies obtained before and during therapy exhibited correction of an isolated mineralization in the second. The response to treatment was reflected in striking changes in tetracycline-labelled calcification fronts in both patients.

Bone Regeneration↗
PubMed1976

Senile and postmenopausal osteoporosis.

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.

Aged↗
PubMed1976

Hyperthyroidism in Graves disease. Current trends in management and diagnosis.

The radioimmunoassay for T3 is now widely available and is a useful diagnostic tool for hyperthyroidism, especially in T3-thyrotoxicosis. It is an essential tool in the management of hyperthyroidism that persists after treatment with normal T4 serum levels or, in euthyroid cases, with low T4 serum levels. In these conditions, it reflects the metabolic state more accurately than serum levels of T4. A promising new test is the response of radioimmunoassayable TSH to protirelin (TRH) administration. An absent response indicates pituitary suppression and thyroid autonomy as seen in frank hyperthyroidism or euthyroid Graves disease, treated or untreated. It is safer and quicker than the conventional T3 suppression test of thyroid radioactive iodine uptake and may replace it at least partly in the future.

Adult↗