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Biomedical subjects

T J Hahn

Publications and source records attributed to T J Hahn.

At least 73 records · Page 4Linked to original sources
PubMed1976

Vitamin D metabolite-binding proteins in human tissue.

Serum and post-microsomal supernatants of human lymphocyte, erythrocyte, skeletal muscle and parathyroid adenoma homogenates were examined for specific binding of 25-hydroxycholecalciferol (25-OHD3) and 1, 25-dihydroxycholecalciferol (1,25-(OH)2D3). Muscle, lymphocytes and parathyroid adenomata extracts contained a 6-S 25-OHD3-binding protein which was not found in erythrocyte extracts, and which was distinct from the smaller serum transport alpha-globulin. A cathodal, 1, 25-(OH)2D3-binding protein, which sedimented at 3-4 S was also detected in parathyroid tissue. These observations suggest the possibility of direct physiologic interaction between vitamin D metabolites and nucleated human tissues other than intestine and bone.

Adenoma↗
PubMed1976

Vitamin D resistance in magnesium deficiency.

Four patients with gastrointestinal disorders, and one patient with chronic alcoholism presented with both hypocalcemia and hypomagnesemia. Pharmacological doses of either ergocalciferol or dihydrotachysterol did not correct the hypocalcemia except in one patient who had a minimal rise in serum calcium. Parathormone levels were high in three patients and exogenous parathormone given to the fourth subject failed to elicit a rise in serum calcium, implying impairment of the calcemic response to parathormone. Magnesium repletion simultaneously corrected the hypomagnesemia and hypocalcemia. Balance data suggested that the rise in serum calcium was in part, at least, due to increased mobilization of minerals from bone. While the mechanism remains speculative, it appears that magnesium facilitates the release of calcium from bone in the presence of adequate amounts of vitamin D and parathormone.

Adolescent↗
PubMed1976

Bone complications of anticonvulsants.

Anticonculsant drug-induced disorders in mineral and bone metabolism are apparently quite common. Current evidence indicates that these drugs derange bone metabolism, both through induction of increased hepatic catabolism of vitamin D and its biologically active products, as well as by direct effects on membrane cation transport systems. The significant clinical manifestions of the disorder include rickets with defective bone development, decreased bone mass with increased risk of pathological fracture and reductions in serum calcium levels which may predispose to increased seizure frequency. There is a broad range of clinical presentation with a number of factors -- drug dose, duration of therapy, vitamin D intake, amount of sunlight exposure, degree of physical activity and presence of other concurrent diseases -- which appear to determine the severity of the clinical manifestations. Current evidence indicates that appropriate vitamin D and calcium supplementation can significantly reduce the clinical manifestations of this disorder. All patients receiving chronic anticonvulsant drug therapy should be carefully evaluted for the presence of drug-induced osteomalacia and treated appropriately with vitamin D. This is especially important in those patients in whom the presence of multiple risk factors indicates an increased likelihood of deranged mineral metabolism.

Anticonvulsants↗
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↗
PubMed1972

Phenobarbital-induced alterations in vitamin D metabolism.

The metabolic fate of intravenously injected vitamin D(3)-1,2-(3)H (D(3)-(3)H) was studied in two normal individuals on chronic phenobarbital therapy. Silicic acid column chromatography of lipid-soluble plasma extracts obtained serially for 96 hr after D(3)-(3)H injection demonstrated a decreased plasma D(3)-(3)H half-life and increased conversion to more polar metabolites. The polar metabolites formed included several with chromatographic mobility similar to known biologically inactive vitamin D metabolites and one with chromatographic mobility identical to 25-hydroxycholecalciferol. Disappearance of this latter material was also accelerated. A child with rickets and a normal volunteer studied before and after a 2 wk course of phenobarbital therapy demonstrated similar alterations in D(3)-(3)H metabolism. When liver microsomes from 3-wk-old Sprague-Dawley rats treated with phenobarbital were incubated with D(3)-(3)H, polar metabolites were produced with chromatographic mobility similar to the plasma D(3)-(3)H metabolites from phenobarbital-treated humans. Similar incubations employing 25-hydroxy-cholecalciferol-26-27-(3)H as the substrate also demonstrated an increased conversion to polar metabolites. The data suggest that the reported increased incidence of osteomalacia observed in patients on chronic anticonvulsant therapy may be the result of an accelerated conversion of vitamin D and its active metabolite, 25-hydroxycholecalciferol, to polar metabolites by druginduced liver microsomal enzymes.

Adult↗
PubMed1972

Effect of magnesium depletion on responsiveness to parathyroid hormone in parathyroidectomized rats.

Hypocalcemia and resistance to exogenous parathyroid hormone have been reported in several clinical states associated with magnesium deficiency. On the basis of such observations, it has been suggested that magnesium depletion per se may result in impaired responsiveness of the adenyl cyclase-adenosine 3',5'-monophosphate (3',5'-AMP) system. To test this hypothesis, 4 wk old male parathyroidectomized rats were maintained on normal or magnesium-deficient diets for 4 wk and their responses to parathyroid hormone compared. Serum magnesium and calcium fell progressively in the magnesium-deficient group. Despite clinical and biochemical evidence of severe magnesium deficiency in these animals, renal production and excretion of 3',5'-AMP in response to parathyroid hormone was normal both in vitro and in vivo. Additionally, administration of either dibutyryl 3',5'-AMP or parathyroid extract to fasting magnesium-depleted rats produced a normal increase in serum calcium. Parathyroid hormone infusion studies demonstrated normal renal and skeletal responsiveness as measured by urinary excretion of calcium, magnesium, phosphate, and hydroxyproline. These data show that the effect of parathyroid hormone on 3',5'-AMP formation and excretion, the responsiveness of skeletal tissue to 3',5'-AMP, and the renal and skeletal system responses to parathyroid hormone are not altered by pure magnesium deficiency in the parathyroidectomized rat.

Adenosine Monophosphate↗