Biomedical subjects
Publications and source records attributed to H Jorgensen.
The Department of Dermatology at the Washington Hospital Center conducts research on drugs and products for various drug companies prior to their approval by the Food and Drug Administration. The purpose of this article is to describe this interesting and rewarding process which can give dermatology nurses the opportunity to assist patients who might not have found effective or affordable treatment for their condition.
In transgenic mice, mature peripheral B lymphocytes in lymphoid follicles, like immature B cells, are rendered tolerant by encounter with self-antigen, provided receptor occupancy by self-antigen exceeds a critical threshold. The tolerant state of the B cell is closely correlated with down-regulation of membrane IgM but not IgD antigen-receptors. Identical changes in antigen-receptor expression occur in a subset of follicular B cells in nontransgenic mice, suggesting that clonally silenced self-reactive cells are common in the peripheral B-cell repertoire.
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Ten patients with disorders of keratinization were treated with oral isotretinoin (13-cis-retinoic acid) on an investigational protocol to test the efficacy, safety, and optimal dosage schedule for using the drug in these rare disorders. Elevations of serum triglyceride levels above the highest normal levels developed in seven of the ten patients, while they maintained normal levels of serum cholesterol. This effect was found to be dose and/or time related and reversible. Moderate elevations of serum triglyceride levels have not been clearly established as a risk factor for the development of coronary artery disease. High levels, however, may precipitate acute pancreatitis. For this reason, the conditions of patients receiving retinoids must be carefully monitored for triglyceride abnormalities throughout their courses of treatment.
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In two patients (father and daughter) with idiopathic hypoparathyroidism, one of whom was resistant to the action of vitamin D2 and AT-10, 1alpha-hydroxycholecalciferol (1alpha-(OH)D3) in doses of 2-5 mug/day restored the serum calcium concentration to the normal range. The calcemic effect of 1alpha (OH)D3 was in both patients due to an increased intestinal calcium absorption and increased calcium mobilization from bone. In one of the patients 1alpha-(OH)D3 also increased the renal tubular calcium reabsorption; in the other it did not have this effect, resulting in hypercalciuria as serum calcium rose. The lack of effect on tubular calcium reabsorption probably accounts for the relative resistance to the action of 1alpha-(OH)C3 in this patient compared with other.
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Bone mineral content was determined in the radius of 29 osteoporotic patients by the photon absorption method. Mineral content was within the normal range in nine of 24 osteoporotic women. Ratios representing the bone mineral content in the proximal and distal areas of the radius did not distinguish osteoporotic subjects or patients with hyperparathyroidism from normal subjects. Ten osteoporotic women had mineral measurements during a two-year period while receiving placebo or an intake of 2,200 mg of phosphorus and 2,400 mg of calcium. No increase in radial mineral content was observed during this regimen or after adding vitamin D. We conclude that the mearurement of mineral in the radius does not always accurately reflect the overall skeletal mass in an individual patient and that prolonged therapy with high phosphorus and calcium intake did not increase the radius mineral content.
In normal, nonmedicated volunteers and in patients with thyroid disorders the plasma half-lives of antipyrine, propylthiouracil, and methimazole were determined after single oral doses. The plasma half-liver plus or minus S.D. of antipyrine, propylthiouracil, and methimazole were 11.9 plus or minus 1.4 hr, 6.7 plus or minus 1.0 hr, and 9.3 plus or minus 1.4 hr, respectively, in normal volunteers, but were shortened to 7.7 plus or minus 1.2 hr, 4.3 plus or minus 0.7 hr, and 6.9 plus or minus 0.6 hr, respectively, in hyperthyroid patients. In hypothyroid patients the plasma half-lives of these drugs were prolonged to 26.4 plus or minus 4.0 hr, 24.7 plus or minus 34.5 hr, and 13.6 plus or minus 4.8 hr, respectively. Return to the euthyroid state restored plasma half-lives to or toward normal. Alterations in plasma drug half-lives during thyroid dysfunction appear to result mainly from accelerated hepatic microsomal drug metabolism in hyperthyroidism and retarded drug biotransformation during hypothyroidism.
Adrenal scintigraphy after i.v. injection of 131I-19-iodocholesterol has been performed in 4 patients with primary aldosteronism, 5 with Cushing's syndrome and 1 patient with phaeochromocytoma. In primary aldosteronism a unilaternal adrenocortical adenoma was demonstrated in 2 patients, while the method failed in 1 patient to visualize a tumour that was localized by measurements of aldosterone concentrations in the adrenal veins and by adrenal venography; in 1 patient none of the methods demonstrated a tumour. In Cushing's syndrome, adrenal scinitgraphy indicated bilateral adrenocortical hyperplasia in 1 patient and visualized the tumour in 2 patients with adrenocortical adenoma. In all patients with Cushing's syndrome due to unilateral adrenocortical tumour, the accumulation of radioactivity in the contralateral adrenal was suppressed. However, a delayed and slight accumulation of the isotope in the suppressed gland contralateral to an adrenocortical carcinoma was misinterpreted and led to exploration on the wrong side since the tumour did not concentrate radioactivity at all. The method failed in 1 patient to localize the adrenocortical tissue responsible for the relapse of Cushing's syndrome after bilateral adrenalectomy for hyperplasia. In the patient with phaeochromocytoma, no radioactivity was found on the tumour. It is conculded that adrenal scintigraphy is a safe and valuable method for localization of adrenal tumours and their differentiation from adrenocortical hyperplasia. Some diagnostic pitfalls do, however, exist, as demonstrated in this series of patients.
Intestinal 47Ca absorption has been determined from blood and stool radioactivity after oral administration of the isotope in nine patients before and during cellulose phosphate treatment. Oral administration of 5 g cellulose phosphate concomitant with 47Ca in 100 mg "carrier" calcium as CaCl2 decreased 47Ca absorption by 80 per cent. Cellulose phosphate, 5 g three times daily, decreased urinary excretion of non-radioactive calcium by 47 percent. Urinary magnesium excretion decreased by 47 percent whereas urinary phosphorus excretion increased by 67%. Calcium and magnesium excretion in urine decrease because cellulose phosphate binds divalent cations within the GI tract. The increased phosphorus excretion is probably due to partial hydrolysis of the substance in the gut.
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