PubMed Health⌕ Search

Biomedical subjects

R E Reitz

Publications and source records attributed to R E Reitz.

At least 19 recordsLinked to original sources
PubMed2001

The prevalence of insulin receptor antibodies in patients with systemic lupus erythematosus and related conditions.

Autoantibodies to the insulin receptor have been demonstrated to antagonize the physiologic actions of insulin, most often resulting in hyperglycemia unresponsive to massive doses of insulin (type B insulin resistance). Patients with these anti-insulin receptor antibodies typically have a coexistent autoimmune disorder, most commonly systemic lupus erythematosus (SLE) or undifferentiated autoimmune syndromes. Attempting to determine the prevalence and significance of anti-insulin receptor antibodies, sera from consecutive patients with SLE and early undifferentiated connective tissue disease (UCTD) were tested for the presence of anti-insulin receptor antibodies by radio-immuno assay. Thirty-eight patients participated in the study. Twenty-six had SLE and 12 had UCTD. One patient with SLE (2.6%) was positive for anti-insulin receptor antibodies. None of the patients demonstrated evidence of insulin resistance, hypoglycemia, ovarian hyperandrogenism, or acanthosis nigricans, findings commonly linked with the presence of anti-insulin receptor antibodies. The results presented here indicate that the incidence of anti-insulin receptor antibodies in patients with SLE or UCTD, without associated history of altered glucose metabolism, is quite low. Because in most cases the disturbance of glucose metabolism dominates the clinical picture at presentation and the associated systemic autoimmune syndrome presents either simultaneously with or subsequent to the diagnosis of diabetes, the measurement of anti-insulin receptor antibodies should be reserved for patients with indications of disordered glucose homeostasis.

Journal Article↗
PubMed1998

Technical and clinical aspects of spectrometric analysis of trace elements in clinical samples.

The capabilities of ICP-MS far exceed the slow, single-element analysis of GFAAS for determination of multiple trace elements. Additionally, its sensitivity is superior to that of DCP, ICP, and FAAS. The analytic procedure for ICP-MS is relatively straightforward and bypasses the need for digestion in many cases. It enables the physician to identify the target trace element(s) in intoxication cases, nutritional deficiency, or disease, thus eliminating the treatment delays experienced with sequential testing methods. This technology has its limitations as well. The ICP-MS cannot be used in the positive ion mode to analyze with sufficient sensitivity highly electronegative elements such as fluorine, because F+ is unstable and forms only by very high ionization energy. The ICP mass spectrometers used in most commercial laboratories utilize the quadrupole mass selector, which is limited by low resolution and, thus, by the various interferences previously discussed. For example, when an argon plasma is used, selenium (m/e 80) and chromium (m/e 52) in serum, plasma, and blood specimens are subject to polyatomic and molecular ion interferences. Low-resolution ICP mass spectrometers can therefore be used to analyze many trace elements, but they are not universal analyzers. High-resolution ICP-MS can resolve these interferences, but with greater expense. With the advent of more research and development of new techniques, some of these difficulties may be overcome, making this technique even more versatile. Contamination during sample collection and analysis causes falsely elevated results. Attention and care must be given to avoid contamination. Proper collection devices containing negligible amounts of trace elements should be used. Labware, preferably plastic and not glass, must be decontaminated prior to use by acid-washing and rinsed with [table: see text] de-ionized water. A complete description of sample collection and contamination has been written by Aitio and Jarvisalo as well as by Chan and Gerson. Lutz et al observed the ranges in blood shown in Table 4. We have adopted the ranges listed in Table 5 in urines of healthy, ambulatory, and community-dwelling individuals through a limited in-house study and review of literature. In conclusion, differentiation of trace element abnormalities (primary intoxication or disease versus secondary underlying disease) can be made only by utilizing results from trace element analyses in clinical specimens, medical history, and careful observation of symptoms. Repeat analysis on a second specimen collection is recommended when contamination is suspected.

Body Fluids↗
PubMed1986

Effects of parathyroidectomy on circulating levels of 1 alpha,25-dihydroxyvitamin D and bone Gla protein in dialyzed patients.

The effects of decreasing serum levels of PTH after parathyroidectomy on circulating levels of 1 alpha,25-dihydroxyvitamin D [1,25-(OH)2D] and bone Gla protein (BGP) were studied in seven patients treated with chronic maintenance dialysis. Before surgery, all patients had extremely elevated levels of PTH, low normal or low levels of 1,25-(OH)2D, high levels of BGP, and histological signs of excess PTH action on bone. The fall in PTH levels after surgery resulted in a further decline in 1,25-(OH)2D concentrations and a reduction in circulating BGP levels. This fall in serum 1,25-(OH)2D and BGP levels was not related to serum calcium or phosphorus. Administration of 1,25-(OH)2D3 from 4-6 months after surgery did not significantly affect serum levels of BGP or PTH. These data indicate that 1,25-(OH)2D is still under regulatory control of PTH in patients without excretory kidney function. This might reflect some remaining endocrine activity of the kidneys in these dialyzed patients or extrarenal production of 1,25-(OH)2D. In addition, the data show that serum BGP levels in renal failure are elevated due not only to impaired clearance but also to PTH-mediated acceleration in bone turnover. Therapy with 1,25-(OH)2D3 in these patients resulted in supraphysiological serum 1,25-(OH)2D levels which did not stimulate BGP production.

Adult↗
PubMed1984

High-dose ketoconazole therapy and adrenal and testicular function in humans.

Ketoconazole, an oral antifungal, when given in conventional doses, transiently blocks testosterone synthesis and adrenal response to corticotropin. Higher therapeutic doses (ie, 800 to 1,200 mg/day), even once daily, caused more prolonged blockade. In some men, the serum testosterone concentrations were always subnormal. Bound and free testosterone values were equally diminished. Oligospermia and azospermia after prolonged therapy were noted. Impotence and decreased libido were found. Gynecomastia appeared more common than with lower doses. Depressed response to corticotropin was pronounced. Urine cortisol excretion was depressed. The blockade appeared related to the serum ketoconazole concentration. Instances of normal hormone levels or responsiveness were associated with low ketoconazole concentrations. The hormonal effects were generally unrelated to duration of therapy, although there may have been partial reversal with continued therapy. These effects appeared reversible with discontinuation of therapy. Patients receiving ketoconazole should be considered potentially unable to mount an adrenal stress response and may require testosterone supplementation.

Adrenal Glands↗
PubMed1982

Ketoconazole blocks adrenal steroid synthesis.

Ketoconazole, a broad-spectrum, antifungal drug that is administered orally, has been shown to inhibit sterol synthesis in fungi. When gynecomastia developed in some patients taking this drug, we investigated the effects of ketoconazole on steroid synthesis in humans and in isolated adrenal cells from rats. In healthy humans, the cortisol response to adrenocorticotropic hormone was significantly blunted 4 hours after a 400-mg or 600-mg dose. The inhibition persisted for up to 8 hours and was absent by 16 hours. This finding indicated that adrenal androgen response was reduced. Easily achieved therapeutic concentrations of ketoconazole virtually eliminated corticosterone production by isolated adrenal cells from rats. Although ketoconazole at currently used doses has never been documented to cause clinical hypoadrenalism, caution is urged in high- or multiple-dose trials. The drug may prove useful as an agent to block steroid synthesis.

Adrenal Cortex↗
PubMed1982

Ketoconazole blocks testosterone synthesis.

Ketoconazole, a new oral drug used to treat systemic and superficial mycoses, inhibits sterol synthesis in fungi. The development of gynecomastia in two patients prompted us to investigate the effect of the drug on testosterone production. After a 200-, 400-, or 600-mg dose, volunteer male testosterone serum concentrations fell markedly, but returned toward baseline eight to 24 hours later as ketoconazole serum concentrations waned. A marked but transient drop in testosterone levels occurred in patients receiving long-term therapy, and continuous testosterone depression was noted in one. A block of synthesis was demonstrated in vitro. Ketoconazole at concentrations achievable in serum with currently used doses blocked basal and gonadotropin-stimulated testosterone production by rat Leydig cells. The diminution of testosterone synthesis could be significant as further therapeutic trials may use larger doses or more than once-daily administration. The paucity of reports of endocrinologic toxicity may relate to the "escape" from the block demonstrated in vivo.

Adult↗
PubMed1981

Management of acute hyperparathyroidism in a community hospital.

Primary hyperparathyroidism is a common entity that routinely lends itself to prompt surgical cure. Infrequently, multiple surgical explorations are required to effect a cure. A case is reported of a 27-year-old man with hypercalcemia and nephrocalcinosis. The initial surgical exploration failed to identify the abnormal parathyroid tissue. Hypercalcemia necessitated rigorous antihypercalcemic therapy; three subsequent operations, including a mediastinal exploration, were unsuccessful. On the fifth exploration, which took barely an hour, a 35-g adenoma was removed from the left superior posterior mediastinum. This report illustrates that a detailed knowledge of the possible locations of aberrant parathyroid tissue and the skills of the operating surgeon are the sine qua non for those patients requiring one or more parathyroid reexplorations.

Acute Disease↗
PubMed1981

Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release.

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.

Adenoma↗
PubMed1977

Calcium, magnesium, phosphorus, and parathyroid hormone interrelationships in pregnancy and newborn infants.

The ability to measure directly human parathyroid hormone (hPTH) and ionized calcium (Ca++) is of fundamental importance in understanding their interrelation in pregnancy and the newborn. hPTH and Ca++ progressively increase throughout pregnancy. Since Ca++ is the direct determinant of hPTH levels, a different "set point" appears to be operative throughout pregnancy. The newborn infant, on the other hand, has higher serum Ca++ levels than its mother, and the infant's plasma hPTH is suppressed to undetectable or low levels. Ca++, total serum Ca, magnesium, and phosphorus are all significantly elevated in the serum of the mother at delivery. An active transport mechanism of all these minerals appears to be operative and lowers the maternal serum levels at the termination of labor in relation to serum levels in the third trimester of pregnancy.

Blood Proteins↗
PubMed1974

Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.

Adult↗