Assessment of physician responses to abnormal results of bone densitometry studies.

OBJECTIVE: To assess how physicians who have ordered bone densitometry studies respond to abnormal results. METHODS: We conducted a retrospective review of cases from physicians affiliated with a community teaching hospital. The study sample consisted of 142 female patients with abnormal bone mineral density (BMD) who had been referred by 50 physicians (internists or gynecologists). A questionnaire was completed for each patient, providing data about further investigations, treatment interventions, and frequency of referral to a specialist in bone diseases. RESULTS: Of the patients diagnosed with osteoporosis on the basis of BMD studies, 20.4% had no further investigations, and 27.8% underwent only mammography. Of all the patients with osteoporosis, 10.6% received no therapy (calcium and vitamin D excluded). The majority of all patients (71.8%) received a combination of calcium and vitamin D. The most common treatment modality was hormone replacement therapy. The second most common treatment strategy was bisphosphonates. The percentage of all referrals to specialists in metabolic bone diseases was low--11.3% in the patients of internists and 14.5% in the patients of gynecologists. CONCLUSION: In this study, the information provided by bone densitometry did not affect management in a substantial percentage of patients. A considerable percentage of patients underwent no further investigations to rule out secondary causes of osteoporosis.

Adrenocorticotropin radioimmunoassay: properties of antisera against synthetic ACTH(1-24) and its clinical application.

Two antisera against synthetic ACTH(1-24) developed in rabbit showed strikingly different affinities toward the ACTH molecule. Both antisera (A-6 and A-7) were highly specific for the COOH-terminal region of ACTH(1-24). Antisera A-6 recognized ACTH(1-39) poorly. Radioimmunoassays (RIAs) using these antisera permitted the rapid (less than or equal to 18 h) quantitation of ACTH(1-24) (A-6) or ACTH(1-39) (A-7) at picogram levels. ACTH levels were determined on silicic acid extracts of rat and human plasma samples by the RIA specific for mid-region of ACTH(1-39) (A-7) and compared with that obtained by an ACTH(34-39) (C-terminal) RIA. In nearly all cases the C-terminal/mid-region ACTH ratios were less than 1.0, indicating that C-terminus of ACTH is more readily degraded by tissue or blood peptidases than are internal sequences. A solid-phase immunoadsorbent RIA specific for the extreme COOH-terminus of ACTH(1-24) was developed by coupling antiserum (A-6) to Sepharose 4B. This assay exhibited the same specificity as the soluble antiserum, yet tolerated relatively high concentrations of protein. Although the assay was suitable for rapid quantitation of ACTH(1-24), a decrease in sensitivity was observed in comparison to a conventional assay.

C-Peptide reserve in insulin-dependent diabetes. Comparative responses to glucose, glucagon and tolbutamide.

Residual beta cell secretory capacity was assessed in short term (2 months to 2 years) and long term (5 to 8 years) insulin-dependent diabetics by measurement of serum C-peptide immunoreactivity during three provocative tests: glucose, tolbutamide, and glucagon. Minimal C-peptide secretion could be detected in only one out of seven long term diabetics by the stimulatory tests. All seven short-term diabetics responded to at least one provocative test of beta cell reserve, although these responses were blunted. The greatest C-peptide responses occurred after glucagon administration (mean increase 0.62 pmol/ml) in short-term responders. Patients who responded to one test did not necessarily respond to another stimulus. There was no correlation between basal C-peptide levels and the ability to provoke further C-peptide secretion by any of the three tests. C-peptide responses did not correlate with % Haemoglobin A1c, mean fasting blood glucose levels, or mean blood glucose concentrations during an oral glucose tolerance test. The data indicate that stimulation tests are only useful in assessing endogenous beta cell reserve in patients with diabetes of less than 5 years duration. In diabetics of longer duration there is little insulin reserve above basal levels.

Screening for hypertension in the emergency department.

Review of emergency department charts at three university-affiliated hospitals showed that less than half of all patients who had elevated blood pressure (BP) recorded were recognized by physicians to be hypertensive. At the primary teaching hospital, less than one third of patients with the greatest BP elevation (greater than 20 mm Hg above normal) were sent for some type of hypertension follow-up care.

Decreased thyroid function and high plasma prolactin levels in rats of the Buffalo strain.

Rats of the inbred Buffalo strain have previously been reported to be susceptible to thyroiditis, as defined by histology. We have studied the endocrinology of the pituitary-thyroid axis of this strain by making direct measurements of the plasma concentrations of TSH and T4 in untreated, adult Buffalo rats of both sexes. Plasma PRL levels were also measured. All hormone determinations were by RIA. In addition, relative thyroid weights were noted and, in many cases, preliminary assessment of thyroid histology was made. Our principle findings were as follows. 1) Decreased thyroid function, in addition to the previously reported histological abnormalities, was found to occur spontaneously among the rats studied. Indications of decreased function included elevations of plasma TSH and thyroid weight and depressions of plasma T4. We estimated the incidence of unequivocal thyroid disease as approximately 3% in each sex. 2) Basal plasma PRL concentrations of Buffalo rats averaged three to four times higher than those of outbred CD rats. Our findings strongly suggest that rats of the Buffalo strain will provide a good model for the study of thyroid failure of varying degrees and concomitant changes in the circulating levels of pituitary hormones.

Membrane receptor function and the loss of glucagon-stimulated adenylate cyclase activity in hepatomas.

Plasma membranes were prepared from homogenates of two well differentiated hepatomas (Morris rat 7787 and Dalton mouse 9815), two poorly differentiated hepatomas (Morris rat 7288-C and Dalton mouse 129), and normal liver. Adenylate cyclase activity and [125I]iodoglucagon binding were measured in the plasma membrane preparations over a wide range of glucagon concentrations. Nether glucagon-stimulated adenylate cyclase activity nor [125I]iodoglucagon binding could be detected in the poorly differentiated hepatomas. Fluoride and epinephrine stimulated adenylate cyclase activity in all hepatomas. Maximum activity of glucagon-stimulated adenylate cyclase and maximum binding of glucagon in the wall differentiated hepatomas were less than those of normal liver. Plasma membranes from liver and hepatomas were solubilized with Lubrol-PX and, after reducing the concentration of detergent, were incubated with [125I]iodoglucagon and then chromatographed on a column of Bio-Gel A 1,5 m. Two peaks containing both protein and [125I]iodoglucagon were found for normal liver but not for the poorly differentiated hepatomas. Fractions from the Bio-Gel column containing the greatest concentration of protein were also subjected to a binding microassay. Material from the poorly differentiated tumors did not bind glucagon in this system, whereas the solubilized normal liver membranes bound up to 1.4 pmol [125I]iodoglucagon/mg protein. This indicates that there is no detectable glucagon receptor in these undifferentiated tumors.