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Ultrasound is an ancillary tool in adrenal imaging in adults and a primary tool in children. Intraoperative sonography is the method of choice for pancreatic endocrine tumors. In the scrotum, the benign adrenal rest tumors must be distinguished from the more common malignant mass.
This study aimed to clinically validate the global skeletal uptake (GSU) of (99m)Tc-methylene diphosphonate ((99m)Tc-MDP), and to compare it with a marker of bone formation (i.e. serum osteocalcin or OC) and an index of bone resorption (i.e. urinary deoxypyridinoline or U-DPD) in different endocrine disorders affecting the skeleton. We studied 29 female patients with thyrotoxicosis (TT), 27 with primary hyperparathyroidism (PHPT), 16 with acromegaly (AC), 15 with Cushing's syndrome (CS), and altogether 110 healthy women matched for age, BMI and menstrual status. In all subjects total body digital scan images (TBDS) were acquired at 5 min and at 4 h after the administration of (99m)Tc-MDP; the whole body retention (WBR) of the tracer was measured by counting two identical sets of rectangular ROIs, and GSU was subsequently calculated by drawing an irregular ROI on 4 h TBDS images. Serum OC was assessed by IRMA and urinary DPD by fluorometric detection after reverse phase high pressure chromatography. In TT patients GSU (40.0 +/- 5.1 vs 36.5 +/- 4.8%), OC (19.1 +/- 11.8 vs 7.1 +/- 2.9 microg/l) and U-DPD (62.4 +/- 42.7 vs 19.5 +/- 5.3 pmol/pmol) were significantly ( p<0.01) higher than in controls. PHPT patients showed GSU (47.2 +/- 6.6 vs 37.8 +/- 5.3%), OC (38.6 +/- 40.9 vs 8.2 +/- 2.5 microg/l), and U-DPD (55.0 +/- 51.3 vs 21.9 +/- 6.1 pmol/pmol) values significantly ( p<0.001) higher than controls. In CS patients, GSU (39.6 +/- 6.4 vs 32.7 +/- 3.5%; p<0.01) and U-DPD (22.8 +/- 8.4 vs 16.5 +/- 2.7 pmol/pmol; p<0.05) were higher, whereas OC (3.6 +/- 2.4 vs 5.2 +/- 1.9 mg/l; p<0,05) was lower than in controls. In AC patients, GSU (34.9 +/- 5.3 vs 35.2 +/- 3.4%) did not differ significantly from controls, whereas OC (16.8 +/- 8.8 vs 6.9 +/- 2.9 microg/l; p<0.001) and U-DPD (30.9 +/- 13.6 vs 21.0 +/- 5.7 pmol/pmol; p<0.01) were higher. Stepwise multivariate linear regression analysis was performed with disease activity, creatinine clearance, age, and years since menopause as predictor variables and GSU or OC or U-DPD as dependent variables. The significant partial regression coefficients ( r) were: in TT, free triiodothyronine (fT3) with GSU ( r = 0.37; p<0.005), Ln OC ( r = 0.30; p = NS), Ln U-DPD ( r = 0.76; p<0.0001), respectively; in PHPT, PTH with GSU ( r = 0.74; p<0.001), Ln OC ( r = 0.50; p<0.05), Ln U-DPD ( r = 0.64; p<0.001); in CS Ln urinary free cortisol with OC ( r = -0.68; p<0.001) and U-DPD ( r = 0.66; p<0.05). Our data suggest that GSU could represent a valuable clinical tool for evaluating bone turnover rate in PHPT, CS, TT but not in AC. The behavior of GSU and OC and U-DPD is non-uniform in disorders characterized by a marked uncoupling between bone formation and resorption.
Somatostatin content in the blood of healthy persons, of patients with cerebral nanism, diabetes mellitus, Icenko-Cushing's disease, and obesity, was studied by radioimmuno--assay. Comparative analysis of somatostatin, somatotropin, glucagon and immunoreactive insulin content in the blood of patients with different endocrine disturbances was carried out. Significant elevation of somatostatin level was revealed in cerebral nanism. An increase in the blood somatostatin concentration of patients with diabetes mellitus, Icenko-Cushing's disease and obesity was accompanied by a fall in somatotropin and glucagon secretion and a rise in the blood insulin level.
The promoting effect of ACTH on carnitine and lipid metabolism was studied in patients with various endocrine hypofunctions. The results were compared with those of normal subjects. In adrenocortical insufficiency, hypothyroidism and hypopituitarism urinary excretion of carnitine was significantly lower than in normal subjects. On intramuscular injection of synthetic beta1-24 ACTH-Z urninary excretion of carnitine in normal subjects increased sixfold on the day of the injection and returned to the pretreatment level on the third day. Serum concentrations of carnitine and FFA increase in parallel with carnitine excretion, while serum triglyceride was lowered in response to ACTH administration. These responses were totally lacking or substantially suppressed in patients with the above endocrine insufficiencies. In hypothyroid and hypopituitary patients substitution therapy restored the responses to ACTH in the same fashion as those in normal subjects. These findings suggest that the promoting effect of ACTH on carnitine and lipid metabolism requires the presence of intact adrenocortical and thyroid functions.
Plasma levels of prolactin, before and after TRH stimulation, progesterone, estradiol, sex-hormone-binding-globulin, androstenedione, testosterone and dehydroepiandrosterone-sulphate were determined in a group of women with benign breast disease and in control group, in order to correlate a possible hormonal disorder to breast pathology. The hormonal pattern in the patients with benign breast disease was characterized by an increased responsiveness of lactotrophes to TRH stimulation and by higher levels of sex hormone binding globulin, probably sustained by an underlying hyperestrogenism.
The pituitary and gonadal response to pulsatile luteinizing hormone-releasing hormone (LH-RH) administration during the first and consecutive second treatment unit (TU) was studied in nine women with clomiphene citrate-resistant polycystic ovary-like disease (PCOD). The control group consisted of eight eumenorrheic women. Luteinizing hormone levels, LH amplitudes, and total urinary excretion/24 hours did not differ between ovulatory and anovulatory TUs, but were significantly higher compared with the control group. Follicle-stimulating hormone (FSH) in PCOD did not differ from normal cycles. Androgen values in the anovulatory TUs were significantly higher compared with the ovulatory TUs (P = 0.001). We conclude that LH-RH therapy may result in ovulation; however, it does not redress the intrinsic abnormality in PCOD and FSH, and androgen levels do not seem to be critical in ovulation induction.
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The diagnostic reliability of CT in pheochromocytoma was evaluated in 12 symptomatic and 2 asymptomatic patients with a total of 1 bladder and 15 adrenal histologically confirmed tumours. Particular attention is drawn to two cases with bilateral sites (one male child, one woman with Sipple's syndrome) and the detection of possible local and distant malignancy. CT is thus an examination of the first order, since it is noninvasive, specific (no false positives) and able to reveal even small tumours.
A 69-year-old man became hypocalcemic under medical observation. The hypocalcemia occurred in the presence of circulating immunoreactive parathyroid hormone (PTH). Common causes of secondary hyperparathyroidism were excluded, as was PTH resistance using PTH infusions. The immunoreactive PTH was examined in detail. PTH immunoreactivity (1) was not retained on a C18 SPE-column, suggesting unusual molecular or physicochemical properties, unlike bona fide PTH; (2) was precipitated with 15% PEG, indicating a molecular size far in excess of native PTH; (3) had an apparent molecular size similar to immunoglobulins on size exclusion chromatography; (4) was retained on affinity chromatography with both Protein A and anti-hIgG antibodies. These data lead us to conclude that the immunoreactive PTH was due to antiidiotypic PTH autoantibodies. No significant quantities of true PTH were found in the patient's serum suggesting that his hypoparathyroidism was a result of PTH deficiency. Autoimmunity might explain the occurrence of both processes if an arrested antiidiotypic antibody cascade is assumed.
An 11-year prospective study was carried out in 180 non-diabetic patients with organ-specific autoimmune diseases to evaluate islet cell antibodies in predicting Type 1 (insulin-dependent) diabetes mellitus. Islet cell antibodies were characterised according to titres, persistence, complement-fixing ability, and pattern. During follow-up, 14 of 46 patients with islet cell antibodies persistently greater than 5 Juvenile Diabetes Foundation Units (JDF-U) (30.4%), none of 23 with islet cell antibodies between 2.5 and 5 JDF-U or fluctuating, and 3 of 109 without islet cell antibodies (2.7%), developed diabetes. The cumulative risk of developing diabetes was 70%, 0%, and 4%, respectively. All the patients who developed diabetes were females. Eight progressed to insulin-dependence acutely, four showed a transient period of non-insulin-dependence, while two were still insulin-free. No difference was found in titres of islet cell antibodies for the risk of diabetes. Complement-fixing islet cell antibodies enhanced the cumulative risk for the disease in patients with conventional islet cell antibodies at low-middle (> or = 2.5-40 JDF-U), but not at high (> or = 80 JDF-U) titres. Forty-two patients with islet cell antibodies were investigated for the whole or the selective pattern. In the presence of the whole pattern the cumulative risk for diabetes rose to 100%, while with the selective pattern it declined to 34%. The whole pattern was found in 83% of patients who developed Type 1 diabetes acutely. In patients with organ-specific autoimmune diseases, the whole islet cell antibody pattern greatly enhances the prediction for diabetes.
The aim of our echocardiographic study was to characterize cardiac function and anatomy of 14 acromegalics (A: 9 women, 5 men; mean age: 42.4 yrs) more closely. The duration of acromegaly in 4 of these patients was between 3 and 12 years; the disease was diagnosed for the first time in the other patients. Double M-mode echocardiography was performed in all patients and the results compared with data obtained from a control group of 24 healthy volunteers (N: 22 men, 2 women; mean age: 23 yrs). The mean left ventricular diameter at end-diastole was greater in the acromegalics than in the controls (A: 55 +/- 6 mm, N: 50 +/- 4 mm; p less than 0.005, means +/- SD). After correction for age and body surface area, it, however, was outside the 95% confidence interval in 5 patients. Left ventricular hypertrophy was present in 3 patients, one of whom had coexistent arterial hypertension. A total of 3 patients were hypertensive. Significantly higher values for the maximal velocity of systolic wall thickening (A: 6.1 +/- 0.6 cm/s, N: 4.2 +/- 0.6 cm/s, p less than 0.001) and diameter change (A: 12.4 +/- 2.0 cm/s, N: 10.6 +/- 1.0 cm/s, p less than 0.005) indicate increased contractility with concurrently increased relaxation; fractional shortening did not differ significantly (A: 38 +/- 5%, N: 37 +/- 5%, ns). The isovolumetric relaxation period at diastole was slightly longer in the acromegalics (A: 70 +/- 17 ms, N: 61 +/- 13 ms, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Diseases like sepsis, AIDS and cancer can induce an increase in endogenous glucose production. Sepsis and cancer induce insulin resistance whereas increased insulin sensitivity is found in AIDS. Non-oxidative glucose disposal is increased in sepsis and cancer but normal in AIDS. These differences in glucose metabolism between these three diseases characterized by wasting preclude energy-requiring changes in glucose metabolism as the common denominator for wasting in all three diseases. Moreover, the energy requirements of the changes in glucose metabolism induced by cancer and sepsis are rather small. Consequently, alterations in glucose metabolism are pathophysiological epiphenomena rather than a cause of wasting in disorders like sepsis, cancer and AIDS.
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