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Biomedical subjects

B Glaser

Publications and source records attributed to B Glaser.

At least 109 records · Page 6Linked to original sources
PubMed1989

Bromocriptine treatment of acromegaly: possible dose dependency of the tumor size-reducing effect.

The effect of long-term, high-dose therapy with bromocriptine (BR) on the clinical and hormonal response, tumor size and neuro-ophthalmological status was studied in seven acromegalic patients. The mean BR dose was 64 mg/day (range 35 to 80) for a mean period of 11 months (range 10 to 12). In six patients there was a clinical improvement already manifest at low BR doses (10 to 20 mg). Serum growth hormone levels fell substantially (greater than 50%) in five patients, and the growth hormone response to thyrotropin-releasing hormone (TRH) and glucose were similar to those previously reported at lower doses of the drug, as were the prolactin and thyroid-stimulating hormone responses to TRH. In three patients, repeat CT scan disclosed a reduction in tumor size. In none of the patients was there evidence of tumor progression, with the possible exception of one patient who developed an impairment of the visual evoked potential response. These results suggest that when compared to previous studies in which lower doses of BR were used, a high BR dose is not superior in terms of clinical response and hormone secretion, but does appear to increase the percentage of patients who respond with a reduction in tumor size.

Acromegaly↗
PubMed1988

Pancreatic polypeptide response to secretin in obesity: effects of glucose intolerance.

Pancreatic polypeptide (PP) may function as a regulator of satiety. Its secretion is impaired in certain animal models of obesity and the administration of PP may improve the hyperphagia and hyperinsulinism seen in these animals. In obese humans, decreased, normal or increased, basal and stimulated concentrations of PP in plasma have been reported. However the advent of diabetes confounds the picture since PP levels in diabetes are generally raised. We have therefore examined the PP responses to intravenous secretin, a known PP secretagogue, in 23 obese subjects, 12 with normal and 11 with abnormal glucose tolerance, and compared the results with those in 23 age and sex-matched healthy controls. The mean maximum PP level in obese subjects with normal glucose tolerance (98 +/- 13 pg/ml) was significantly less than that in normal subjects (218 +/- 23 pg/ml) but in obese subjects with abnormal glucose tolerance, it was significantly greater (578 +/- 115 pg/ml). Within each of the 3 study groups taken separately, PP response to secretin was not correlated with glucose or insulin levels, or with the degree of obesity. Thus, obesity per se appears to be associated with impaired PP responses, which may be masked by abnormalities in glucose tolerance.

Adult↗
PubMed1988

Effects of secretin on the normal and pathological beta-cell.

Secretin is a gastrointestinal hormone that stimulates insulin secretion and enhances the insulin response to glucose. The mechanism by which secretin acts on the beta-cell has not been extensively studied. The plasma insulin responses to secretin (2 U/kg), expressed as the percent increase relative to basal plasma insulin concentrations, were similar in normal (n = 23) and obese subjects with normal glucose tolerance (n = 12), but were decreased in obese subjects with abnormal glucose tolerance (n = 11). The insulin response to secretin was directly proportional to the basal insulin concentration in these three groups. The effects of secretin on beta-cell function was not altered by propranolol (n = 6), atropine (n = 8), or surgical vagotomy (n = 10). Patients with single islet cell tumors secreting insulin (n = 18) had no plasma insulin response to secretin, whereas patients with noninsulin-secreting pancreatic tumors (gastrinomas; n = 6) and patients in whom single insulinomas had been removed (n = 7) responded normally. Two adult patients with multiple B-cell adenomas and hyperplasia (not associated with multiple endocrine neoplasia type I) hyperresponded to secretin, whereas patients with multiple endocrine neoplasia, type I, without hyperinsulinism responded normally. One patient with nesidioblastosis had no response to secretin, indicating that the pathophysiology of this entity is distinct from that of other forms of islet hyperplasia. These data suggest that secretin stimulates beta-cells directly rather than through cholinergic, adrenergic, or vagal peptidergic neural mechanisms. In addition, the ability to respond to secretin appears to be lost in patients with single insulinomas and nesidioblastosis, but not in those with multiple B-cell adenomas and hyperplasia. The lack of a plasma insulin response in patients with single insulinomas and the high normal or exaggerated response in patients with multiple B-cell adenomas and hyperplasia may prove useful in differentiating these entities.

Adenoma↗
PubMed1988

Improved beta-cell function after intensive insulin treatment in severe non-insulin-dependent diabetes.

In Type II, non-insulin-dependent diabetes, insulin secretion is often reduced to the point where oral hypoglycaemic agents fail to control the plasma glucose level. We studied 12 patients (age 41-66 years; 4 lean, 8 obese) with Type II diabetes mellitus for 1-25 years who were uncontrolled despite maximal dose glibenclamide and metformin. After withdrawal of medication, blood glucose control was determined by measuring glucose before and 2 h after each meal for 48 h, and beta-cell function by insulin or C-peptide response to glucagon and to iv glucose. Following these tests, intensive insulin treatment (CSII) was initiated, and near-euglycaemia (mean of 7 daily glucose determinations less than 7.7 mmol/l) was maintained for 16.6 +/- 1.5 days, at which time the tests were repeated. Mean daily insulin requirement was 61 +/- 9 IU (0.81 +/- 0.09 IU/kg). Glucose control was improved after cessation of CSII (mean glucose 12.7 +/- 0.6 mmol/l after vs 20 +/- 1.5 mmol/l before, P less than 0.005). Maximum incremental C-peptide response improved both to glucagon (214 +/- 32 after vs 134 +/- 48 pmol/l before, P = 0.05) and to glucose iv bolus injection (284 +/- 53 vs 113 +/- 32 pmol/l, P less than 0.05). Peak insulin response, measured after iv glucose infusion, also tended to be higher in the post-CSII test (42 +/- 18 vs 22 +/- 5.6 mU/l). Basal and stimulated proinsulin concentrations were high relative to C-peptide levels during the pre-treatment period, but returned to normal after CSII.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Bioassay of thyroid-stimulating immunoglobulin in cryopreserved human thyroid cells: optimization and clinical evaluation.

We have explored the method of Rapoport et al. (J Clin Endocrinol Metab 1984;58:332-8) for the bioassay of thyroid-stimulating immunoglobulin (TSI) in cultured human thyroid cells, to optimize the assay and to evaluate its utility in clinical diagnosis and management of patients with autoimmune thyroid disease. Here we describe the procedure ultimately adopted, its major properties, and the results it has yielded in various clinical states. Clinical sensitivity of the assay was established by demonstrating TSI activity in all of 60 cases of active Graves' disease. We observed in these patients a nonlinear correlation between concentrations of TSI and of triiodothyronine, as well as between TSI concentration and the clinical severity of the thyrotoxicosis. Specificity of the assay was demonstrated by finding no TSI bioactivity in 13 patients with toxic adenoma, five with cold nodule, and 18 of 19 with nontoxic goiter. Remission of Graves' disease in 25 patients was invariably accompanied by undetectable concentrations of TSI; evidently this assay may be useful in identifying patients who are likely to go into remission. TSI activity was present in eight of 11 patients with euthyroid ophthalmopathy (unilateral and bilateral) associated with a normal response to the thyrotropin-releasing hormone test and absence of increased titers of antithyroid antibodies, suggesting that this assay may provide a powerful tool in the clinical diagnosis of this disorder.

Antibodies↗
PubMed1987

Thyrotrophin receptor blocking antibodies: incidence, characterization and in-vitro synthesis.

The prevalence and characteristics of TSH receptor blocking activity were examined in patients with different thyroid disorders. Studies were also performed on the in-vitro synthesis and immunoregulation of the blocking antibody. Blocking activity was tested by measuring the inhibition of TSH-stimulated cAMP production of cultured human thyroid cells by patient immunoglobulin (Ig) preparations. The following patients were investigated (number of cases in parentheses): Hashimoto's thyroiditis (33); primary myxoedema (17); euthyroid ophthalmopathy (8); active Graves' disease (19); cold nodule (5); non-toxic goitre (14); toxic adenoma (8); toxic multinodular goitre (9) and 22 normal controls. TSH receptor blocking activity was only detected in primary hypothyroidism with the following characteristics: (i) Such activity was present in only 16% of the patients (both goitrous, i.e. Hashimoto's thyroiditis, and non-goitrous, i.e. primary myxoedema), and in three patients with previously active Graves' hyperthyroidism who had become hypothyroid. (ii) Blocking activity seems to be associated with the Ig fraction of serum as indicated by protein A adsorption. (iii) The block-positive samples did not bind 125I-TSH, which seems to rule out an antibody directed against TSH. (iv) The specificity of the blocking activity seems to be directed towards the TSH-(thyroid stimulating immunoglobulin, TSI) receptor-mediated cAMP response since no inhibition of prostaglandin E1-stimulated cAMP production was found. Moreover, all cases in which an inhibitory effect was demonstrated towards TSH also exhibited blocking of TSI-stimulated cAMP, with a high correlation between the degree of inhibition of the TSH to that of the TSI response (r = 0.89, P less than 0.001, n = 11). The blocking activity may contribute to the pathogenesis of some cases of primary hypothyroid autoimmune thyroiditis, both goitrous and non-goitrous, as well as in the evolution of hyper- to hypothyroidism. By culturing peripheral blood lymphocytes, as well as B/T lymphocyte co-cultures isolated from three patients with blocking activity present in serum, the in-vitro synthesis of the blocking antibody was demonstrated for the first time. Moreover, in-vitro secretion of the antibody by patients B lymphocytes, as well as T cell regulation of autoantibody production, were also shown.

Adult↗
PubMed1987

Toxic multinodular goiter: a variant of autoimmune hyperthyroidism.

The aim of this study was to examine whether at least a subgroup of patients with toxic multinodular goiter may have autoimmune thyroid disease. Thyroid-stimulating immunoglobulin (TSI) activity, measured by a sensitive bioassay employing cultured human thyroid cells, was determined in patients with toxic multinodular goiter and other thyroid disorders. All patients with active Graves' disease (n = 47) had detectable serum TSI activity, whereas TSI was undetectable in patients with thyroid disease not believed to be of autoimmune origin: toxic adenoma (n = 13), cold nodule (n = 5), and nontoxic goiter (n = 19), with a single exception in the latter group. Toxic multinodular goiter (n = 26) was diagnosed based on clinical and laboratory evidence of hyperthyroidism associated with a multinodular goiter on palpation and scintiscan. The toxic multinodular goiter group was then subclassified according to scintiscan pattern (type A, diffuse but uneven distribution of technetium uptake; type B, multiple discrete nodules of varying size and function). All but 1 of the 11 TSI-positive toxic multinodular goiter patients had a type A scintiscan pattern. The patients with the type A scintiscan pattern were younger and more often had elevated antithyroid antibody titers, ophthalmopathy, and concurrent development of goiter and hyperthyroidism (rather than long-standing goiter preceding hyperthyroidism) compared to the type B patients. Thus, a subgroup of patients with clinically defined toxic multinodular goiter (type A) probably have autoimmune hyperthyroidism (a variant of Graves' disease), while in another subgroup (type B) hyperthyroidism is not related to an autoimmune etiology (a variant of toxic adenoma).

Adenoma↗
PubMed1986

Magnetic resonance imaging of the pituitary gland.

Magnetic resonance imaging (MRI) was performed on 22 patients with a wide spectrum of pituitary disease and on 17 control subjects, in order to determine whether MRI is useful in localising and determining the extent of involvement of large and small pituitary tumours. The results indicate that MRI, with an 0.5 T superconducting magnet (Elscint, Israel), can be used to visualise large pituitary tumours and to determine the extent of parasellar and suprasellar involvement. The 'empty sella' syndrome can also be easily and confidently diagnosed. Some microadenomas can be visualised despite the relatively thick slices (0.7 cm) used in this study. These findings suggest that MRI in its current state of development is very useful in evaluating large pituitary lesions. With further technical refinements, improving the spatial resolution and decreasing slice thickness, this technique may come to be of some importance in the evaluation of pituitary microadenomas.

Acromegaly↗
PubMed1985

Leydig-cell tumor of the ovary: visualization using 131I-19-iodocholesterol scintigraphy.

A Leydig (Hilus)-cell tumor of the ovary was diagnosed in a 54-year-old woman with severe hirsutism and virilization. This case is unique in that it was diagnosed in a postmenopausal female 24 years after ovarian irradiation for sterilization, and the tumor was successfully localized preoperatively using 131I-19-iodocholesterol scintigraphy. This nuclear scanning technique may be of use in documenting the biologic activity of ovarian masses and in localizing functioning ovarian tumors which are too small to palpate or to localize by other means.

19-Iodocholesterol↗
PubMed1985

Do cyclic AMP concentrations in saliva reflect PTH biologic activity?

The aim of this study was to investigate whether the concentration of cAMP in saliva might reflect the biologic activity of parathyroid hormone (PTH), as nephrogenous levels of cAMP reflect parathyroid function. Patients with primary hyperparathyroidism (HPT) with elevated levels of PTH, nephrogenous cAMP, and serum calcium were found to have cAMP levels not significantly different from control subjects. When the levels of these parameters were reduced following parathyroidectomy, salivary cAMP concentrations were not affected. Similarly, an oral calcium loading test (which decreased both PTH and nephrogenous cAMP in normal subjects) failed to influence salivary cAMP levels. Basal salivary cAMP concentrations were low in secondary hyperparathyroid patients due to chronic renal failure and rose almost fivefold following dialysis despite the stable plasma cAMP levels and salivary flow rate. We conclude that salivary cAMP concentrations do not appear to be influenced by changes in circulating biologically active PTH. However, salivary cAMP concentrations do change in response to certain perturbations; this suggests that they are regulated by some other modulator(s).

Adolescent↗
PubMed1985

Cellular immune functions in patients with primary hyperparathyroidism: effects of histamine and cimetidine.

The possibility of a link between parathyroid hyperfunction and cellular immune functions was studied in primary hyperparathyroid (1 degree HP) patients. The effect of cimetidine on lymphocyte functions in 1 degree HP patients and control subjects was also investigated. Histamine-induced suppressor activity of lymphocytes from 1 degree HP patients was significantly greater than that of controls. Cimetidine addition to both normal and 1 degree HP lymphocyte cultures abolished histamine-induced suppression. In vivo administration of cimetidine, while ineffective towards normal lymphocytes, depressed phytohemagglutinin stimulation of 1 degree HP lymphocytes, indicating possible immunological damage caused by this drug, which is frequently used in the treatment of patients with 1 degree HP.

Cimetidine↗
PubMed1985

L-Thyroxine-induced leukopenia in a patient with Hashimoto's disease: involvement of suppressor-cytotoxic T cells.

A study of in vitro reactivity to L-T4, as assessed by peripheral blood lymphocyte transformation, was carried out in a patient with Hashimoto's disease who developed leukopenia during treatment with L-T4. L-T4 stimulated lymphocyte transformation in this patient. The proliferating cells were of T lineage and further typing demonstrated that they bore the OKT8 antigen. Cell-mediated immune reactions mediated by OKT8+T cells might have caused the leukopenia, although other mechanisms involving cytotoxic antibodies or antibody-dependent cell-mediated cytotoxicity cannot be excluded.

Female↗
PubMed1985

Study of vitreous liquifaction by NMR spectroscopy and imaging.

The vitreous gel is primarily composed of collagen, hyaluronic acid, and water (98-99%) and can break down into a liquid state devoid of collagen. The liquifaction of vitreous gel that occurs with age and in certain other disease states is believed to be important in the pathogenesis of retinal tears and detachments. The authors report measurements of water proton relaxation times and water proton nuclear magnetic resonance (NMR) imaging to study the process of vitreous liquifaction in extracted vitreous and in the intact bovine eye. A comparison is made between macroscopic viscosity, longitudinal (T1) and transverse (T2) relaxation times obtained on an NMR spectrometer and proton NMR images. Vitreous liquifaction as measured by a decrease in macroscopic viscosity resulted after treatment of vitreous with collagenase and to lesser degree with hyaluronidase. A shortening of relaxation times accompanied the drop in viscosity. An area of brightness or increased proton signal intensity corresponding to a focus of liquifaction was seen by NMR imaging only after injection with collagenase. The authors believe NMR imaging to be a useful new diagnostic modality by which vitreous liquifaction can be studied in the intact eye. The vitreous provides a new model for studying changes in proton relaxation times of protein solutions in biologic systems.

Animals↗
PubMed1984

Nuclear magnetic resonance imaging of the vitreous body.

Imaging with proton nuclear magnetic resonance is a valuable new tool for studying the vitreous body of the eye. It is particularly suited for the detection of vitreal liquefaction and intraocular hemorrhage because of the dependence of the signal on the physical environment of water. Conversely, the vitreous body provides a new model for studying changes in proton relaxation times of protein solutions in biological systems.

Animals↗
PubMed1984

Pancreatic polypeptide-producing tumors. Silent lesions of the pancreas?

Eight patients with pancreatic polypeptide (PP)-producing islet cell tumors and one patient with pseudo-PP-producing tumors were examined. Their age range was 20 to 74 years. Clinical features included abdominal pain in four patients, weight loss in four patients, diarrhea in two patients, gastrointestinal bleeding in two patients, and jaundice in one patient. The range of the basal serum level of PP was 394 to 35,100 pg/mL. In two patients the PP-producing tumors were associated with multiple endocrine neoplasia. Two patients had diffuse hepatic metastases at the time of diagnosis and four patients had disease limited to the pancreas. Pancreaticoduodenectomy and 80% pancreatectomy were performed in four and two patients, respectively. Immunohistochemical staining was positive for PP and neuron-specific enolase in all cases and was negative for other peptides except in one specimen with microadenomatosis. Patients who underwent curative resection are asymptomatic with normal serum levels of PP.

Abdomen↗
PubMed1984

Effect of acute cimetidine administration on indices of parathyroid hormone action in healthy subjects and patients with primary and secondary hyperparathyroidism.

To evaluate the acute effect of histamine H2-receptor blockade with cimetidine on PTH concentrations and its endogenous biological activity, we studied the effect of iv administration of cimetidine (50-mg bolus followed by 500 mg/60 min infusion) in normal subjects and patients with primary and secondary hyperparathyroidism. No significant changes in serum concentrations of calcium, phosphate, or immunoreactive C-terminal PTH were found in any group. However, the control group had decreased calciuria, increased phosphaturia, and decreased tubular reabsorption of phosphate, while the primary hyperparathyroid group had increased phosphaturia, increased nephrogenous cAMP excretion, and decreased tubular reabsorption of phosphate. In both of these groups, the finding suggest an increase in PTH-like biological activity. These findings suggest that cimetidine is not useful in the diagnosis or medical management of hyperparathyroidism. In fact, the changes in renal calcium and phosphorous excretion indicative of PTH-like biological activity along with a decrease in creatinine clearance in the primary hyperparathyroid group suggest a relative contraindication to the use of this drug in these patients.

Adult↗