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Biomedical subjects

B Grubeck-Loebenstein

Publications and source records attributed to B Grubeck-Loebenstein.

106 records · Page 6Linked to original sources
PubMed1982

[Thyroid function in healthy premature infants and in premature infants with the hyaline membrane syndrome ].

The serum concentrations of thyrotropin (TSH), thyroxine (T4), trijodothyronine (T3) and of 3,3',5', trijodothyronine (reverse T3, rT3) were followed up during the first 4 weeks of life in 5 healthy premature infants and in 6 premature infants with hyaline membrane syndrome and artificial ventilation. TSH and T4 concentrations remained unchanged in both groups. T3 levels increased during the observation period and were significantly lower in the sick prematures on days 1 and 3 (p less than 0,02). T3 and the rT3/T3 ratio was increased in healthy and in the sick prematures, the sick prematures showing higher values, and decreased in both groups during the first week of life. We found no significant correlation between TSH and the peripheral thyroid hormone levels as well as no relation between the respiratory compliance-indicating degree of lung maturity-and the T3 or T4 concentrations. Postpartal T3 or T4 serum levels were correlated significantly with the duration of artificial ventilation. Our data indicate that a "low T3 syndrome" was present in all prematures after birth and that respiratory distress syndrome increased conversion of T4 to rT3. From our results we cannot conclude that substitution therapy with thyroid hormones may be useful in premature infants with the hyaline membrane syndrome.

Humans↗
PubMed1982

Impaired secretion of TSH in critically ill patients with 'low T4-syndrome'.

Thyroid and pituitary function was studied in 10 male and 6 patients female during critical non-endocrine disease. Low concentrations of TT3 were observed in each case. Seven patients out of whom 3 survived, presented with low levels of TT4 due to deficiency in TBG in the presence of normal values of FTI and FT4, whereas a 'low T4-syndrome', characterized by low concentrations of both TT4 and FT4 was seen in 9 patients, 8 of whom died 1 to 16 days after evaluation of pituitary function. A diminished response of TSH to iv TRH (400 micrograms), as observed in 4 patients with normal FT4 and in all patients with 'low T4-syndrome', was not accompanied by a concomitant lack in stimulated release of LH, FSH and Pr1 in the majority of cases. However, the secretory maximum of LH and FSH following stimulation by LRH (100 micrograms iv) was delayed in 10 and in 9 patients, respectively, including patients both with normal and subnormal concentrations of FT4. From the above it appears that low stimulated concentrations of TSH in the presence of subnormal concentrations of FT4 indicate an extremely poor prognosis in critically ill patients. The abnormal behaviour of TSH in this group of patients cannot be explained by generalized pituitary insufficiency or by an increase in FT4.

Adult↗
PubMed1982

Pituitary-thyroid dysfunction in severe non-thyroidal disease: "low-T4 syndrome".

Thyroid function tests were obtained from 335 consecutive patients admitted to an intensive care unit. Twenty patients suffering from severe non-endocrine diseases (septicaemia, fulminant hepatic and renal failure, acute pancreatitis, polytrauma, cerebral haemorrhage) were found to have serum thyroxine levels in the hypothyroid range (less than 4 micrograms/dl). Serum concentrations of total thyroxine (2.3 +/- 0.2 micrograms/dl), triiodothyronine (0.23 +/- 0.03 ng/ml), and thyroxine binding globulin (15.1 +/- 1.3 micrograms/ml) were reduced, but were above normal for reverse triiodothyronine (0.43 +/- 0.06 ng/ml). Response of TSH secretion to iv TRH was found to be either normal, lowered or absent. Primary hypothyroidism was excluded, as no enhanced TSH response was observed in any case. Although decreased thyroxine levels may be due to increased thyroid hormone degradation it appears that associated impaired TSH responsiveness to TRH may result from illness-related inhibition of pituitary TSH release. Although the finding of decreased thyroid hormone levels is not rare in care patients, it represents an index of poor prognosis. Differentiation between this "low-T4 syndrome" and true hypothyroidism depends essentially on clinical symptoms and course of disease.

Acute Disease↗
PubMed1981

The role of "diabetogenic" hormones on carbohydrate and lipid metabolism following oral glucose loading in insulin dependent diabetics: effects of acute hormone administration.

To evaluate the relative role of "diabetogenic" hormones as insulin antagonists in severe derangements of diabetic control, glucagon, cortisol, growth hormone and adrenaline were administered by continuous intravenous infusion, separately and in combination, to ketosis-prone insulin-dependent diabetics (n = 11). The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Raising plasma hormone concentrations acutely into the range seen in severe diabetic states (glucagon 517 +/- 70 pg/ml; cortisol 32 +/- 3 micrograms/dl; growth hormone 14 +/- 3 ng/ml) did not alter significantly blood glucose profile and insulin requirement (control 11.3 +/- 1.1 U; glucagon 11.6 +/- 2.0 U; cortisol 11.1 +/- 0.4 U; growth hormone 12.9 +/- 1.4 U), except for adrenaline (plasma level 550 +/- 192 pg/ml), which caused a marked rise in blood glucose levels and a threefold increase in insulin demand (31.1 +/- 3.7 U). Combined infusion of all hormones did not potentiate significantly the latter effect (38.3 +/- 4.7 U). The effectiveness of metabolic control by insulin was assessed by a marked decrease in plasma nonesterified free fatty acids and ketone bodies upon its administration after glucose ingestion in all groups studied. It is concluded that from the hormones investigated within this study adrenaline exerts the strongest diabetogenic action during its short term administration followed by that of growth hormone. Whereas it may well be that over-insulinization of the patients by the glucose controlled insulin infusion system has overcome and disguised the smaller diabetogenic effects of cortisol and glucagon.

Adult↗
PubMed1981

Antidiabetic action of somatostatin after oral glucose loading: due to suppression of glucagon and growth hormone or of intestinal carbohydrate absorption?

To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). Thus the integrated amounts of insulin required for glucose hormone were temporarily suppressed by somatostatin. It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. Our findings favour inhibition of intestinal carbohydrate absorption as the determining cause for the "antidiabetic" action of somatostatin.

Adult↗
PubMed1981

The impact of euglycemia and hyperglycemia on stimulated pituitary hormone release in insulin-dependent diabetics.

To study the influence of different blood glucose (BG) concentrations on the release of pituitary hormones, the effect of the simultaneous iv administration of LRH (200 micrograms), TRH (400 micrograms), and arginine (30 g/30 min) upon the serum concentrations of LH, FSH, TSH, PRL, and GH was determined in six male insulin-dependent diabetics. BG concentration was clamped by feedback control and an automated glucose-controlled insulin infusion system at euglycemic (BG 4-5 mmol/liter) or hyperglycemic (BG, 14-18 mmol/liter) levels. Increments in serum concentrations of LH, FSH, TSH, and PRL were similar in the euglycemic and hyperglycemic steady states, whereas the GH response to arginine was suppressed during the hyperglycemic clamp (P less than 0.01). Omission of exogenous insulin during hyperglycemia did not modify the observed hormonal responses. Thus, the release of LH, FSH, TSH, and PRL in response to adequate acute stimuli at the pituitary level is not modulated by hyperglycemia in insulin-dependent diabetes, while arginine-induced GH release is suppressed. Since the effect of arginine on GH is most likely mediated by an action on the hypothalamus, the data suggest that elevated glucose concentrations may exert their modulatory influence on GH secretion at the hypothalamic rather than at the pituitary level.

Adult↗
PubMed1981

Alterations in thyroxine metabolism in Crohn's disease.

To evaluate the possible alterations in thyroxine metabolism in patients with Crohn's disease (C.D.), the serum concentrations of thyroxine (T4), triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), and thyroxine binding globulin (TBG) were determined in 23 patients with C.D. and in 25 healthy controls. While concentrations of T4 and rT3 in patients with C.D. were similar to those seen in healthy controls, serum T3 was lower in patients with C.D. (0.93 +/- 0.4 ng/ml) than in controls (1.20 +/- 0.3 ng/ml, p less than 0.005). TBG concentrations were elevated in two patients with C.D., and below normal in two others. However, the group mean of TBG concentrations in patients with C.D. (23.7 +/- 6.9 micrograms/ml) was similar to that of healthy controls (21.9 +/- 3.6 micrograms/ml, p greater than 0.05). Changes in peripheral deiodination of thyroxine, enhanced in some cases by treatment with glucocorticoids and/or increased turnover of T3 may be the cause of the decreased concentration of T3 in some patients with Crohn's disease.

Adolescent↗
PubMedDate not supplied

The role of adrenergic mechanisms in the blood pressure regulation of leg-amputees.

An increased occurrence of hypertension has been reported among leg-amputees. In order to investigate whether leg amputation is followed by an elevation of sympathetic tone, possibly enhanced by continuous mechanical irritation of the amputation stump by wearing a prosthesis, blood pressure (BP), pulse-rate (PR) and plasma catecholamines (norepinephrine, NE, and epinephrine, E) were measured in six hypertensive leg-amputees during prosthesis walking as well as during irritation of the amputation stump by vacuum suction in the supine position. Six patients suffering from essential hypertension and six normotensive subjects served as control groups. Basal levels of plasma NE and E did not differ in the three investigated groups. Mechanical stump(limb) irritation as well as walking induced a rise of NE but not of E, accompanied by a rise of BP and PR in amputees as well as in the control subjects. Elevation of NE and BP was most accentuated in hypertensive amputees when walking with prosthesis. Within each investigated group there was a positive correlation between NE and mean arterial blood pressure (MAP), (p less than 0.001 in hypertensive amputees and non-amputees, p less than 0.05 in normotensives). We conclude that mechanical limb irritation induces a rise of BP by sympathetic nervous stimulation. Thus wearing of a vacuum-prosthesis may support a consistent rise in BP.

Adult↗
PubMedDate not supplied

APP peptides stimulate lymphocyte proliferation in normals, but not in patients with Alzheimer's disease.

We hypothesized that metabolic products of the Alzheimer beta amyloid precursor protein (APP) might be targets for cells of the immune system. To test this hypothesis, peripheral blood lymphocytes from young and old healthy blood donors and patients with Alzheimer's disease were analysed for their responsiveness upon stimulation with amyloid beta protein as well as with four other synthetic peptides corresponding to parts of the APP sequence. Stimulation of resting blood lymphocytes from young and old healthy blood donors resulted in IL-2 receptor expression and proliferation in both age groups. In contrast, lymphocytes from the majority of patients with Alzheimer's disease did not proliferate, when stimulated with APP peptides, while their proliferative response to anti-CD3 was unimpaired. This lack of proliferative responsiveness to APP peptides was not due to apoptosis, but could reflect T cell anergy, as it was accompanied by unimpaired IL-2 receptor expression. The results suggest that autoreactive lymphocytes with specificity for metabolic products of APP occur in healthy individuals. These cells may be of relevance for the elimination of potentially amyloidogenic substances. This mechanism could be impaired in patients with Alzheimer's disease.

Adolescent↗
PubMedDate not supplied

Immunity and aging.

Explore the source record for details and available documents.

Aged↗
PubMedDate not supplied

Influenza vaccination in a healthy geriatric population: preferential induction of antibodies specific for the H3N2 influenza strain despite equal T cell responsiveness to all vaccine strains.

Cellular as well as humoral immune reactivity were studied in healthy young (< 30 years; n = 12) and older (> 65 years; n = 12) individuals before as well as 1 month after immunization with a trivalent whole virus influenza vaccine. Before vaccination, peripheral blood mononuclear cell proliferation in response to in vitro stimulation with each of the virus strains was low in both groups. No antibodies against either the H1N1 or the B strain were found in most individuals, while 91% of the young and 75% of the elderly persons had low but protective antibody titres to the H3N2 strain. Vaccination led to a significant enhancement of peripheral blood mononuclear cell reactivity to all three influenza strains in both age groups. However, there was a significant difference in the humoral immune response between the groups. While there was a vigorous antibody response to all three vaccine strains among young persons, protective titres against the H1N1 and the B strains were only just reached in the old. In contrast, antibody production to the H3N2 strain was most abundant in the majority of elderly individuals, leading to significantly higher titres in the old than in the young group. In conclusion, the results demonstrate the preferential induction of antibodies to one particular influenza strain despite equal T cell recruitment to all vaccine strains in healthy aged individuals after immunization with a trivalent influenza vaccine. Our findings underline the complexity of immunological alterations to be expected after vaccination in healthy elderlies.

Adult↗
PubMedDate not supplied

The aging immune system: primary and secondary alterations of immune reactivity in the elderly.

The function of the immune system is known to decline in the elderly. The present communication will show that, similar to the situation in children, it is necessary to distinguish between primary and secondary alterations of the immune reactivity in the elderly. The primary immunological change in the elderly is the age-dependent intrinsic decline of immune responsiveness that is also observed in healthy persons, i.e., those selected according to the criteria of the SENIEUR Protocol of EURAGE (European Community Concerted Action on Aging). Secondary immunological changes are due to underlying diseases and various environmental factors, including diet, drug intake, physical activity, etc. While primary immunodeficiencies of the elderly are not, or only to a very minor extent, presently influenced by therapeutic measures, secondary alterations of the immune function offer further possibilities for corrective measures. Clinically, the consequences of impaired immune function in the elderly include increased susceptibility to infectious disease, the emergence of tumors, and increased autoimmune reactions, the latter albeit often without concomitant autoimmune disease. In fact, autoimmune diseases in generally begin to develop at younger ages, but their consequences are major factors affecting the quality of life of the elderly. Investigations of basic molecular and cellular aspects of the aging immune system are, therefore, of theoretical, clinical and socioeconomic interest.

Aging↗
PubMedDate not supplied

The possible role of the immune system in Alzheimer's disease.

Currently, there is little doubt that the immune system plays a role in the neurodegenerative process in Alzheimer's disease (AD). Inflammatory proteins such as complement components, enzymes, eicosanoids, and cytokines are found in association with cerebral amyloid plaques and may exacerbate the fundamental pathology of AD, by stimulating Amyloid beta (A beta) production, supporting its aggregation and increasing its cytotoxicity. Activated microglia and astrocytes are the main source of these proteins, and A beta may trigger their release. Interestingly, there are also indications that the immune system may play a protective role against the development of AD. Microglial cells have been shown to degrade A beta, and recent evidence suggests that autoreactive A beta-specific T cells may be relevant to the elimination of the peptide. This mechanism seems, however, impaired in the majority of patients with AD. The immune system seems thus to represent a natural line of defense against the accumulation of dangerous amyloidogenic substances. Impairment of this specific immunological defense mechanism and the failure to eliminate a toxic metabolite can be the basis for a chronic nonspecific inflammatory process in the brain, as described above. AD is a good example how an immune response initially aiming at maintaining the integrity of the body may fail and consequently lead to tissue destruction and neuronal loss.

Alzheimer Disease↗
PubMedDate not supplied

Release and vasoactive actions of catecholamines during inhibition of prostaglandin synthesis in normal man.

To assess the effect of prostaglandin inhibition upon the vasoactive actions of endogenous and exogenous catecholamines in healthy man, indomethacin (150 mg/day for 3 days) was administered to six healthy men in the sodium-repleted state. Pretreatment with indomethacin did not interfere with the response of blood pressure and pulse rate to orthostasis (10 minutes), a cold pressor test (2 minutes), and the intravenous (i.v.) administration of norepinephrine (NE) (50, 100, and 200 ng kg-1 min-1). Basal plasma concentrations of epinephrine (E) and NE as well as the concentrations of E during orthostasis and cold pressor test remained uninfluenced by pretreatment with indomethacin. While the release of NE during orthostasis appeared to be suppressed in the indomethacin-treated state, it was unchanged during the cold pressor test. These results indicate that inhibition of endogenous prostaglandin synthesis may suppress the release of NE, but does not have a major impact on the vasoactive actions of endogenous and exogenous catecholamines in normal men.

Adult↗
PubMedDate not supplied

The effect of TSH and TSI on the thyroglobulin expression of cultured human thyroid cells.

Human thyroid cells in culture stimulated by TSH and TSI were used in order to detect thyroglobulin expression. After three days stimulation the cells were incubated with monoclonal thyroglobulin antibody and FITC-conjugated antiglobulin. Fluorescent index (the intensity of fluorescence related to hundred analysed cells) was estimated for each experimental group. The most effective stimulation of the thyroglobulin expression was detected after TSH stimulation at the concentration of 0.1 mU/ml. TSI from active Graves' patients provoked the highest expression of thyroglobulin at concentration of 1.0 mg/ml, but the fluorescence index was lower than after TSH stimulation. The thyroglobulin expression was intracellular, large, partly confluent granules were detectable mainly in the perinuclear area. Antigen expression on the surface of cultured thyroid cells could not be detected. The morphology of thyroglobulin expression as detected by immunofluorescence, was the same after TSH and TSI stimulation. It is concluded, that both stimulating factors, i.e. TSH and TSI, are involved in the thyroglobulin expression of human thyroid cells.

Autoantibodies↗