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Biomedical subjects

H Braunsteiner

Publications and source records attributed to H Braunsteiner.

At least 19 recordsLinked to original sources
PubMed1992

High prevalence of viral infection in adults with homozygous and heterozygous alpha 1-antitrypsin deficiency and chronic liver disease.

OBJECTIVE: To determine the prevalence of chronic liver disease in adults with homozygous (Pi ZZ) and heterozygous (Pi Z) alpha 1-antitrypsin deficiency and to assess the presence of other possible risk factors for the development of chronic active hepatitis and cirrhosis of the liver in these patients. DESIGN: Cross-sectional study. SETTING: A referral-based university hospital. PATIENTS: Consecutive patients (164) with the Pi ZZ and Pi Z phenotype with and without chronic liver disease. MEASUREMENTS: The presence of antibody to hepatitis C virus (anti-HCV) was determined using an assay incorporating synthetic peptide antigen from capsid protein (United Biomedical [UBI] assay) and a second-generation enzyme immunoassay (Abbott test); the presence of antibody to hepatitis B virus (anti-HBV) was determined using radioimmunoassays incorporating hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg); assays for antinuclear antibody and antimitochondrial antibody (M2 subtype) were also done, and alcohol abuse was assessed by history. RESULTS: Among patients with cirrhosis (32%), 62% were anti-HCV positive by the Abbott test (P = 0.006), and 41% were anti-HCV positive by the UBI assay (P = 0.007). Thirty-three percent of patients with cirrhosis had hepatitis B virus (HBV) infection (P = 0.01); 41% had a history of alcoholism; and 12% had features of autoimmune liver disease. Only five patients (9%) with cirrhosis had no other risk factor for chronic liver disease. Among patients with chronic active hepatitis (7%), 80% were anti-HCV positive by the Abbott test (P = 0.002), and 75% were anti-HCV positive by the UBI assay (P less than 0.001). Thirty percent of patients with chronic active hepatitis had HBV infection (P = 0.023); 18% had autoimmune hepatitis; and 8% abused alcohol. Only two patients (17%) had no additional risk factor for the development of chronic active hepatitis. Among patients with steatosis of the liver (48%), 5% were anti-HCV positive by the Abbott test, and none were anti-HCV positive by the UBI assay; 18% had serologic evidence of past HBV infection, and 28% abused alcohol. Among patients without chronic liver disease (13%), no viral infection could be found; 9% were alcoholics. CONCLUSIONS: Chronic liver disease in patients with alpha 1-antitrypsin deficiency is associated with a high prevalence of viral infection; this infection, rather than alpha 1-antitrypsin deficiency alone, may be the cause of the liver disease in such patients.

Adolescent↗
PubMed1992

Successful treatment of recurrent hepatic Candida infection with fluconazole after chemotherapy for acute leukemia: a case report.

Hepatic candidiasis represents an increasingly difficult problem in immunocompromised patients. It has been recognized as a variant of disseminated candidiasis after a period of neutropenia. Establishment of diagnosis is difficult since liver biopsy as well as culture may be negative, in spite of the presence of fungus. Hepatic lesions are generally not detectable by ultrasound examination or computed tomography until the neutrophil count has returned to normal. The aim of this case report is to describe the problems related to the diagnosis and treatment of hepatic candidiasis following chemotherapy for acute leukemia. The report also provides further evidence that fluconazole, a new broad-spectrum antifungal drug, can be safely and effectively used for the long-term treatment of deep-seated hepatic candidiasis.

Adult↗
PubMed1992

Regulation of human T lymphoblast growth by sensory neuropeptides: augmentation of cholecystokinin-induced inhibition of Molt-4 proliferation by somatostatin and vasoactive intestinal peptide in vitro.

The effects on proliferation of Molt-4 lymphoblasts of cholecystokinin (CCK-8), somatostatin-14 (SS), vasoactive intestinal peptide (VIP) and substance P (SP) were investigated using different combinations of the peptides, peptide analogs and their antagonists. In vitro proliferation of the cells was measured by a colorimetric assay for cell growth and survival. Results indicate that SP and SP (3-11) stimulated, whereas CCK-8, VIP and SS inhibited, proliferation in a dose-dependent manner (P < 0.05). Unsulfated CCK-8 had no effect on growth of Molt-4 lymphoblasts, and a specific antagonist of CCK, at a concentration 10(-6) M, diminished the inhibitory effect of CCK-8 on Molt lymphoblasts (P < 0.05). This suggests that the inhibitory action of CCK-8 was mediated by peripheral-type CCK receptors. SS and VIP, at equimolar concentrations of 10(-6) M, significantly augmented the CCK-8-induced inhibition of Molt-4 lymphoblast proliferation. However, none of the inhibiting neuropeptides suppressed stimulation of Molt-4 lymphoblast proliferation in response to SP. These data suggest a role of sensory neuropeptides including CCK in modulating human T lymphoblast proliferation during neuroendocrine interactions with the immune system.

Humans↗
PubMed1992

In vivo activation of circulating monocytes by exogenous growth hormone in man.

Animal studies have shown that administration of growth hormone improves wound healing. Monocyte activation is a prerequisite for optimal repair of damage. In vitro, human recombinant growth hormone was shown to be a potent human monocyte chemoattractant. It induced random migration and chemotaxis at picomolar concentrations of recombinant human growth hormone; combinations of growth hormone with other chemoattractants deactivated the chemotactic response. Other functions of monocytes that are activated by growth hormone include release of superoxide anion and production of cytokines. In order to test activation of human monocytes by growth hormone in vivo, we investigated the effects of recombinant human growth hormone administration on monocyte migration in nine healthy young adults. After a single dose of recombinant human growth hormone (4 IU subcutaneously injected), random migration of circulating monocytes significantly increased, whereas chemotaxis of monocytes that was maximally stimulated with f-Meth-Leu-Phe decreased (p < .05). The alterations paralleled the concomitantly measured plasma levels of growth hormone. After recombinant human growth hormone administration, no changes were seen in plasma levels of proinflammatory cytokines. These in vivo data on monocyte migration are comparable to effects of growth hormone on monocyte migration in vitro and strongly suggest that recombinant human growth hormone can activate circulating monocytes in man.

Adult↗
PubMed1992

Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with rheumatic diseases.

The neuroendocrine polypeptide hormone beta-endorphin (beta-END), which is released from various tissues including the anterior pituitary gland and cells of the immune system, has recently been implicated as having an immunoregulatory role. We used a radioimmunoassay to measure beta-END levels in circulating mononuclear leucocytes from normal subjects and patients with various rheumatic diseases. Levels of beta-END in leucocytes from patients were lower than in leucocytes from healthy subjects (P less than 0.001). Whereas levels of beta-END in leucocytes from patients with the various rheumatic disorders were not significantly different, an inverse correlation was found between beta-END levels in leucocytes and expression of rheumatoid factor (P less than 0.025) and erythrocyte sedimentation rate (P less than 0.025). This study demonstrates decreased content of beta-END in cells of the immune system related to parameters of inflammatory activity in rheumatic diseases.

Blood Sedimentation↗
PubMed1992

Priming of polymorphonuclear neutrophils by atrial natriuretic peptide in vitro.

In ischemia-reflow states of coronary artery disease, the activation of PMN precedes the initiation of tissue damage. Release of atrial natriuretic peptide (ANP) from myocytes occurs within minutes after the onset of myocardial ischemia, which suggests a possible role of ANP in PMN activation. To investigate this possibility, we tested the effects of ANP on functions of PMN in vitro. ANP is a potent signal for priming the PMN respiration burst to secrete superoxide anion. Phorbol 12-myristate 13-acetate, opsonized zymosan, or FMLP could all be used as triggering stimuli to demonstrate the priming of PMN activation by ANP. Only ANP fragments 1-28 and 7-28 enhanced respiration burst activity but identical preparations of ANP fragments 13-18 or 1-11 failed to do so. This structure-activity relationship is typical of receptors for ANP found in other tissues. In addition, ANP stimulated the release of beta-glucuronidase From PMN triggered by FMLP. The observed inhibition by ANP of FMLP-stimulated chemotaxis of PMN may be due to their enhanced adhesiveness. These data show that a classic cardiac hormone is involved in regulating important functional activities of PMN. These data support the possibility that ANP could act as a preinflammatory substance in ischemia-reperfusion states and myocardial necrosis.

Atrial Natriuretic Factor↗
PubMed1992

[Snuff aspiration as a cause of recurrent pulmonary infiltrations in a 60-year-old patient with chronic renal failure].

Pulmonary infiltrations associated with renal failure demand several diagnostic procedures to exclude autoimmune disorders affecting both organ systems or to find an infectious cause of the disease. We report the case of a 60 year-old man with chronic renal failure and recurring pulmonary infiltrations. On admission to hospital all diagnostic parameters for systemic vasculitis, infectious or neoplastic disease were negative, including the histological report on transbronchial biopsies. Eventually, follow-up biopsies taken 3 months later showed vegetable fibres and necrosis due to intensive snuff abuse during the previous months. After the patient stopped taking snuff the pulmonary infiltrations improved quickly. Uraemic neuropathy, which may have facilitated aspiration, as well as the reduced pulmonary and systemic defence mechanisms due to chronic renal failure probably contributed to a considerable degree to the development of pulmonary infiltration.

Biopsy↗
PubMed1991

Priming of normal human neutrophils by tachykinins: tuftsin-like inhibition of in vitro chemotaxis stimulated by formylpeptide or interleukin-8.

Tachykinins have priming effects on polymorphonuclear neutrophils, since they may activate the neutrophils to exhibit an exaggerated inflammatory response to phlogistic mediators. In order to investigate mechanisms involved in this action, we determined the influence of substance P and neurokinin A on chemotaxis of human neutrophils towards gradients of formymethionyl-leucyl-phenylalanine or recombinant human interleukin-8. As seen with other neutrophil-priming agents such as tumor necrosis factor-alpha, exposure of neutrophils to substance P or neurokinin A had an inhibitory effect upon a stimulated migration, with effective concentrations being in the nanomolar range. Tuftsin, a known neutrophil activating peptide, similarly inhibited stimulated migration. Analysis of structure-activity relationships revealed that activity of tachykinins is located in amino-terminal, tuftsin-like sequences. The inhibition of stimulated migration was partly reversed by (Pro1)-tuftsin, a partial tuftsin receptor antagonist, which suggests that the effects of amino-terminal tachykinins involves activation of tuftsin receptors of neutrophils.

Amino Acid Sequence↗
PubMed1991

Inhibitory effect of 2-chlorodeoxyadenosine on granulocytic, erythroid, and T-lymphocytic colony growth.

Previous studies have shown that 2-chloro-2'-deoxyadenosine (CdA) is markedly toxic to normal and malignant human lymphocytes in vitro and in vivo. Recent clinical trials have shown that CdA is a very promising drug for the treatment of lymphoid malignancies. The present investigations were designed to test the effect of CdA on the in vitro clonal growth of both myeloid progenitors and T-lymphocyte colony-forming cells (CFU-TL) obtained from normal human bone marrow and peripheral blood. Cells were exposed to CdA in doses up to 1280 nmol/L. To reduce indirect effects of CdA mediated by accessory cells, monocyte- and T-lymphocyte-depleted bone marrow cells were used for our investigations. The results show a marked inhibition of myeloid progenitor and lymphocyte colony-forming cells in a dose-dependent manner, correlating with maturation stage in that the immature progenitor cells are more sensitive to this drug. Furthermore, our studies suggest that a sequence of metabolic events previously described for lymphocytes may be operative in myeloid progenitor cells because a minimal exposure time of 48 hours is required to obtain a marked inhibition. CdA toxicity was proposed to be linked with phosphorylation by deoxycytidine-kinase (E.C. 2.7.1.74), the levels of which have been found to be high in lymphocytes, but low in granulocytes. However, the marked inhibition of myeloid progenitor cells shown in these studies suggests that other factors such as modulation of the effect of CdA by the ambient levels of other deoxynucleosides might influence the apparent sensitivity of myeloid cells.

2-Chloroadenosine↗
PubMed1991

Long-term effect of intensified insulin treatment on lipid parameters in diabetes mellitus type I.

Premature atherosclerosis is often found in patients with diabetes mellitus (DM) type I, and alterations in lipid metabolism seem to play an important role in the development of this complication. Intensified insulin therapy improves glycemic control parameters significantly. To evaluate the effect of this optimized insulin treatment (OIT) not only on glycemic control, but also on plasma lipids, 24 patients with DM type I (19 men and 5 women, 18 to 61 years) were switched from a standard insulin therapy to a regimen of OIT which has been maintained for more than 3 years now. After 2 years on OIT a reduction of HbA1c values from 8.1% to 7.5% (p less than 0.01) was accompanied by an increase in HDL cholesterol from 52 to 67 mg/dl (p less than 0.05) and a decrease of triglyceride levels from 319 to 67 mg/dl (p less than 0.001). At the end of the second year on OIT some of the patients exhibited a reversal of the favorable trend in HbA1c and lipid values. Intensified instructions regarding the implementation of OIT were therefore repeated and resulted in a renewed improvement of overall HbA1c, HDL cholesterol and triglyceride levels to 6.43%, 67 mg/dl, and 78 mg/dl, respectively. Our findings underline the value of OIT not only for glycemic control, but also for the control of plasma lipids considered to be major risk factors for coronary artery disease.

Adolescent↗
PubMed1991

[An idiopathic floating left-ventricular thrombus].

Four weeks after appendicectomy a 28-year-old man developed dragging pains in the left calf. Left popliteal, posterior tibial and dorsalis pedis arteries could not be palpated. Angiography revealed an embolic occlusion of the left superior femoral artery at the level of the adductor canal. Echocardiography demonstrated a pedunculated left ventricular thrombus, 3.5 x 2.0 cm, as a possible source of the embolus. After successful trifurcation embolectomy and saphenous vein patch-plasty acenocoumarol, 4 mg/d and heparin, 3 x 7500 IU/d were administered. Because the thrombus failed to shrink, systemic thrombolysis, initially 750,000 IU streptokinase and 3000 IU heparin i.v., was begun. After five days the thrombus diameter had decreased to 0.7 cm. But because thrombus movement had increased, streptokinase was replaced by 70 IU/d ancrod i.v. The thrombus completely disappeared within two weeks. The patient was symptom-free during the period of anticoagulation with acenocoumarol. Six months later echocardiography confirmed the absence of thrombus in the left ventricle.

Acenocoumarol↗
PubMed1991

Suppression of thyroid function by interferon-alpha 2 in man.

Profound biological changes occur in patients treated with interferon. Observations of endocrine changes prompted us to examine the effects of subcutaneous alpha-interferon administration in single doses on circulating levels of thyroid stimulating hormone, total thyroxine, and total triiodothyronine in 10 volunteers (5 healthy subjects and 5 patients with hepatitis C). Blood samples were taken on an out-patient basis immediately before and 2, 12, 24, 48, and 72 h after administration of 1, 3, or 5 x 10(6) units of recombinant alpha-interferon. Application of the different dose levels was randomly assigned. Plasma samples were stored at -80 degrees C; after collection of samples had been completed hormone levels were measured using commercially available test kits. At all time points before and after injection of alpha-interferon, standard deviations of measured hormone levels of healthy control subjects and patients overlapped to a considerable extent. At a dose level of 5 x 10(6) units, alpha-interferon significantly increased cortisol levels as described, and decreased the level of thyroid stimulating hormone in the group receiving alpha-interferon as compared to placebo-treated healthy volunteers. The effects occurred 12 h after injection. Maximum suppression of thyroid stimulating hormone levels was observed 24 h after injection, when serum levels of thyroxine and triiodothyronine also were significantly reduced. We conclude that subcutaneous alpha-interferon treatment with doses as low as 5 x 10(6) units affects the control of thyroid function.

Adult↗
PubMed1991

In vitro activation of neutrophils of the aged by recombinant human growth hormone.

Several functions of polymorphonuclear neutrophils (PMNL) have been found to be altered in the aged. As the neuroendocrine network, in particular growth hormone (GH), may interfere with the regulation of nonspecific host defense mechanisms, a recently described PMNL-priming activity of recombinant human (rH) GH in vitro was investigated. Oxidative metabolism of PMNL from young and old subjects was studied by measuring reduction of nitroblue tetrazolium (NBT) or cytochrome c. In the absence of stimulating agents, PMNL from old subjects reduced NBT to a significantly lesser extent than did PMNL from young subjects. Addition of rHGH to PMNL from old subjects reversed the suppressed spontaneous oxidative metabolism. No differences between young and old were observed for the increase of stimulated oxidative metabolism. The results suggest that altered PMNL function in the aged may be reversed by rHGH and that the ability of PMNL to respond to rHGH does not decline with age.

Adult↗
PubMed1991

Priming of normal human neutrophils by recombinant human growth hormone.

Growth hormone (GH) plays an important role in the development, maintenance and function of the immune system. Previous data has demonstrated that GH is also a newly defined macrophage-activating factor. Activation of polymorphonuclear neutrophils (PMN) by GH has not yet been examined. This paper presents studies demonstrating the effects of GH on the migratory behaviour and respiratory burst of PMN. In a modified Boyden chamber chemotaxis assay, GH did not stimulate PMN locomotion when added directly to the cells but potently inhibited formylpeptide-stimulated chemotaxis with effective concentrations in the picomolar range. The migration inhibition observed is known from studies on PMN priming-factors to be due to enhanced adhesiveness of PMN to artificial surfaces such as nitrocellulose, suggesting that GH stimulates PMN adhesiveness. Priming of PMN by GH was confirmed by direct demonstration of a stimulatory effect on reduction of nitroblue tetrazolium. These findings suggest that GH may be involved in the regulation of PMN functions.

Cell Adhesion↗