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Biomedical subjects

T Sauerbruch

Publications and source records attributed to T Sauerbruch.

At least 199 records · Page 11Linked to original sources
PubMed1997

[The Churg-Strauss syndrome with cerebral seizures and terminal kidney failure].

HISTORY AND CLINICAL FINDINGS: A 67-year-old man with known bronchial asthma was admitted to hospital because of deteriorating general state of health, fever, progressive renal failure and confusional states. INVESTIGATIONS: Erythrocyte sedimentation rate was 70/95 mm and the concentration of C-reactive protein raised to 30 mg/dl. WBC count was 19,000/microliter with 39% eosinophilia. Anticytoplasmatic antibodies (cANCA) had a high titre (1:160). On admission the creatinine level was 5.6 mg/dl. Renal biopsy indicated marked glomerular and tubulo-interstitial scarring. Chest radiograms showed transient pulmonary infiltrates. Churg-Strauss syndrome (CSS) was diagnosed on the basis of the clinical and biochemical findings. TREATMENT AND COURSE: Haemodialysis was instituted to counteract the renal failure with water retention. Inflammatory parameters and clinical symptoms rapidly responded to administration of corticosteroids (prednisolone, initially 250 mg/d for 3 days, then 150 mg/d for 5 days followed by slowly decreasing doses). Two weeks after starting prednisolone he had secondary generalised seizures. Magnetic resonance imaging (MRI) of the skull demonstrated marked hyperintense focal changes which in their pattern were characteristic of cerebral vasculitis. As a steroid-refractory condition had to be assumed, cyclophosphamide was also given (100 mg/d). Within 6 weeks the clinical symptoms gradually regressed and the MRI changes became practically normal. CONCLUSION: Early combined immunotherapy should be given if CSS runs a complicated course, rather than the usually recommended corticosteroid monotherapy.

Aged↗
PubMed1997

[Symptoms, tumor stage and primary treatment in patients with colorectal carcinoma].

OBJECTIVE: To obtain population-related data, previously not available for Germany, regarding primary symptoms, diagnosis and treatment of patients with colorectal carcinoma. PATIENTS AND METHODS: During 1994, in the catchment area of Bonn (town of Bonn, districts of Euskirchen and Rhein-Sieg), there were 354 cases of newly diagnosed colorectal carcinoma. For all of them initial symptoms, primary diagnosis, cancer stage at time of diagnosis as well as surgical and conservative treatment were prospectively documented. By comparing entries from all relevant hospitals and doctors with those of the pathology institutes of the region, data of about 98% of all these patients were recorded. RESULTS: The average age of the patients was older (median of 69 for men, 72 for women) with more far metastases than in comparable groups reported by German university surgical departments. Only 4.6% of the group had occult blood in the stool as the only symptom. Most of the patients had local or regional metastases (T3-4: 63.9%; N1-3: 41%, respectively). Operations intended to be curative were possible in only 65.9% of the cohort. Adjuvant radiotherapy and/or chemotherapy was given to 11.7%, using current consensus recommendations.

Adenocarcinoma↗
PubMed1997

The low-dose monoethylglycinexylidide test: assessment of liver function with fewer side effects.

The hepatic metabolism of lidocaine (1 mg/kg intravenously) to its metabolite monoethylglycinexylidide (MEG-X) is the basis of the standard MEG-X test. To reduce the lidocaine-induced side effects, we evaluated the MEG-X formation after 0.5 and 1 mg/kg lidocaine intravenously in subjects with normal (n = 5) and severely impaired liver function (n = 7) (study I). From this study, a low-dose test (MEG-X concentration 30 minutes after 50 mg lidocaine intravenously [MEG-X30min] normalized to standard MEG-X test results) was developed. Sensory side effects from this low dose and from the standard MEG-X test were compared in a double-blind, randomized, cross-over study (study II) comprising 15 individuals with normal liver function and 45 patients with cirrhosis (15 Child A, 15 Child B, and 15 Child C). In study I, MEG-X formation rate was dose-independent in patients with severely impaired liver function. In study II, normalized MEG-X test results (ranging from < or = 4 to 120 microg/L) were virtually identical to the standard test results (mean difference: -1.9 microg/L; 95% confidence interval [CI]: -5.3; 1.5 microg/L). Fewer individuals experienced side effects (30% vs. 53%) with the low-dose test (P = .0013). In a multivariate analysis, the Child-Pugh score was inversely related to the occurrence of side effects. The low-dose MEG-X test gives almost identical results to the standard MEG-X test and is associated with fewer side effects, which occur less often in individuals with more severely compromised liver function.

Adult↗
PubMed1997

Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis.

To investigate the role of nitric oxide (NO) with respect to kidney function and liver cirrhosis, we evaluated renal function, as well as cyclic guanosine monophosphate (cGMP) and NOx (nitrite/nitrate [NO3-/NO2-]) as indirect markers of NO formation in plasma and urine at rest and during amino acid (aa)-induced glomerular hyperfiltration in patients with Child A liver cirrhosis and portal hypertension (n = 12), and in healthy controls (n = 10). Baseline filtration rate (GFR) and effective renal plasma flow (ERPF) were significantly lower in patients with cirrhosis than in controls (GFR: mean 88 +/- SD 16 mL/min vs. 106 +/- 15 mL/min, P = .01, ERPF: 477 +/- 93 vs. 561 +/- 72 mL/min, P = .002). In both groups amino acid (aa) infusion increased GFR, ERPF, as well as cGMP and urinary NOx. Changes in GFR were similar in cirrhotic patients and controls (28.3% +/- 14% in cirrhotics and 26% +/- 11% in controls), but the degree of aa-induced changes in ERPF was more marked in patients with liver cirrhosis (31.8% +/- 17% vs. 18.6% +/- 12%, P = .02). Plasma levels of NOx and cGMP were similar in either group at baseline and during aa infusion, whereas NOx and cGMP excretion in cirrhotics was constantly 14% to 24% lower than in the control group. We conclude that patients with compensated liver cirrhosis and portal hypertension already have an impaired kidney function. In addition our data suggest a cirrhosis-related dissociation between ERPF and GFR during aa stimulation. Further studies are warranted to find out whether a local imbalance between vasoconstrictors and vasodilators, e.g., decreased local NO formation, plays a key role for this phenomenon.

Adult↗
PubMed1997

Effect of cytochrome P450 induction on phosphorus metabolites and proton relaxation times measured by in vivo 31P-magnetic resonance spectroscopy and 1H-magnetic resonance relaxometry in human liver.

Experimental and clinical studies have led to the hypothesis that the phosphodiester signal obtained by 31P magnetic resonance (MR) spectroscopy may be a specific marker for the hepatic induction of oxidative metabolism (P450 induction) by phenobarbitone or ethanol. Systematic studies in humans are lacking. Therefore, we studied 10 volunteers who received rifampin (600 mg/d) for 6 days, resulting in a documented induction of oxidative metabolism as measured by an increase in urinary 6-beta-hydroxycortisol output in all volunteers (P = .0004). 31P-MR spectroscopy and 1H-MR relaxometry were performed before and after hepatic P450 induction. As shown by 31P-MR spectroscopy, the median phosphomonoester concentration (PME) relative to nucleoside triphosphate (NTP) increased by 21% from 0.63 (range, 0.40-0.89) before induction to 0.76 (0.49-1.67) after induction (P = .0451). The median level of phosphodiesters (PDE) relative to NTP increased by 28% from 4.82 (3.41-6.67) before induction to 6.18 (4.63-11.63) after induction (P = .0091). An increase in the level of inorganic phosphates (Pi) relative to NTP was observed, but changes were not significant. As shown by 1H-MR relaxometry, a nonsignificant trend of the liver parenchyma to shorter relaxation times was observed after P-450 induction. In conclusion, both PME/NTP and PDE/NTP ratios (measured by in vivo 31P-MR spectroscopy) increased significantly after hepatic induction with rifampin. Further clinical studies with 31P-MR spectroscopy must take into account the potential effects of P450-inducing agents.

Adult↗
PubMed1997

Serum selenium versus lymphocyte subsets and markers of disease progression and inflammatory response in human immunodeficiency virus-1 infection.

Serum selenium levels were determined cross-sectionally in 57 HIV-infected patients who were classified according to the Centers for Disease Control (CDC) 1993 classification system. Mean serum selenium levels were lower in CDC stage II (58.7 +/- 12.2 micrograms/L; p < 0.01; n = 18) and stage III (47.6 +/- 11.3 micrograms/L; p < 0.01; n = 19) HIV-infected patients, than in healthy subjects (80.6 +/- 9.6 micrograms/L; n = 48) and stage I patients (73.6 +/- 16.5 micrograms/L; n = 20). Serum selenium levels were positively correlated with CD4 count, CD4/8 ratio, hematocrit, and serum albumin (r = 0.42; r = 0.39; r = 0.48; and r = 0.45; p < 0.01, respectively) and inversely with serum levels of thymidine kinase (r = -0.49; p < 0.01; n = 49) and beta 2-microglobulin (r = -0.46; p < 0.001; n = 49). In addition, serum selenium levels in 20 randomly selected AIDS-free individuals (CDC I: n = 10; CDC II: n = 10) were inversely correlated with serum concentrations of interleukin-8 (IL-8) and soluble tumor necrosis factor receptors (sTNFR) types I and II. There was no correlation with serum immuneglobulin A and total serum protein levels. The results show that the progressive deprivation of serum selenium in HIV-infection is associated with loss of CD(4+)-cells and with increased levels of markers of disease progression and inflammatory response.

Adult↗
PubMed1997

Anomalous expression of costimulatory molecules B7-1, B7-2 and CD28 in primary biliary cirrhosis.

BACKGROUND: T lymphocytes require two important signals for efficient activation: 1) recognition of antigens bound to self major histocompatibility complex antigens, and 2) simultaneous stimulation via so-called costimulatory molecules. Interaction of the costimulatory B7 molecules on antigen presenting cells with CD28 on T lymphocytes appears to be particularly important, as it modifies secretion of cytokines, especially interleukin 2. In primary biliary cirrhosis biliary epithelial cells aberrantly express major histocompatibility complex class II antigens and may function as antigen presenting cells. METHODS: We studied expression of HLA-DR, B7-1, B7-2 and CD28 on cryostat liver sections in 16 patients with primary biliary cirrhosis, three patients each with autoimmune hepatitis and primary sclerosing cholangitis and nine patients with chronic viral hepatitis (five hepatitis B, four hepatitis C) using mouse monoclonal antibodies in an indirect immunoperoxidase technique. RESULTS: In advanced primary biliary cirrhosis, HLA-DR was found on 57% of bile ducts, B7-2 on 5% of bile ducts, and B7-1 could not be detected on any bile duct. Neither B7-1 nor B7-2 was seen on bile ducts in the four patients with early primary biliary cirrhosis. HLA-DR+ bile ducts also lacked expression of B7 molecules in autoimmune hepatitis. In contrast, HLA-DR, B7-1 and B7-2 were expressed simultaneously on professional antigen presenting cells such as macrophages in epitheloid granulomas. CONCLUSION: HLA-DR+ biliary epithelial cells in primary biliary cirrhosis insufficiently co-express B7-1 or B7-2 molecules. Therefore, they must either use different costimulatory molecules, or otherwise are deficient in lymphocyte activation. Since recognition of antigen in the absence of B7-CD28 interaction may lead to anergy of lymphocytes, this might contribute to the impaired cytokine secretion found in primary biliary cirrhosis.

Antigens, CD↗
PubMed1997

Cholestasis associated with mesalazine therapy in a patient with Crohn's disease.

BACKGROUND/AIMS: Mesalazine is a widely prescribed medication, developed as an alternative to sulfasalazine in the treatment of inflammatory bowel disease. In contrast to sulfasalazine, there are only a few case reports on its causing hepatic injury. We here report on a patient with cholestasis after mesalazine therapy for Crohn's disease of the ileum. METHODS/RESULTS: The patient, a 30-year-old man, developed clinical signs of severe hepatic injury 4 months after treatment with mesalazine (4 g/day) including biopsy-proven hepatocellular cholestasis with minimal focal mononuclear inflammatory infiltration. Contrary to previous reports, no symptoms of generalized hypersensitivity were seen. The patient's illness was resolved by discontinuing the mesalazine treatment and he recovered completely in 40 days. CONCLUSIONS: This case reinforces the possibility of a causal relationship between mesalazine treatment and toxic hepatic injury without systemic hypersensitivity.

Adult↗
PubMed1997

Semiquantitation of intrahepatic MDR3 mRNA levels by reverse transcription/competitive polymerase chain reaction.

BACKGROUND/AIMS: Knockout mice lacking mdr2, the murine analogue of human MDR3 P-glycoprotein, develop chronic non-suppurative cholangitis. Recently, a deficiency in MDR3 messenger RNA (mRNA) has been reported in a subtype of progressive familial intrahepatic cholestasis. Thus, reduced MDR3 gene expression could be involved in human cholestatic liver diseases. METHODS: We developed a sensitive and specific reverse transcription/competitive polymerase chain reaction for the semiquantitation of intrahepatic MDR3 mRNA levels. Using this method we determined the MDR3 mRNA levels in 52 liver specimens from primary biliary cirrhosis (n=11), chronic hepatitis B (n=5), chronic hepatitis C (n=14), non-cholestatic cirrhosis (n=9) and controls (n=13). RESULTS: MDR3 mRNA was detected in all specimens with some variation in mRNA levels. No significant differences in the mean MDR3 mRNA levels were present between the groups studied, including normal controls. CONCLUSIONS: We found no evidence for deficient or severely reduced intrahepatic MDR3 mRNA in primary biliary cirrhosis, nor were mRNA levels altered significantly by virus-induced inflammation or by cirrhosis. The reverse transcription/competitive polymerase chain reaction assay described here should be a useful tool in the semiquantitative study of MDR3 mRNA levels in small tissue specimens.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1997

Serum selenium, plasma glutathione (GSH) and erythrocyte glutathione peroxidase (GSH-Px)-levels in asymptomatic versus symptomatic human immunodeficiency virus-1 (HIV-1)-infection.

OBJECTIVES: Antioxidant defense status was investigated in HIV-infected patients by measuring serum selenium, erythrocyte glutathione peroxidase (GSH-Px) activity, plasma thiol (-SH) and glutathione (GSH) concentrations along with the assessment of the clinical stage and surrogate markers of HIV-disease. DESIGN, SETTING AND SUBJECTS: Serum selenium levels were determined cross-sectionally in 104 sequentially selected HIV-infected patients (83 outpatients and 21 patients with ongoing AIDS defining events). The patients were classified into three stages of the disease, I, II and III according to the 1993 Centers For Disease Control (CDC) classification system for HIV-infection. GSH-Px activities, plasma SH and plasma GSH concentrations were determined in a subset of 24 patients at stage I and 12 patients at stage III with an active AIDS-defining disease. RESULTS: Mean serum selenium levels were lower in CDC stage II (68.7 +/- 20.9 micrograms/l; P < 0.01; n = 34) and stage III (51.4 +/- 14.7 micrograms/l; P < 0.01; n = 37) HIV-infected patients than in healthy subjects (89.2 +/- 20.9 micrograms/l; n = 72) and stage I patients (82.3 +/- 20.5; microgram/l; n = 33). Serum selenium levels were positively correlated with CD4-count (r = 0.42; P < 0.001; n = 104) and inversely with levels of soluble tumor necrosis factor receptors type II (r = -0.58; P < 0.01; n = 35), neopterin (r = -0.5; P < 0.001; n = 80) and beta 2-microglobulin (r = -0.4; P < 0.001; n = 94). Hepatitis C virus (HCV) and HIV-coinfected patients at CDC stages I and II showed markedly lower selenium concentrations compared to HIV-infected patients without concomitant HCV-infection. Serum selenium and GSH-Px activity in hospitalized AIDS patients was significantly lower as compared to asymptomatic patients and healthy subjects, whereas plasma SH and GSH concentrations were lower in both, asymptomatic -and AIDS-patients, than in the controls. CONCLUSION: The results show that stages I-III of HIV-disease are characterized by significant impairments of antioxidative defenses provided by selenium, GSH-Px, SH-groups and GSH.

Adult↗
PubMed1997

Effect of oral pancreatic enzyme administration on digestive function in healthy subjects: comparison between two enzyme preparations.

BACKGROUND: Intraduodenal proteases exert a negative feedback on pancreatic secretion. AIM: To investigate the effect of two pancreatic enzyme preparations (enteric-coated tablets, and capsules with enteric-coated microtablets) on postprandial pancreatic and bile acid secretion, gastroduodenal motility and release of gastrin and pancreatic polypeptide in healthy humans. METHODS: Twenty healthy males were studied on two different days one week apart. After an overnight fast a nine-lumen motility tube was positioned with the distal tip at the Treitz angle. On each study day, 30 min after an interdigestive migrating motor complex-phase III, a semi-liquid test meal was given either alone (n = 20) or with enzymes (3 tablets (n = 10) or 2 capsules with microtablets (n = 10); 40,000 U lipase and 2000 proteases) in a randomized order, and the study continued over 2 h. Motility was continuously recorded with four ports in the antrum and three in the duodenum, using a low-compliance pneumohydraulic perfusion system. Secretion of human-specific pancreatic elastase and bile acids was measured by a standard duodenal intubation perfusion technique. Plasma concentrations of gastrin and pancreatic polypeptide were measured by specific radioimmunoassays. RESULTS: Postprandial pancreatic secretion was significantly reduced by administration of microtablets (median 82 mg/2 h vs. 70 mg/2 h, P < 0.02) but not by tablets (median 59 mg/2 h vs. 58 mg/2 h. N.S.). No changes were observed in bile acid secretion, antroduodenal motility or release of gastrin and pancreatic polypeptide. CONCLUSIONS: Oral administration of pancreatic enzymes at normal therapeutic doses significantly inhibits postprandial pancreatic secretion in healthy humans, when capsules with enteric-coated microtablets are given. Exogenous pancreatic enzymes have no significant effect on bile acid secretion, gastroduodenal motility and hormone release.

Administration, Oral↗
PubMed1997

Inadequate erythropoietin response to anaemia in HIV patients: relationship to serum levels of tumour necrosis factor-alpha, interleukin-6 and their soluble receptors.

Severe anaemia is a frequent complication in advanced HIV infection. In our study we investigated the interaction between cytokine network, HIV infection and erythropoietin (Epo) response with increasing anaemia levels. No correlations could be established between circulating tumour necrosis factor (TNF)-alpha and any of the examined parameters. However, a negative correlation was found between haemoglobin values and soluble TNF receptor levels (sTNF-R-I: r = -0.54; P < 0.001; sTNF-R II: r = -0.47; P < 0.001) as well as interleukin-6 levels (r = -0.29; P < 0.01). In contrast, no significant increase in log[Epo], counterbalancing haemoglobin decline and paralleling the rise in sTNF receptors, was found. In patients classified as stage III, according to the Centers for Disease Control (CDC) classification, the erythropoietin response was significantly more impaired than in patients from CDC groups I and II (P < 0.01). The results of this study suggest that similar to its action in vitro, activation of the TNF/TNF-R system may impair erythropoietin production in HIV-associated anaemia. Due to the brief half-life of TNF-alpha, this activation is particularly reflected by elevations of soluble TNF receptor levels.

Adult↗