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Biomedical subjects

N Teich

Publications and source records attributed to N Teich.

At least 19 recordsLinked to original sources
PubMed2006

[A 32-year-old patient with diarrhoea and acute kidney failure].

A 32-year-old male patient presented in the emergency department of our hospital with acute vomiting and diarrhoea. He reported occasional non-severe diarrhoea over several years in the past. Furthermore, at the time of presentation the patient had had anuria for several days. A prerenal and postrenal origin of the renal failure was excluded. A renal biopsy was performed and histopathological examination displayed findings consistent with a haemolytic-uraemic syndrome but no signs of glomerulonephritis. MRI examination of the small bowel revealed inflammatory alterations typical for Crohn's disease, even without histological verification. We describe haemolytic-waemic syndrome as manifestation of Crohn's disease for the first time.

Acute Kidney Injury↗
PubMed2006

[Invasive and non-invasive diagnostic methods for evaluation of hypovolemia in acute pancreatitis].

Severe acute pancreatitis leads to a dramatic fluid loss in the intraperitoneal space which may result in circulatory decompensation. Sequestration of fluid can amount up to 40 percent of the circulating blood volume. The amount of fluid and electrolyte replacement is often misjudged leading to a higher rate of complications and a higher mortality rate of the disease. Furthermore, subsequent and adequate fluid resuscitation seems to influence the prognostic course of the disease by improving the perfusion and oxygenation of the pancreas. Otherwise volume overload may cause cardiopulmonary decompensation in the case of synchronous cardiopulmonary comorbidities. Therefore, an important part of treatment relies on careful haemodynamic monitoring, if necessary managed in an intensive care unit. Usually most patients with acute pancreatitis will be treated on a non-intensive medical ward which allows a differentiated and continuous haemodynamic monitoring only to a limited extent. Apart from monitoring circulatory parameters and measuring central venous pressure, there are other clinical methods, laboratory tests and radiological diagnostic procedures to determine the amount of intravascular fluid deficit and the individual volume demand of patients with acute pancreatitis. Prospective clinical trials for evaluation of pancreatitis-specific volume management do not exist so far. The aim of this review is to provide background information on invasive and non-invasive diagnostic methods for detection of circulatory hypovolemia in acute pancreatitis.

Blood Volume↗
PubMed2005

[Resuscitation by laypersons: lack of knowledge of first-aid measures in Germany].

BACKGROUND AND OBJECTIVE: Sudden cardiac death is a leading cause of death. In Germany, only 10% of patients will survive reanimation. The prognosis is mainly determined by the first-aid skills of accidental witnesses. METHODS: The reaction of 1007 German-speaking adults (462 males, 545 females, median age 39 years) was investigated in an emergency scenario with symptoms of sudden cardiac death in an acquaintance. Afterwards a self-assessment of their first-aid skills, such as cardiac compression and mouth-to-mouth ventilation was made. RESULTS: 94% of the interviewees would call professional aid at once. Diagnostic skills, as searching for pulse or checking for breath would be done by 26 and 21%, respectively. The most frequently mentioned therapeutic skill was positioning the victim in stable lateral position (37%), but very less frequently cardiac compression (6%) and mouth-to-mouth resuscitation (10%). When asked, 51 (81%) of those interviewed regarded their skills in cardiac compression and mouth-to-mouth resuscitation as adequate. To some extent there were differences in favor of young people and those from East Germany. CONCLUSION: These representative data suggest that (a) ABC-like first-aid rules are largely unknown among the population; (b) the value of a stable lateral position is overestimated and (c) first-aid skills of elderly persons are worst. A significant improvement of first-aid skills of the German population is mandatory in order to improve in future the outcome of sudden cardiac death.

Adolescent↗
PubMed2005

[Clinical implications of genetic risk factors of chronic pancreatitis].

The identification of a specific mutation in the human cationic trypsinogen gene in large kindreds with hereditary pancreatitis was the key to understand the genetic background of chronic pancreatitis. Rapidly, other variants within the same gene were identified-even in small families with a minority of patients. Later, mutations of the most important intrapancreatic trypsin inhibitor SPINK1 were found with high prevalence in patients with idiopathic, tropical and alcoholic chronic pancreatitis. We summarize interesting genetic and biochemical findings, point to clinical features and review recommendations for genetic analysis, follow-up and cancer prevention.

Carrier Proteins↗
PubMed2004

Endoluminal gastroplication: what are the predictors of outcome?

BACKGROUND: Endoluminal gastroplication (EndoCinch) has emerged as an endoscopic anti-reflux therapy, but predictive factors for symptom relief have not been established. The aim of this study was to evaluate the major determinants to predict outcome in patients treated with EndoCinch. METHODS: A total of 53 consecutive patients, treated with EndoCinch at a single center were included in this prospective study. Inclusion criteria were symptoms of chronic heartburn, dependency on proton-pump inhibitors, documented pathological esophageal acid exposure, and a hiatal hernia smaller than 3 cm in length. All patients underwent endoscopy, 24-h pH monitoring, esophageal manometry, barium esophagram, and a detailed questionnaire regarding their symptoms before treatment. Patients were stratified into a responder and a non-responder group using a questionnaire at 3-month follow-up. A multivariate analysis was performed. RESULTS: The success rate was 64% (34/53 patients). Three variables weresignificantly predictive for successful endoscopic anti-reflux treatment at the multivariate level: presence of typical symptoms (P=0.01), complete symptom relief with acid suppressive therapy (P=0.01), and normal lower esophageal sphincter pressure (P = 0.04). Not predictive of outcome were age, body mass index, esophagitis, other manometric findings, hiatal hernia size, or pathological level of pH <4/24 h. Barium esophagram did not add any additional predictive information. CONCLUSIONS: Since no single factor can predict outcome after EndoCinch, a careful patient selection is mandatory to maximize the success rate. The ideal candidate for EndoCinch is a gastroesophageal (GERD) patient with a normal lower esophageal sphincter pressure, whose typical symptoms completely resolved with acid suppressive therapy.

Adult↗
PubMed2003

[Sporadic acute hepatitis E in Germany: an underdiagnosed phenomenon?].

Hepatitis E virus infection is the leading cause of enterically transmitted hepatitis worldwide. Case reports of hepatitis E in individuals in Germany so far related to travel to endemic areas. A 33-year-old man presented with painless jaundice. By serology and liver biopsy, no cause of hepatitis could be identified. After discharge transaminases were persistently elevated. Serology (IgG and IgM) confirmed acute hepatitis E. The transaminases declined to normal values within six months. Detailed anamnestic questioning revealed no travel to an endemic region or contact with individuals who had visited such areas. In addition to our patient, a total of 34 cases of acute hepatitis E were reported to the Robert-Koch-Institute (German center of disease control) in 2001. In five of them, the disease had obviously been acquired in Germany. These data indicate that community acquired hepatitis E virus infection may occur sporadically in Germany and should be considered as a cause of seronegative (non-A-non-B-non-C) hepatitis.

Acute Disease↗
PubMed2002

Relevance of variants in serum antiproteinases for the course of chronic pancreatitis.

BACKGROUND: Mutations of the pancreatic serine protease inhibitor, Kazal type 1 (SPINK1), the cationic trypsinogen (PRSS1) and the cystic fibrosis transmembrane conductance regulator (CFTR) were reported to be genetic risk factors of chronic pancreatitis (CP). The aim of this study was to determine the role of genetic variants of the main serum antiproteinases alpha-1-antitrypsin (AAT) and alpha-2-macroglobulin (A2M) for the course of chronic pancreatitis. METHODS: 124 patients with non-alcoholic chronic pancreatitis (with PRSS1 or SPINK1 mutations or idiopathic pancreatitis) and 64 healthy controls were investigated for the AAT mutations PiS and PiZ, and the PiM determining variants R101H, V213A, E376D. In 101 subjects, the 'bait region' of A2M was sequenced. A pentanucleotide deletion in the bait region of A2M was analysed in 147 chronic pancreatitis (CP) patients and 87 controls. RESULTS: The lowest prevalences of V213A and E376D were found in PRSS1 patients, whereas an increased rate of these mutations was present in the SPINK1 group, and the highest prevalence was found in patients with idiopathic pancreatitis. The prevalence of PiM variants was higher in patients with early onset CP than in late onset (P < 0.05 for E376D). The coding region of the bait region of A2M was of wild type in all investigated subjects. The A2M pentanucleotide deletion showed a homogenous distribution in patients and controls. CONCLUSIONS: Our study suggests a moderating, but not predominant, role of AAT variants in the course of chronic non-alcoholic pancreatitis.

Adolescent↗
PubMed2001

Clinical characterization of patients with hereditary pancreatitis and mutations in the cationic trypsinogen gene.

PURPOSE: We determined the clinical manifestations of hereditary pancreatitis in nearly 30 families. PATIENTS AND METHODS: The two trypsinogen mutations N29I and R122H were identified in a group of 550 patients with chronic pancreatitis of unclear origin. The following criteria were used to characterize the severity of chronic pancreatitis (one point each): calcifications, cysts, dilation of the pancreatic duct, diabetes, hospital treatment, and operation. Stages were defined as stage 0 (no points), stage 1 (one to two points), stage 2 (three to four points), and stage 3 (more than four points). Smoking and drinking habits were also recorded. RESULTS: Six families with the N29I mutation (25 subjects with the mutation) and 21 families with the R122H mutation (76 subjects with the mutation) were identified. The median ages for the onset of disease were 11 years in N29I and 10 years in R122H patients. The severity of chronic pancreatitis and symptoms were similar for both mutations. About 26% (n = 26) of the 101 subjects carrying a mutation were asymptomatic, and 42% (n = 42) had mild disease (stage 1). Twenty-nine percent (n = 29) had moderate disease (stage 2), and only 4% (n = 4) had severe disease (stage 3). CONCLUSIONS: Symptoms of patients with the N29I or R122H trypsinogen mutation were generally similar. The majority of subjects with trypsinogen mutations had mild disease or was asymptomatic.

Adolescent↗
PubMed2001

[Pathogenetic concepts of chronic pancreatitis].

Summary. The understanding of the pathogenesis of chronic pancreatitis is limited. Several theories (i. e. obstruction hypothesis) were suggested in the past but could not be confirmed by experimental data. As a formal description of the course of the disease, the necrosis-fibrosis concept seems to be very attractive. According to this theory, there is no significant difference in the pathogenesis of acute and chronic pancreatitis. A major step was the identification of mutations of the cationic trypsinogen, the secretory trypsin inhibitor (SPINK 1) and the cystic-fibrosis protein (CFTR) in some patients. Investigation of these mutations may significantly contribute to a better understanding of the pathogenesis of chronic pancreatitis.

Adult↗
PubMed2000

Chronic pancreatitis associated with an activation peptide mutation that facilitates trypsin activation.

BACKGROUND & AIMS: Mutations of the cationic trypsinogen have been described in hereditary pancreatitis. We report a new trypsinogen mutation in the activation peptide of the proenzyme in a family with chronic pancreatitis. METHODS: The coding region of the cationic trypsinogen gene was sequenced after polymerase chain reaction amplification. The following peptides homologous to the N-terminal end of cationic trypsinogen were synthesized (one-letter code, mutated amino acid underlined): wild-type peptide, APFDDDDKIVGG; pD22G, APFDDDGKIVGG; pK23R, APFDDDDRIVGG. The sequences of pD22G and pK23R correspond to the recently identified mutation K23R and to the mutation described here (D22G). To mimic trypsinogen activation, these peptides were digested with trypsin for 30 minutes at pH 5.0-8. 0, and the fragments were analyzed by high-performance liquid chromatography. RESULTS: In a family with clinical evidence of hereditary chronic pancreatitis, a missense mutation of codon 22 (GAC-->GGC) of the cationic trypsinogen was found. This mutation results in a substitution of aspartic acid by glycine; therefore, the mutation was called D22G. Chromatographic analysis of tryptic digests of the peptides pD22G and pK23R showed hydrolysis rates of 22% and 75%, respectively, whereas the wild-type peptide was hydrolyzed at only 6%. The cleavage rates were reduced at lower pH, and no hydrolysis occurred without trypsin. CONCLUSIONS: The activation peptides of the trypsinogen variants D22G and K23R could be released at a higher rate than in wild-type trypsinogen, resulting in increased amounts of trypsin in the pancreas, which could initiate pancreatitis.

Adult↗
PubMed2000

Mutations of the cystic fibrosis gene, but not cationic trypsinogen gene, are associated with recurrent or chronic idiopathic pancreatitis.

OBJECTIVE: We investigated whether mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene and cationic trypsinogen gene are associated with recurrent acute, or chronic idiopathic pancreatitis. METHODS: Twenty patients with idiopathic pancreatitis (11 women, nine men; mean age, 30 yr) were studied for the presence of a CFTR mutation by screening the genomic DNA for more than 30 mutations and variants in the CFTR gene. Selected mutations of the cationic trypsinogen gene were screened by Afl III restriction digestion or by a mutation-specific polymerase chain reaction (PCR). In each patient exons 1, 2, and 3 of the cationic trypsinogen gene were sequenced. Patients with a CFTR mutation underwent evaluation of further functional electrophysiological test (intestinal current measurement). RESULTS: No mutation of the cationic trypsinogen gene was detected. A CFTR mutation was detected in 6/20 (30.0%) patients. Three patients (15.0%) had a cystic fibrosis (CF) mutation on one chromosome (deltaF508, I336K, Y1092X), which is known to cause phenotypical severe cystic fibrosis. One patient was heterozygous for the 5T allele. In addition, two possibly predisposing CFTR variants (R75Q, 1716G-->A) were detected on four patients, one of these being a compound heterozygous for the missense mutation I336K and R75Q. No other family member (maternal I336K; paternal R75Q; sister I1336K) developed pancreatitis. An intestinal current measurement in rectum samples of patients with a CFTR mutation revealed no CF-typical constellations. CONCLUSIONS: CFTR mutations are associated with recurrent acute, or chronic idiopathic pancreatitis, whereas mutations of the cationic trypsinogen mutation do not appear to be a frequent pathogenetic factor.

Adult↗
PubMed1999

The pancreatitis-associated protein in hereditary and chronic alcoholic pancreatitis.

The pancreatitis-associated protein (PAP) was investigated in patients with hereditary and chronic alcoholic pancreatitis. Blood levels of pancreatic enzymes and PAP were measured in nine families with hereditary pancreatitis; in three of them, the mutation N21I, and in six, the R117H variant of the cationic trypsinogen were present. In all family members, similar to controls, only normal values of the PAP were found. There was no evidence for polymorphism of the PAP gene in patients with hereditary or alcoholic pancreatitis. Immunohistochemically PAP was detected in the apical parts of the acinar cells but not in ducts, interstitial tissue, islets, or blood vessels. Intensity of PAP labeling was directly related to the deterioration of the acinar units, and its concentration was inversely related to chymotrypsinogen immunoreactivity in the same tissue. Similar immunohistochemical findings were present in chronic alcoholic and hereditary pancreatitis. We conclude that there is a lack of PAP polymorphism in hereditary and alcoholic pancreatitis and that expression of the PAP in both groups of patients is related to the degree of cellular damage of the pancreas.

Acute-Phase Proteins↗