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Biomedical subjects

N Homann

Publications and source records attributed to N Homann.

At least 19 recordsLinked to original sources
PubMed2007

The Luebeck interview for psychosocial screening in patients with inflammatory bowel disease.

BACKGROUND: Psychosocial factors play an important role in the course of inflammatory bowel disease (IBD). However, a simple, valid psychosocial screening instrument that is suitable for short patient-physician contacts does not exist. Therefore, the Luebeck semistructured Interview for Psychosocial Screening was developed as a rating tool for psychosocial stress in IBD patients (LIPS-IBD). METHOD: The entire interview requires approximately 10 minutes. Interrater reliability was tested. Depression, anxiety, social support, impact of the disease, global level of psychosocial stress, and demand for psychosocial support were rated in 92 patients with IBD on 5 point Likert scales. Patients from the in- and out-patient clinic for gastroenterology were included. In addition, patients filled out self-report questionnaires regarding depression, anxiety, social support, and impact of the disease. Indices of disease activity (Colitis Activity Index, Crohn's Disease Activity Index) were recorded. RESULTS: Both patients and physicians found the interview feasible. Reliability was good, with interrater reliability ranging from .76 to .94. Convergence with self-report instruments was also high (r = .5-.6). Ratings of depression and impact of the disease were correlated with indices of disease activity. DISCUSSION: LIPS helps to identify patients with high levels of psychosocial stress and provide them with more detailed psychologic assessments. It was found to be a suitable instrument for daily clinical routine. It is potentially a valuable screening tool to obtain reliable, valid, and useful information in daily practice in IBD treatment settings.

Adult↗
PubMed2004

[Massive pulmonary embolism after endoscopic therapy for gastric variceal bleeding].

A 60-year-old woman with alcoholic cirrhosis of the liver was admitted to the ICU because of haemodynamic instability, hematemesis and presumed acute variceal bleeding. An upper endoscopy was performed and varices of the distal esophagus and an actively bleeding varix of the gastric fundus were detected. The bleeding was successfully treated with 2 consecutive injections of 0.5 ml n-butyl-2-cyanoacrylate and 0.5 ml lipiodol. The patient was intubated prior to the endoscopy to avoid blood aspiration. However, severe hypoxaemia with a need for prolonged mechanical ventilation and signs of right heart strain developed after endoscopy. A chest X-ray and CT scan of the thorax documented an extensive embolisation of the pulmonary arteries. The patient's varices were retreated with band ligation but rebleeding occurred. Finally, a TIPS application was needed to stop recurrent haemorrhage. This case demonstrates that embolisation of the pulmonary arterial bed is a rare complication of endoscopic sclerotherapy for gastric variceal bleeding. The severity of this complication may depend on the volume of liquid acrylate being injected and pre-existing lung tissue alterations. Since histoacryl is not lysable, severe pulmonary emboli with lung tissue damage and pulmonary hypertension may occur. Factors contributing to this complication are analysed and therapeutic alternatives are discussed.

Endoscopy, Gastrointestinal↗
PubMed2004

Increased cancer risk in heavy drinkers with the alcohol dehydrogenase 1C*1 allele, possibly due to salivary acetaldehyde.

BACKGROUND: Chronic ethanol consumption is associated with an increased risk of upper aerodigestive tract cancer. As acetaldehyde seems to be a carcinogenic factor associated with chronic alcohol consumption, alcoholics with the alcohol dehydrogenase (ADH) 1C*1 allele seem to be particularly at risk as this allele encodes for a rapidly ethanol metabolising enzyme leading to increased acetaldehyde levels. Recent epidemiological studies resulted in contradictory results and therefore we have investigated ADH1C genotypes in heavy alcohol consumers only. METHODS: We analysed the ADH1C genotype in 107 heavy drinkers with upper aerodigestive tract cancer and in 103 age matched alcoholic controls without cancer who consumed similar amounts of alcohol. Genotyping of the ADH1C locus was performed using polymerase chain reaction based on restriction fragment length polymorphism methods on leucocyte DNA. In addition, ethanol was administered orally (0.3 g/kg body weight) to 21 healthy volunteers with the ADH1C*1,1, ADH1C*1,2, and ADH1C*2,2 genotypes, and 12 volunteers with various ADH genotypes consumed ethanol ad libitum (mean 211 (29) g). Subsequently, salivary acetaldehyde concentrations were measured by gas chromatography or high performance liquid chromatography. RESULTS: The allele frequency of the ADH1C*1 allele was found to be significantly increased in heavy drinkers with upper aerodigestive tract cancer compared with age matched alcoholic controls without cancer (61.7% v 49.0%; p = 0.011). The unadjusted and adjusted odds ratios for all cancer cases versus all alcoholic controls were 1.67 and 1.69, respectively. Healthy volunteers homozygous for the ADH1C*1 allele had higher salivary acetaldehyde concentrations following alcohol ingestion than volunteers heterozygous for ADH1C (p = 0.056) or homozygous for ADH1C*2 (p = 0.011). CONCLUSIONS: These data demonstrate that heavy drinkers homozygous for the ADH1C*1 allele have a predisposition to develop upper aerodigestive tract cancer, possibly due to elevated salivary acetaldehyde levels following alcohol consumption.

Acetaldehyde↗
PubMed2002

The impact of blepharospasm and cervical dystonia on health-related quality of life and depression.

The aim of the study was to evaluate and compare health-related quality of life (HR-QoL) and depression in essential blepharospasm (BSP) and idiopathic cervical dystonia (CD), to identify the clinical and demographic factors associated with poor HR-QoL in both disorders and to analyse the effect of Botulinum Toxin A (BtxA) therapy. Two hundred-twenty consecutive patients with BSP (N = 89, 62 % women, mean age 64 years, mean disease duration 7 years) and CD (N = 131, 64 % women, mean age 53 years, mean disease duration 8 years) recruited from routine referrals to eight Austrian dystonia clinics were included. HR-QoL was measured by the Short Form 36 (SF-36) and depression by the Beck Depression Inventory (BDI). At baseline, patients with CD and BSP scored significantly worse in all eight SF-36 domains compared with an age-matched community sample. In addition, 47 % of patients with CD and 37 % of those with BSP were depressed. Women with BSP scored significantly lower in all SF-36 domains and were more depressed than male patients. In contrast, there was no significant effect of gender on HR-QoL and depression in CD. Neck pain had a significant impact on all SF-36 domains and represented the main determinant of depression in CD. Although BtxA therapy resulted in a significant improvement of clinical symptoms in BSP and CD, HR-QoL did not improve in BSP and only two of the eight SF-36 domains improved significantly in patients with CD. The present study for the first time demonstrated that BSP has a substantial impact on health status emphasizing the need for psychological support with interventions aimed at treating depression in these patients. Our results provide further evidence for the profound impact of CD on HR-QoL and indicate the importance of an adequate management of neck pain in addition to reducing the severity of dystonia in CD. The mismatch between objective BtxA derived improvement of dystonia and lack of change of HR-QoL as determined by the SF-36 illustrates the need for optimized disease specific quality of life rating scales in patients with craniocervical dystonia.

Aged↗
PubMed2001

Poor dental status increases acetaldehyde production from ethanol in saliva: a possible link to increased oral cancer risk among heavy drinkers.

Epidemiological data support evidence that poor dental status increases oral cavity cancer risk especially among heavy alcohol consumers, but the causality of this finding is unclear. The enzymatic conversion of ethanol by the physiological oral microflora may lead to an accumulation of the highly carcinogenic intermediate acetaldehyde. This study was conducted to evaluate the role of dental status on the microbial production of acetaldehyde from ethanol in saliva. The microbial acetaldehyde production from ethanol was related to the dental score in 132 volunteers. After adjustment for smoking, alcohol consumption, age and gender, poor dental status was shown to lead to an approximately twofold increase in salivary acetaldehyde production from ethanol (P=0.02). Our results could be an important factor underlying the role of poor dental hygiene and status in oral cancer risk associated with ethanol drinking.

Acetaldehyde↗
PubMed2001

Alcohol and cancer.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Helmut K. Seitz and Shohei Matsuzaki. The presentations were (1) Alcohol dehydrogenase-2 and aldehyde dehydrogenase-2 genotype and cancer risk for upper aerodigestive tract in Japanese alcoholics, by Akira Yokoyama; (2) The role of acetaldehyde in alcohol-associated carcinogenesis, by Nils Homann; (3) High salivary acetaldehyde levels after a moderate dose of alcohol in ALDH2-deficient subjects, by Satu Väkeväinen; (4) Alcohol and vitamin A interactions, by Xian Dong Wang; and (5) Alcohol and colorectal cancer, by Helmut K. Seitz.

Acetaldehyde↗
PubMed2001

Increased rectal cell proliferation following alcohol abuse.

BACKGROUND: Epidemiological data indicate an increased risk for rectal cancer following chronic alcohol consumption. As chronic ethanol ingestion leads to rectal hyperregeneration in experimental animals, indicating a state of increased susceptibility to carcinogens, we studied cell proliferation in alcohol abusers. METHODS: Rectal biopsies were taken from 44 heavy drinkers and 26 controls. Cell proliferation, including proliferative compartment size, was measured by immunohistological staining for proliferative cell nuclear antigen (PCNA) and Ki67, and by in situ hybridisation for histone H3. Quantification of cell proliferation using PCNA staining was evaluated in 27 alcohol abusers and 12 controls. In addition, immunohistology was performed for cytokeratins and gene products of Rb1, bcl-2, and p53. RESULTS: Heavy drinking resulted in increased cell proliferation of the rectal mucosa, as shown by increased detection of different proliferation markers. However, cell differentiation regarding cytokeratin expression patterns was unchanged as well as regulatory factors involved in carcinogenesis and/or apoptosis. CONCLUSION: Chronic alcohol abuse leads to rectal mucosal hyperproliferation in humans, a condition associated with an increased cancer risk.

Adult↗
PubMed2001

Overexpression of p53 in tumor-distant epithelia of head and neck cancer patients is associated with an increased incidence of second primary carcinoma.

Second primary carcinoma is a peculiar feature of head and neck cancer and represents a form of treatment failure distinct from the recurrence of the primary tumor. Whether altered p53 expression in tumor-distant epithelia at the time of diagnosis is of clinical value as a biomarker for second primary carcinoma development has not been rigorously answered because of the lack of long-term follow-up studies involving a sufficiently large patient cohort. In this prospective study, we have investigated p53 expression in tumor-distant epithelia and in the corresponding primary tumors of 105 head and neck cancer patients by immunohistochemistry on frozen sections. After a median follow-up of 55 months, the clinical course of disease parameters, i.e., local recurrences, lymph node and distant metastasis, incidence of second primary carcinoma, and survival, was evaluated. Overexpression of p53 in tumor-distant epithelia was found in 49 patients (46.7%), and it was independent of the p53 protein status of the primary tumor and of the tumor site, size, stage, and grading. Mucosal p53 overexpression was not associated with local primary recurrences, lymph node or distant metastases, or overall survival. Importantly, mucosal p53 overexpression, but not overexpression in the primary tumors, was significantly associated with an increased incidence of second primary carcinomas (P = 0.0001; Fisher's exact test). When the times to second primary tumor occurrence were analyzed by the Kaplan-Meier method, the difference remained significant (P = 0.005; log rank test). We conclude that IHC staining for p53 overexpression in tumor-distant epithelia provides a simple and rapid tool to identify head and neck cancer patients at increased risk of developing second primary tumors. Because p53 overexpression in these epithelia in our patient cohort was specifically associated with second primary cancer but not with recurrences, at least a fraction of the second primary cancers appears to have resulted from genetic events in the mucosa ("field cancerization").

Carcinoma, Squamous Cell↗
PubMed2000

Microbially produced acetaldehyde from ethanol may increase the risk of colon cancer via folate deficiency.

High alcohol and low folate intake are independent risk factors for colorectal cancer. Acetaldehyde has been postulated to be a factor responsible for ethanol-associated carcinogenesis. High levels of acetaldehyde accumulate in the large intestine via the microbial oxidation of alcohol. Acetaldehyde degrades folate in vitro. Thus, it is possible that high intracolonic acetaldehyde levels break down folate in the colon. Our aim was to test the effect of high alcohol and acetaldehyde concentrations in the gut on systemic and local intestinal folate levels in rats. Twenty rats received 3 g/kg of ethanol twice a day for 2 weeks with or without concomitant ciprofloxacin administration. Twenty control rats received saline with or without ciprofloxacin. All rats were fed a diet with normal folate content. Alcohol treatment led to very high intracolonic acetaldehyde levels (387 +/- 185 microM), which were markedly decreased by concomitant ciprofloxacin treatment (21 +/- 4 microM). Erythrocyte, serum and small intestinal folate levels were unaffected by alcohol treatment. Alcohol administration decreased significantly colonic mucosal folate levels by 48%, and this effect was prevented by ciprofloxacin. We conclude that alcohol administration for 2 weeks leads to local folate deficiency of colonic mucosa in rats, most probably via the degradation of folate by the high levels of acetaldehyde microbially produced from ethanol. Our findings offer a unique explanation for the increased risk of colonic cancer associated with alcohol intake and folate deficiency.

Acetaldehyde↗
PubMed2000

[Alcohol and cancer].

Numerous studies have identified alcohol as the main risk factor for cancer of the upper GI tract such as pharynx, larynx and esophagus. Alcohol consumption is also associated with an enhanced risk for hepatocellular, breast and colorectal cancer. Animal experiments have demonstrated, that alcohol per se is not carcinogenic but rather exerts tumor-promoting and cocarcinogenic properties in animal models. These findings may be explained by recent experimental and epidemiological studies which have focused on the first metabolite acetaldehyde as the main tumorigenic substance of alcohol abuse. Other possible tumor promoting effects of alcohol are the existence of carcinogenic congeners in alcoholic beverages, an increased solubility of carcinogens by alcohol, a reduced intake and bioavailability of possible cancer protective substances, an inhibition of detoxification of carcinogenic compounds or increased activation of procarcinogens by cytochrome P450IIE1 which is induced by alcohol and a suppressed immune function. Alcohol also leads to a direct local mucosal damage, which results in a chronically increased cell division and thus an increased cancer risk.

Alcohol-Related Disorders↗
PubMed2000

Increased salivary acetaldehyde levels in heavy drinkers and smokers: a microbiological approach to oral cavity cancer.

The pathogenetic mechanisms behind alcohol-associated carcinogenesis in the upper digestive tract remain unclear, as alcohol is not carcinogenic. However, there is increasing evidence that a major part of the tumour-promoting action of alcohol might be mediated via its first, toxic and carcinogenic metabolite acetaldehyde. Acetaldehyde is produced from ethanol in the epithelia by mucosal alcohol dehydrogenases, but much higher levels derive from microbial oxidation of ethanol by the oral microflora. In this study we investigated factors that might alter the composition and quantities of the oral microflora and, consequently, influence microbial acetaldehyde production. Information about dental health, smoking habits, alcohol consumption and other factors was obtained by a questionnaire from 326 volunteers with varying social backgrounds and health status, e.g. oral cavity malignancy. Paraffin-induced saliva was collected and the microbial production of acetaldehyde from ethanol was measured. Smoking and heavy drinking were the strongest factors increasing microbial acetaldehyde production. Whether poor dental status may alter local acetaldehyde production from ethanol remained unanswered. Bacterial analysis revealed that mainly gram-positive aerobic bacteria and yeasts were associated with higher acetaldehyde production. Increased local microbial salivary acetaldehyde production due to ethanol among smokers and heavy drinkers could be a biological explanation for the observed synergistic carcinogenic action of alcohol and smoking on upper gastrointestinal tract cancer. It offers a new microbiological approach to ethanol-associated carcinogenesis at these anatomic sites.

Acetaldehyde↗
PubMed1999

Ciprofloxacin decreases the rate of ethanol elimination in humans.

BACKGROUND: Extrahepatic ethanol metabolism is postulated to take place via microbial oxidation in the colon, mediated by aerobic and facultative anaerobic bacteria. AIMS: To evaluate the role of microbial ethanol oxidation in the total elimination rate of ethanol in humans by reducing gut flora with ciprofloxacin. METHODS: Ethanol was administered intravenously at the beginning and end of a one week period to eight male volunteers. Between ethanol doses volunteers received 750 mg ciprofloxacin twice daily. RESULTS: A highly significant (p=0.001) reduction in the ethanol elimination rate (EER) was detected after ciprofloxacin medication. Mean (SEM) EER was 107.0 (5.3) and 96.9 (4.8) mg/kg/h before and after ciprofloxacin, respectively. Faecal Enterobacteriaceae and Enterococcus sp. were totally absent after medication, and faecal acetaldehyde production capacity was significantly (p<0.05) decreased from 0.91 (0.15) to 0.39 (0.08) nmol/min/mg protein. Mean faecal alcohol dehydrogenase (ADH) activity was significantly (p<0. 05) decreased after medication, but ciprofloxacin did not inhibit human hepatic ADH activity in vitro. CONCLUSIONS: Ciprofloxacin treatment decreased the ethanol elimination rate by 9.4%, with a concomitant decrease in intestinal aerobic and facultative anaerobic bacteria, faecal ADH activity, and acetaldehyde production. As ciprofloxacin has no effect on liver blood flow, hepatic ADH activity, or cytochrome CYP2E1 activity, these effects are probably caused by the reduction in intestinal flora.

Acetaldehyde↗