Biomedical subjects

Christoph Hanck

Publications and source records attributed to Christoph Hanck.

3 recordsLinked to original sources

PubMed2004

Alcoholic pancreatitis.

Without doubt, alcohol consumption is one of the most important considerations in adults with acute or chronic pancreatitis. Understanding chronic pancreatitis as a complex disorder in which complimentary factors are required for recurrent acute and late chronic pancreatitis to develop in subsets of patients is critical for the early diagnosis and management of these individuals. Recent pathophysiological and genetic findings represent the beginning of major diagnostic and treatment breakthroughs that are likely to continue for the foreseeable future. The information provided in this article should provide the physician with a fresh perspective and remind the clinician of the importance of an accurate and complete history, and the need to document the actual alcohol consumption, pattern of drinking, and raise appropriate concerns if signs of alcoholism are detected. If alcohol-associated pancreatitis is detected, then limitation of pancreatic damage, limitation of progression, or preventative intervention should become the major concern.

Alcohol Drinking↗

PubMed2003

Genetic polymorphisms in alcoholic pancreatitis.

Chronic, excessive alcohol consumption is clearly associated with acute and chronic pancreatitis. However, both clinical and laboratory studies have demonstrated that alcohol consumption alone does not directly cause pancreatitis. Growing evidence suggests that environmental and possibly genetic cofactors must also be present before the mechanisms protecting the pancreas from pancreatitis are circumvented and pancreatitis develops. The discovery that mutations in the cationic trypsinogen gene (R122H, N29I) predisposed to acute and chronic pancreatitis focused attention on possible genetic predispositions. Mutations in the cationic trypsinogen gene, however, are rarely associated with alcoholic chronic pancreatitis. Mutations in the SPINK1 gene (e.g. N34S) provide a threefold increased risk, and cystic fibrosis transmembrane conductance regulator (CFTR) mutations continue to be investigated. However, the major cofactor associated with alcoholic chronic pancreatitis is yet to be identified.

Acute Disease↗

PubMed2003

Differential expression of toll-like receptors 2 and 4 in patients with liver cirrhosis.

OBJECTIVE: Toll-like receptors (TLR) 2 and 4 were shown recently to mediate lipopolysaccharide (LPS)/endotoxin effects in vivo. Absence of clinical features, such as fever and leucocytosis, frequent infections, and up-regulation of anti-inflammatory cytokines suggest systemic differential regulation of LPS effects in patients with chronic endotoxinaemia due to liver cirrhosis. DESIGN: Regulation of TLR2 and TLR4 represents a possible pathway to control LPS-induced immune responses in liver cirrhosis. METHODS: We compared the expression of TLR2 and TLR4 in peripheral blood mononuclear cells (PBMC) (n = 28) and in liver biopsies (n = 20) of controls and of patients with liver cirrhosis by applying the reverse transcriptase polymerase chain reaction technique. The data were correlated to serum levels of LPS and CD14. RESULTS: Expression of TLR2 was up-regulated (P < 0.01 to P < 0.05) in the PBMC of patients with high serum endotoxin levels, while TLR4 expression in patients at Child-Pugh stage A was down-regulated, irrespective of the origin (alcoholic or viral) of cirrhosis. A strong and significant correlation between expression of TLR2 and serum LPS (r = 0.638, P < 0.01) and soluble CD14 (r = 0.550, P < 0.05) was observed. Intrahepatic expression of TLR2/4 was not altered significantly in patients with liver cirrhosis. CONCLUSION: Our data indicate LPS-driven regulation of TLR2/4 in patients with liver cirrhosis, suggesting involvement in mechanisms of systemic LPS hyporesponsiveness.

Drosophila Proteins↗