Outcome of incisional hernia repair in patients 80 years and older: results from the Herniamed-Registry.

INTRODUCTION: More and more often complex abdominal surgeries are performed in the elderly. Together with the ageing population these patients are at risk for incisional hernias. We aimed on assessing outcomes following incisional hernia surgery in patients 80 years and older. MATERIAL AND METHODS: Using the Herniamed-Registry, a prospective multi-institutional database, data on patients undergoing surgery for incisional hernias were retrospectively assessed. 46,040 patients were included and divided by age. Intraoperative-, general-, and postoperative complications as well as 1-year follow-up outcomes were assessed and compared between patients 80 years and older vs younger than 80 years. RESULTS: Intra- (2.3% vs 1.5%; p < 0.001) and postoperative (8.6% vs 7.2%; p = 0.001) complications, general complications (5.5% vs 3.0%; p < 0.001), as well as reoperations (3.8% vs 3.0%; p = 0.007) were more likely to occur in elderly patients. By contrast, recurrences (3.6% vs 4.5%; p = 0.007), pain at rest (7.3% vs 10.1%; p < 0.001) and on exertion (11.3% vs 18.3%; p < 0.001), as well as pain requiring treatment (5.4% vs 7.7%; p < 0.001) was less likely in the group of patients aged ≥ 80 years. CONCLUSION: Incisional hernia repair in patients 80 years and older is associated with a slightly higher complication risk but is quite acceptable and also have improved pain scores. The recurrence difference is also clinically unimportant.

Serotonin: a double-edged sword for the liver?

Since the discovery of the impact of serotonin in liver regeneration, this molecule has gained considerable attention in liver physio-pathology. Platelet-derived serotonin initiates liver regeneration after partial hepatectomy in various rodent models. Serotonin agonism stabilizes the hepatic microcirculation and prevents small-for-size liver graft failure. Similarly, serotonin receptor agonists improve the sinusoidal perfusion of aged liver and restore the deficient liver regeneration in old mice through a pathway dependent on vascular endothelial growth factor. Beside hepatocyte proliferation, cholangiocytes have been shown to be able to deploy serotonin as an autocrine/paracrine signal to regulate regeneration of the biliary tree. Increasing evidence indicates that serotonin is involved in many pathological conditions of the liver. For example, serotonin promotes tissue repair after ischemia/reperfusion injury. Reactive oxygen species generated by serotonin degradation contribute to steatohepatitis in rodent models. Serotonin aggravates viral hepatitis, again through vasoactive effects on the microcirculation, and plays a crucial role in the progression of hepatic fibrosis. Finally, serotonin may facilitate tumor growth of primary liver carcinoma like cholangiocarcinoma and hepatocellular carcinoma. These findings make serotonin both friend and foe for the liver. Whichever, these new data emphasize the potential of serotonin as a pharmacological target in liver disease.

Role of serotonin in the hepato-gastroIntestinal tract: an old molecule for new perspectives.

Beside its role as a neurotransmitter in the central nervous system, serotonin appears to be a central physiologic mediator of many gastrointestinal (GI) functions and a mediator of the brain-gut connection. By acting directly and via modulation of the enteric nervous system, serotonin has numerous effects on the GI tract. The main gut disturbances in which serotonin is involved are acute chemotherapy-induced nausea and vomiting, carcinoid syndrome and irritable bowel syndrome. Serotonin also has mitogenic properties. Platelet-derived serotonin is involved in liver regeneration after partial hepatectomy. In diseased liver, serotonin may play a crucial role in the progression of hepatic fibrosis and the pathogenesis of steatohepatitis. Better understanding of the role of the serotonin receptor subtypes and serotonin mechanisms of action in the liver and gut may open new therapeutic strategies in hepato-gastrointestinal diseases.

Systematic analysis of oxidative degradation of polysaccharides using PAGE and HPLC--MS.

Oxidation of polysaccharides yields hydroxyaldehydes and hydroxycarboxylic acids. Aldehydes and carboxylic acids were separately conjugated to 8-aminonaphthalene-1,3,6-trisulfonic acid (ANTS) or tyrosine t-butyl ester (TBT). The ANTS-labeled derivatives were separated by molecular size on PAGE gels and detected by fluorescence. TBT-labeled derivatives were separated by reverse phase chromatography on a C18-HPLC column and analyzed by positive ion electrospray mass spectroscopy (HPLC--MS). This combination of procedures allowed a systematic analysis of carbohydrate oxidation products.

Effect of a short maximal physical exercise on the eosinophil cationic protein.

Eosinophil cationic protein (ECP) has been shown to be a marker of eosinophil granulocyte activation. In 10 healthy young subjects the plasma concentrations of ECP were measured before and after a graded maximal bicycle exercise test. The analyses were carried out 30 min before and immediately before exercise, immediately after exercise and 20 and 45 min later. The post-exercise values were corrected for plasma volume changes which were calculated from hematocrit and hemoglobin values. Immediately post-exercise the ECP increased significantly (p < 0.01) from 1.25 +/- 0.28 at rest to 2.40 +/- 0.59 micrograms/l. Twenty and 45 min later the values normalized and significant differences from the pre-exercise values could no longer be measured. The results provide strong evidence for an activation of eosinophil granulocytes after a short maximal exercise.