Endothelial dysfunction in metabolic syndrome.

Metabolic syndrome (MS) or insulin resistance syndrome is the result of multiple metabolic abnormalities associated with cardiovascular disease. Since 1988, when Reaven first described MS, many researches have been conducted in order to understand its pathophysiology, epidemiology, prognostic implications and therapeutic strategies. Numerous metabolic abnormalities found in the metabolic syndrome, including hyperglycemia, excessive fatty acids and insulin resistance, cause an endothelial cell dysfunction by affecting nitric oxide synthesis or degradation. Although the exact mechanism by which metabolic syndrome induces endothelial dysfunction remains to be clarified, there are many possibilities of vascular endothelial damage and increase in cardiovascular risk in these patients. The most frequent metabolic, hormonal, hemostatic abnormalities in patients with metabolic syndrome that may contribute to endothelial dysfunction are: hyperinsulinemia, hyperglycemia, increase in fatty acid levels, hypertriglyceridemia, decrease in HDL-cholesterol, increase in small dense LDL-cholesterol, increase in apolipoprotein B, increase in insulin-1 growth factor levels, increase in tissue angiotensin II levels, increase in plasminogen activator inhibitor-1, increase in C reactive protein, increase in oxidative stress.

Anemia--a complication of antiviral treatment in chronic viral hepatitis C.

Anemia is an important and frequent secondary effect of the treatment with pegylated interferon and ribavirin in patients with chronic viral C hepatitis. Ribavirin produces more often hemolytic anemia, while pegylated interferon may determine medullary suppression. The level of hemoglobin beneath 10 g/dL is considered by most authors as being the reference level for anemia secondary to the antiviral treatment. Beneath this hemoglobin value it is recommended to reduce or to stop the treatment with ribavirin, to administer recombinant human erythropoietin or blood transfusion, based on the severity of the anemia. The growth rate of the serum erythropoietin in the first few weeks of treatment is correlated with the necessity of decreasing the doses or even to stop the treatment with ribavirin. The SVR (sustained viral response) rate of the patients is reduced when the ribavirin doses are reduced due to anemia.

[Ultrasound guided percutaneous drainage in the treatment of local septic complications of chronic pancreatitis]. / Utilizarea drenajului percutan ecoghidat în tratamentul complicatiilor septice locale ale pancreatitei cronice.

AIM: To evaluate results of ultrasound guided percutaneous catheter drainage (PCD) for local septic complications of chronic pancreatitis. MATERIAL AND METHOD: Between 1999 and 2002, PCD was used in 19 patients with chronic pancreatitis for 6 infected acute pseudocysts, 3 post-necrotic abscesses, 3 abscesses following pancreatic resections, 6 abscesses with none of the precipitating factors present (no acute episode or recent surgical/endoscopic interventions) and a tuberculous peritoneal empyema. In 17 patients, collections were unilocular. RESULTS: Trocar technique was used in 14 patients and Seldinger technique in 5. Sixteen patients were successfully treated with PCD alone (mean drainage duration = 32 days) without abscess recurrence during the follow-up period (mean = 35.6 month). Surgical treatment was necessary in 3 patients. Pseudocyst recurrence occurred in another patient after 9 months. CONCLUSION: PCD should be considered as the initial therapy for chronic pancreatitis local septic complications. Surgery is reserved for patients in whom PCD fails.

[Acute diffuse peritonitis of a rare cause]. / Peritonita generalizata de cauza rara.

The authors report a rare case of acute onset of non-Hodgkin lymphoma with diffuse peritonitis due to bowel perforation of secondary jejunal involvement. The admission diagnosis in the 18-years-old male with acute abdominal pain for 4 days, guarding on physical examination and pneumoperitoneum on abdominal ultrasonography was peptic ulcus perforation. The palpable splenomegaly and cervical lymph nodes on ultrasonography examination might have raised suspicion of lymphoma. Surgical exploration revealed the peritonitis origin--jejunal perforation, proximal to a stenosing tumor, a gastric tumor and confirmed the splenomegaly. Small bowel resection--end to end anastomosis--and gastric tumor biopsies were performed. The pathological diagnosis was diffuse large B-cell non-Hodgkin lymphoma. Some therapeutic considerations on digestive tract secondary lymphoma are made.