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A 23-year old female patient is referred to our intensive care unit from another hospital because of progredient neurological deterioration with sopor. One week before, she had experienced non-specific pain in her upper right stomach combined with vomitus and nausea. For two days, she had been treated with ciprofloxacin 2 × 500 mg / d by her primary care physician. Except for appendectomy in childhood, no other diseases were reported. Clinical investigation: Physical examination reveals mild scleral and dermal jaundice. There is tenderness of the upper right abdomen. Initially, no neurological pathological findings are obvious. Laboratory results show an increase of liver aminotransferases, bilirubin, and ammonia. The toxicological screening is negative.Hepatic encephalopathy due to acute hepatic failure is diagnosed and detoxification of ammonia with lactulose is started. Transiugular liver biopsy confirms lobular hepatitis with cytolysis. Because of progressive deterioration additional treatment to prevent cerebral oedema is initiated. Consecutively serum osmolality decreases, and ammonia and neurological status normalize.This report illustrates toxic acute liver failure after treatment with ciprofloxacin.

Circulating polymorphonuclear neutrophils (PMNs) are known to contribute to the pathophysiology of myocardial ischemia and reperfusion injury. The present study was designed to examine whether the duration of ischemia in myocardial infarction, the type of coronary intervention (angioplasty vs. angioplasty plus stenting) and duration of the procedure itself modulate the inflammatory responses of PMNs.In patients with acute myocardial infarction (AMI; n = 20) neutrophil beta-2-integrin Mac-1 (CD11b/CD18) and L-selectin (CD62L) were determined at different time points before and after PTCA or PTCA plus stenting. After PTCA alone but not after PTCA plus stenting a significant rise in Mac-1 (136 +/- 43%) was demonstrated. This elevation decreased after 60 minutes if the duration of the recanalization procedure was shorter than 30 minutes but remained elevated after longer interventions. After delayed intervention a significant and more pronounced increase of Mac-1 (142 +/- 37%) was observed, while early intervention prevented this increase. After PTCA alone or delayed intervention a significant shedding of L-selectin (77 +/- 20%; 77 +/- 23%) was demonstrated. Early intervention or PTCA plus stenting caused no significant changes in L-selectin.It is concluded that PMN activation is attenuated by early and short intervention as well as by stenting. Induction of PMN activation might contribute to the superior outcome following stenting and early intervention compared to conventional PTCA in particular when performed delayed.

In the past years coronary atherosclerosis and plaque rupture have been characterized not only as a problem of growth of smooth vascular cells, of activated thrombocytes and coagulation but also of inflammation.Several studies have demonstrated the importance of C-reactive protein as a marker for cardiovascular complications. Also interleukin-6, tumor necrosis factor-alpha and adhesion molecules are discussed as predictors of a poor prognosis in patients with acute coronary syndromes.A positive troponin T test is correlated with an increased rate of early complications; thus, these patients benefit from an aggressive therapy with GP IIb/IIIa receptor antagonists and acute coronary intervention. The C-reactive protein is predictive for late complications such as restenosis, reinfarction and death due to cardiac events; these patients benefit from close controls and from an anti-inflammatory therapy with acetylsalicyclic acid and statins.