The pathogenic mechanism of hepatorenal syndrome is not well established. We investigated the circulatory function in cirrhosis before and after the development of hepatorenal syndrome. Systemic and hepatic hemodynamics and the activity of endogenous vasoactive systems were measured in 66 patients who had cirrhosis with tense ascites and normal serum creatinine levels; measurements were repeated at follow-up in 27 cases in whom hepatorenal syndrome had developed. At baseline, mean arterial pressure and cardiac output were significantly higher, and hepatic venous pressure gradient, plasma renin activity, and norepinephrine concentration were significantly lower in patients who did not develop hepatorenal syndrome compared with those presenting with this complication. Peripheral vascular resistance was decreased to the same extent in the two groups. Plasma renin activity and cardiac output were the only independent predictors of hepatorenal syndrome. Hepatorenal syndrome occurred in the setting of a significant reduction in mean arterial pressure (83 ؎ 9 to 75 ؎ 7 mmHg; P < .001), cardiac output (6.0 ؎ 1.2 to 5.4 ؎ 1.5 L/min; P < .01), and wegded pulmonary pressure (9.2 ؎ 2.6 to 7.5 ؎ 2.6 mmHg; P < .001) and an increase in plasma renin activity (9.9 ؎ 5.2 to 17.5 ؎ 11.4 ng/mL ⅐ hr; P < .001), norepinephrine concentration (571 ؎ 241 to 965 ؎ 502 pg/mL; P < .001), and hepatic venous pressure gradient. No changes were observed in peripheral vascular resistance. In conclusion, these data indicate that hepatorenal syndrome is the result of a decrease in cardiac output in the setting of a severe arterial vasodilation. (HEPATOLOGY 2005;42:439-447.)
In a prospective study in AIDS patients with chronic diarrhea, the overall prevalence of intestinal cryptosporidiosis was 15.6% (43/275). The prevalence was higher in homosexual patients (33.3%) than in intravenous drug abusers (10.6%) (p < 0.001). Extraintestinal infection was present in 30% (13/43) of the patients with known intestinal cryptosporidiosis. Eight of the 13 (61.5%) patients with extraintestinal cryptosporidiosis had Cryptosporidium in the bile and 7 of 13 (16.28%) had it in the sputum. Of the seven patients with Cryptosporidium in the sputum, four had respiratory symptoms and an abnormal chest radiograph, although another pulmonary pathogen was isolated simultaneously. Two other patients from whom Cryptosporidium was the sole respiratory pathogen isolated had no respiratory symptoms and normal chest radiographs. The seventh patient had pulmonary symptoms, interstitial infiltrate on chest radiograph and excessive activity on a pulmonary Gallium scan; Cryptosporidium was the only organism detected in induced sputum and bronchoalveolar lavage specimens. The mean CD4+ lymphocyte count in patients with extraintestinal cryptosporidiosis was 55 cells/mm3.
We report the first hepatitis E infection case detected in a slaughterhouse worker. The identified strain belonged to genotype 3, subtype 3f. Partial sequence analysis of the strain isolated from his serum showed a percentage of nucleotide homology ranging from 83.4% up to 97.3% compared with European human and swine strains, respectively. These findings point strongly to hepatitis E virus as a vocationally acquired illness by means of the manipulation of infected organs from pigs.
We report the second case of an adult fulfilling all diagnostic criteria for GAGD. We propose that the activated LP CD4+ T lymphocytes, as well as those atypically located in the epithelium, may play a pathogenic role. The alphaE/beta7- IEL could constitute a diagnostic marker of intestinal autoimmunity in the cases when autoantibodies are not evidenced, and mucosal TNF-alpha might represent a novel therapeutic target in this severe disease.
The correction of hepatopulmonary syndrome (HPS) after liver transplantation (LT) remains controversial. The aims of our study were to: 1) analyze whether LT reverses HPS; 2) note any relationship between HPS and the systemic hemodynamic disturbance; and 3) note changes in circulating sex hormones and the possible association with pulmonary and systemic hemodynamic changes. Systemic hemodynamic parameters, cardiac output and systemic vascular resistance (SVR), sex hormones, and intrapulmonary vasodilatation assessed by contrast transesophageal echocardiography, and gas exchange abnormalities were investigated in 19 patients with advanced cirrhosis prior to and 6 months (176.8+/-30 days) after LT. LT was followed by a marked reduction in cardiac output (6.6+/-1.7 vs 3.5+/-0.5 l/min; p<0.001) and SVR (1039+/-460 vs 1978+/-294 dyn x sec x cm(-5); p<0.005). Before LT, circulating estradiol and progesterone levels were invariably elevated (66+/-22 pg/ml and 1.8+/-1.1 ng/ml, respectively, normal values <31 pg/ml and 0.35 ng/ml, respectively), and dropped after LT (28+/-12 pg/ml p<0.001 and 0.38+/-0.2 ng/ml; p<0.001, respectively). Seventeen of 19 patients had intrapulmonary vasodilatation and increased alveolar-arterial oxygen difference, thereby fulfilling diagnostic criteria for HPS. Patients with HPS presented higher cardiac output (p<0.05), lower SVR (p<0.01), and higher progesterone and estradiol levels than patients without HPS (p<0.05). LT produced normalization of intrapulmonary vasodilatation in all patients. LT normalized hyperdynamic circulation and is a useful therapeutic option in patients with HPS. Normalization of sex hormone levels after LT suggests that they could play a pathogenic role in the development of HPS.
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