B Fenn | PubMed Health

PubMed2000

Ischemic hepatitis: clinical presentation and pathogenesis.

BACKGROUND: The pathophysiology of ischemic hepatitis, otherwise known as "shock liver," is poorly understood, although it is believed to be the result of a reduction in systemic blood flow as typically occurs in shock. The aim of this study was to investigate the importance of this phenomenon as well as other clinical features in patients with ischemic hepatitis. METHODS: We identified a cohort of 31 patients (case group) who met the most commonly accepted definition of ischemic hepatitis (an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper limit of normal, excluding known causes of acute hepatitis or hepatocellular injury, in an appropriate clinical setting). We also evaluated the clinical features and serum aminotransferase levels in a cohort (the control group) of 31 previously healthy patients who sustained major nonhepatic trauma at San Francisco General Hospital, a major trauma center. Both groups of patients had documented systolic blood pressures <75 mm Hg for at least 15 minutes. Clinical and hemodynamic (invasive and noninvasive) data were recorded. RESULTS: Despite the marked reduction in blood pressure, no patient in the control group developed ischemic hepatitis. The mean (+/- SD) peak serum aspartate aminotransferase level in the control group was only 78 +/- 72 IU, in contrast with a mean peak of 2,088 +/- 2,165 IU in the case group. All 31 patients with ischemic hepatitis had evidence of underlying organic heart disease, 29 (94%) of whom had right-sided heart failure. CONCLUSIONS: Systemic hypotension or shock alone did not lead to ischemic hepatitis in any patient. The vast majority of patients with ischemic hepatitis had severe underlying cardiac disease that had often led to passive congestion of the liver. These data lead us to propose that right-sided heart failure, with resultant hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event.

Acute Disease↗

PubMedDate not supplied

Trimellitic anhydride-sensitive mouse as an animal model for contact urticaria.

The respiratory allergen trimellitic anhydride (TMA) has been shown to induce IgE production and immediate ear swelling in mice sensitized to it. We studied whether TMA sensitivity could be used as an animal model for immunological contact urticaria. BALB/C mice were sensitized to TMA by topical applications. Groups of animals were pretreated on the ears with the glucocorticosteroid (GCS) betamethasone-17,21-dipropionate, the antihistamine (AH) diphenhydramine hydrochloride, the non-steroidal anti-inflammatory drug (NSAID) indomethacin or vehicle (VEH). Ears were challenged with TMA and ear thickness was measured at baseline and 1, 2, 4, 8 and 24 h after challenge. Trimellitic anhydride caused a significant biphasic ear swelling response with an early peak at 1-2 h, a plateau at 4 h and a late peak at 24 h. However, there was also an early swelling by TMA in non-sensitized mice, suggesting that non-immunological as well as immunological mechanisms contribute to early swelling by TMA. Glucocorticosteroid suppressed significantly the early and to some extent the late TMA responses, while AH suppressed only early and NSAID only late TMA responses. Ear swelling in TMA-sensitive BALB/C mice may represent a combination of immunological and non-immunological contact urticaria and allergic contact dermatitis. Mice sensitive to TMA may be helpful in defining pharmacological agents affecting contact urticaria and the model is perhaps suitable for identification of some immunologically mediated contact urticants.

Administration, Topical↗