Hepatic involvement in hypereosinophilia: sonographic findings.

Hypereosinophilic syndrome may cause eosinophil-related tissue damage to various organs. The purpose of this paper is to describe sonographic findings in 13 patients with hypereosinophilia in whom the liver was involved. The diagnosis in these 13 patients was based on liver biopsy in seven patients with bone marrow biopsy in six patients. Eight patients had hypereosinophilic syndrome and five patients had clonorchiasis. All 13 patients had mild to marked hepatomegaly. Seven of 13 patients showed multiple round or oval hypoechoic (n = 6) or variably echogenic (n = 1) lesions measuring 1 to 2 cm with poorly defined margins in both lobes of the liver. Four patients had one or two hypoechoic lesions 3 to 4 cm in size, with geographic pattern and poorly defined margins. Two patients showed diffuse hepatomegaly with increased parenchymal echogenicity. The number of lesions and the extent of diffuse lesions seem to be proportional to the degree of eosinophilia. Hypereosinophilia may produce multiple small focal hepatic lesions or diffuse segmental or lobar echogenic lesions simulating primary or metastatic tumor of the liver.

Hypoxemia and liver cirrhosis (hepatopulmonary syndrome) in eight patients: comparison of the central and peripheral pulmonary vasculature.

PURPOSE: To evaluate the pulmonary vasculature in patients with hepatopulmonary syndrome. MATERIALS AND METHODS: Conventional computed tomographic (CT) scans in eight patients with hepatopulmonary syndrome were retrospectively evaluated to compare the diameters of the pulmonary trunk, right and left main pulmonary arteries, and peripheral pulmonary vasculature in the right posterior basal segment with those in eight healthy subjects and in four patients with normoxemic cirrhosis. With thin-section CT, the ratio of segmental arterial diameter to adjacent bronchial diameter in the right lower lobe in four patients with hepatopulmonary syndrome was compared with that in four patients with normoxemic cirrhosis. RESULTS: In patients with hepatopulmonary syndrome, the peripheral pulmonary vasculature was significantly dilated compared with that in control subjects and in patients with normoxemic cirrhosis (P = .002); however, the central pulmonary arteries were not significantly dilated (P > .05). At thin-section CT, the ratio of segmental arterial diameter to adjacent bronchial diameter was significantly greater than that in patients with normoxemic cirrhosis (P < .05). CONCLUSION: In patients with hepatopulmonary syndrome, the peripheral pulmonary vasculature is significantly dilated. Dilatation of the peripheral pulmonary vasculature may be helpful in the diagnosis of hepatopulmonary syndrome.

Limited blood-brain barrier transport of polyamines.

Transport of polyamines across the blood-brain barrier of adult rats was examined by measuring the amount of radioactivity that reached the forebrain 5 s after a "bolus" intracarotid injection. The values were expressed by the brain uptake index (BUI), which is the percentage of material transported in relation to freely diffusible water in a single passage through the brain. Transport was restricted as indicated by the respective BUI values, presented as means +/- SD (number of animals): putrescine, 5.3 +/- 0.8 (11); spermidine, 6.1 +/- 1.3 (7); and spermine, 5.8 +/- 0.5 (4). A kinetic study of the transport of [14C]putrescine showed that transport due to passive diffusion accounted for the majority of the observed influx (66% at 1 mM putrescine). However, a small saturable component exists with a Km value of 4-5 mM and a Vmax of 30 nmol X min-1 X g-1. This Km value is considerably higher than the circulating levels of the polyamine in the normal mature animal, and thus is unlikely to be of physiological significance. Competition studies indicated that putrescine does not interact with carriers for adenosine, arginine, choline, or leucine.