Fourteen patients with liver cirrhosis of differing severity participated in a one-dimensional chemical shift imaging 31P MRS study of the liver. Patients were divided into two groups according to the severity of their liver disease using Child's classification and the aminopyrine breath test (AB test). Seven normal volunteers without liver disease acted as controls. The phosphomonester (PME) peak in normal subjects was 4.77% (95% confidence interval, CI: 4.11-5.42) of total phosphorus. The PME peak was significantly elevated in both mild cirrhosis [5.80% (95% CI: 5.46-6.14), p = 0.0051, vs normal subjects] and severe cirrhosis [9.64% (95% CI: 8.71-10.57), p = 0.0002, vs normal subjects and p = 0.001, vs mild cirrhosis]. There was a significant negative linear correlation (r = 0.88, p < 0.01) of PME with the percentage dose of 14CO2 excreted over 2 h in the AB test. pH values in patients with mild cirrhosis [7.45 (95% CI: 7.35-7.55)] but not severe cirrhosis [7.36 (95% CI: 7.25-7.47)] were significantly elevated (p = 0.04) compared to normal subjects [7.29 (95% CI: 7.17-7.41)]. Comparison of the peak area of PME at TR = 0.5 s against that using TR = 5.0 s in cirrhotic liver suggested no reduction in T1 of phosphorus metabolites in cirrhosis. A relationship between the severity of liver cirrhosis and a relative increase in PME was demonstrated and this was not due to a reduction of T1. This study highlights the clinical potential of 31P MRS as a non-invasive means of assessing the severity of liver cirrhosis.

Adult↗

PubMedDate not supplied

CT demonstration of brain infarcts due to deep venous thrombosis in systemic lupus erythematosus.

Rapid development of low density bilateral lesions in the brain due to deep venous thrombosis in Systemic Lupus Erythematosis is described. To the best of our knowledge, this type of symmetry, distribution and appearance of brain infarcts in CT due to deep venous thrombosis has not been reported previously.

Adult↗

PubMedDate not supplied

The effect of vasopressin on hepatic artery flow in the rat.

The effects of vasopressin infusion on hepatic artery flow was studied in rats. Hepatic artery ligation followed by the infusion of vasopressin (0.08 microU/g body weight per min) decreases portal venous flow and liver blood flow. Vasopressin infusion results in an increase in hepatic artery flow and liver blood flow both of which are abolished by subsequent hepatic artery ligation. The increase in hepatic artery flow and the decrease in portal venous flow following the infusion of vasopressin is discussed in relation to the management of patients presenting with bleeding oesophageal varices.

Animals↗

PubMedDate not supplied

Circulating levels of arginine vasopressin before and during the infusion of the hormone in patients presenting with bleeding oesophageal varices.

Circulating levels of antidiuretic hormone (ADH) were measured in patients presenting with bleeding oesophageal varices before and during treatment with arginine vasopressin. There was no significant difference in the circulating levels of ADH before and during treatment with arginine vasopressin in patients in which the hormone successfully controlled haemorrhage and those in which it did not. It is concluded that the failure of vasopressin to control variceal haemorrhage in approximately 40% of patients presenting for treatment cannot be attributed to higher circulating levels of the hormone in these subjects.

Arginine Vasopressin↗

PubMedDate not supplied

Mechanism of action of isosorbide-5-mononitrate in reducing portal pressure in cirrhotic patients with cirrhosis and portal hypertension.

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Humans↗