[STUDY ON THE MECHANISM OF THE ORIGIN OF BANTI'S SYNDROME].
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The data obtained in a retrospective analysis, angiographic and hepatoscintigraphic examinations of 86 patients (aged from 12 to 64 years) with liver cirrhosis (LC) treated during the period from 1998 through 2003 were analyzed. Among them there were 64 men and 22 women. The investigations performed have shown that the angiographic data obtained in LC patients determine not only the topographic interaction of the major and collateral vessels of the porto-lienal pool that is of principal significance in the decision for the method of surgical correction in portal hypertension but also allow an estimation of the picture of the hepatopetal blood flow inversion. The data obtained allowed the authors to define three degrees of reduction of the hepatopetal blood flow. A conclusion was made that the degree of reduction of the hepatopetal blood flow when compared was the findings of angiographic and radionuclide examinations were of great prognostic significance for an estimation of the necessary decompression and possible maximal preservation of the hepatopetal blood flow with respect to the preoperative level.
In anesthetized patients during abdominal surgery, hepatic artery and portal vein flows were measured simultaneously utilizing an ultrasonic transit-time volume flowmeter. The total hepatic blood flow was 994.6 +/- 52.4 ml/min. The hepatic artery flow and the portal vein flow were 260.0 +/- 23.8 ml/min and 730.8 +/- 41.3 ml/min, respectively. The ratio of hepatic artery flow to portal vein flow was 0.37 +/- 0.04. A significant increase in hepatic artery flow (p less than 0.01) followed portal vein occlusion, whereas no significant change was observed in portal vein flow after hepatic artery occlusion. Common hepatic artery occlusion resulted in a significant decrease in hepatic artery flow (p less than 0.05), but no significant change was observed in portal vein flow. The present study firstly demonstrated that ultrasonic transit-time volume flowmeter is a device to quantitatively assess hepatic artery and portal vein flows with good reproducibility and stability in human subjects. This easy and simple technique seemed to have wide clinical application to abdominal surgery and would have a promising in studying splanchnic blood flows in various situations such as in cases of hepatectomy and portal hypertension.
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In 1982 Weinstein coined the term HELLP syndrome to describe a special group of pre-eclamptic women who had evidence of hemolysis, elevated liver enzymes and low platelets. The question of whether the HELLP syndrome exists as a distinct entity or is a part of a spectrum of pregnancy complications has long been a source of speculation and debate among obstetricians and internists. A review of the literature indicates that the syndrome occurs in post-partum from 20% to 30% of the cases; maternal mortality from 1% to 4% and perinatal mortality from 5% to 40%. Hypertension and proteinuria are frequently associated with HELLP syndrome, but may also be absent. The syndrome is a group of clinical and pathological manifestations resulting from an insult that leads to intravascular platelet activation (thrombocytopenia) and micro-angiopathic hemolytic anemia (elevated total bilirubin and LDH). Endothelial damage and vasospasm are responsible of hepatic hypoperfusion that results in liver damage, as indicated by a rise in circulating liver enzymes. Since natural evolution of HELLP syndrome is the disseminated intravascular coagulation (CID), the interruption of pregnancy is mandatory and irrespective of the gestational age. This is the reason of an high incidence of cesarean section. Visser and Wallemburg (1995) treated 128 pre-eclamptic patients with HELLP syndrome with volume expansion and pharmacologic vasodilatation under invasive haemodynamic monitoring; they tried to delay delivery with the aim of enhancing fetal maturity. A complete reversal of HELLP occurred in 43% of patients. Further investigations will be necessary to confirm this interesting experience.
A number of circulating breakdown products of collagen or other components of extracellular matrix, matrix degrading metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) have been proposed as markers of hepatic fibrosis. However, the published results lack consistency. Since many of the patients with fibrosis studied were alcoholics, the question was raised whether recent alcohol consumption may affect the results obtained. Using sandwich-type assays of radioimmunoassay technology with corresponding antibodies, we studied eight markers of liver fibrosis: laminin, tenascin, undulin, TIMP-1, collagen VI, procollagen type III (PIIINP), hyaluronic acid (HA) and MMP-2. A group of 10 alcoholics was studied after significant alcohol consumption and following 2 weeks of abstinence, verified with repeated breath alcohol measurement. Laminin was significantly reduced at 1 week (22%) and at 2 weeks (30%). Similarly, tenascin and undulin were also significantly decreased. By contrast, TIMP-1, collagen VI, PIIINP, HA and MMP-2 did not significantly change. The mode of action of alcohol on these tests is unknown. These differences must be considered when using those measurements to assess liver fibrosis.
There is much debate about the way in which epithelial tumors metastasize. It has been proposed that the bone marrow (BM) acts as a tumor cell reservoir. We injected human hepatocellular carcinoma (HCC) cells (Mahlavu cell line) into the livers, circulation or BM of NOD/SCID mice and circulating tumor cells were quantified. When injected under the Glisson capsule, a primary tumor developed and continuously yielded circulating tumor cells. Liver tumor removal led to a very low level of Mahlavu cells both in blood and BM 30 days later. When Mahlavu cells (cultured or from BM of primary mice femurs) were intravenously injected into mice, the number of cells in the bloodstream (BS) steadily decreased, whereas the BM was not significantly colonized. When Mahlavu cells were directly injected into one femur, the controlateral femur was not colonized. Microscopic analysis and a sensitive PCR assay (<1 Mahlavu cell/nuclear cells) both failed to detect human tumor cells in other organs regardless of injection route. In conclusion, our model strongly supports the hypothesis that HCCs continuously release cells into the BS. However, in sharp contrast with the current hypothesis, the BM is not specifically colonized by tumor cells but could store them at a very low level.
Circulating liver membrane antibodies (LMAb) were examined in 71 patients with non-insulin-dependent diabetes mellitus (NIDDM) without liver dysfunction and 16 cases of KK mouse as a model of obese diabetic animals. LMAb were detected in 10 NIDDM patients (14.1%). Fasting blood glucose, glycosylated serum albumin (G-Alb), and glycosylated hemoglobin A1 (HbA1) levels were compared with LMAb-positive and negative groups. The G-Alb levels and HbA1 levels of the LMAb-positive group were significantly higher (p less than 0.05 and p less than 0.01, respectively) than those of the LMAb-negative group. In addition, there were no differences in histological findings in KK mouse liver between the LMAb-positive and negative cases. These results revealed that the state of continued high blood glucose directly or indirectly influence the autoimmunity and clinical features of NIDDM patients.
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BACKGROUND/AIMS: Tolerance of damaged rat livers for intermittent ischemia was assessed. Clinically, tolerance of operative ischemia by diseased livers, long thought minimal, is being reexamined. METHODOLOGY: A rat model using 0.04% thioacetamide-induced liver damage followed by pedicle occlusion was used to study partial hepatic ischemia in injured livers in terms of survival, hepatic tissue blood flow, beta-ATP content, liver enzymes and histology. Prior to continuous ischemia (150 min) or intermittent ischemia (alternating every 15 min with reperfusion for 10 cycles) animals were divided into mild (B) and severe (A) thioacetamide-induced injury groups according to the hepatic clearance rate of indocyanine green from plasma. RESULTS: The survival rates for 1 week after intermittent ischemia were 43%, 77%, and 93% in groups A and B and in controls (group C), respectively. No group A or B animals receiving continuous ischemia survived. Hepatic tissue blood flow and liver beta-ATP levels in serum were significantly higher in group A than in other groups. Marked damage also was observed histologically in group A. CONCLUSIONS: Intermittent liver circulation blockage may be relatively safe in a damaged liver, but a more severe degree of damage predisposes to serious ischemia-reperfusion injury.