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Biomedical subjects

P Caraceni

Publications and source records attributed to P Caraceni.

At least 37 records · Page 2Linked to original sources
PubMed1998

Prevention of reoxygenation injury by sodium salicylate in isolated-perfused rat liver.

Sodium salicylate can be used as a chemical trap for hydroxyl radicals, the most damaging reactive oxygen species. Because reactive oxygen species are involved in the pathogenesis of hepatic hypoxia/reoxygenation injury, the goal of this study was to determine if trapping hydroxyl radicals with salicylate would prevent or at least ameliorate such injury. Isolated rat livers, continuously perfused with Krebs-Henseleit bicarbonate buffer in the presence or absence of salicylate (2 mM), were exposed, after 30 min of recovery, to 60 min of hypoxia, followed by 30 min of reoxygenation. During reoxygenation, control livers experienced a sharp increase in the rate of lactic dehydrogenase release, taken as index of cell injury, protein carbonyl content, and malondialdehyde, taken as index of protein oxidation and lipid peroxidation, respectively. The presence of salicylate in the solution perfusion significantly reduced the rate of lactic dehydrogenase release, protein carbonyl content, and malondialdehyde production during reoxygenation. Hepatic histology documented a significantly reduced cell injury in salicylate-perfused livers compared to control livers. These data suggest that the hydroxyl radical chemical trap sodium salicylate, acting as an antioxidant, may represents an effective agent to reduce liver injury due to hypoxia/reoxygenation in a model of isolated-perfused rat liver.

Animals↗
PubMed1998

Lamivudine treatment for acute hepatitis B after liver transplantation.

BACKGROUND/AIMS: Acute hepatitis caused by recurrent or de novo hepatitis B virus (HBV) infection after liver transplantation frequently induces aggressive disease leading to liver failure. The aim of this study was to determine the efficacy and safety of lamivudine treatment in post-transplant acute hepatitis B. METHOD: Twelve patients with acute hepatitis B were started on lamivudine 100 mg p.o. daily within 8 weeks of the appearance of HBsAg. One patient was excluded after 1 month because of hepatocellular carcinoma recurrence. Patients were followed for an average of 68.6 weeks (range 32-108), and were clinically and biochemically evaluated on a monthly basis. They had a histological assessment at baseline, after at least 6 months, and whenever clinically indicated. RESULTS: Basal HBV-DNA ranged between 13 and 1288 pg/ml and serum alanine aminotransferase between 97 and 1036 U/l. HBV-DNA became undetectable within 8 weeks and transaminases normalized within 24 weeks in all cases. At the last visit, eight patients (73%) remained HBV-DNA negative by liquid hybridization and had normal or close to normal alanine aminotransferase. Five patients (45%) were also HBsAg negative and HBV-DNA negative by polymerase chain reaction. HBV-DNA and transaminase breakthrough occurred in three patients (27%). Histology after 6-9 months showed chronic hepatitis in seven patients. Lamivudine was well tolerated without serious adverse reactions. CONCLUSIONS: These results indicate that lamivudine treatment induces sustained inhibition of viral replication and normalization of transaminases in the majority of post-transplant patients with acute hepatitis B. HBsAg loss may be achieved in a considerable number of cases. Although viral resistance is relatively frequent, early initiation of lamivudine appears to be effective and safe.

Acute Disease↗
PubMed1997

Rat hepatocytes isolated from alcohol-induced fatty liver have an increased sensitivity to anoxic injury.

The aim of this study was to determine whether rat hepatocytes isolated from steatotic or nonsteatotic livers have different thresholds for injury due to anoxia-reoxygenation. Rats were fed ethanol or control diets for 8 weeks. Histology showed that more than 75% of the hepatocytes in alcohol-fed and less than 3% in control animals contained fatty vacuoles. The glycogen content was significantly reduced in steatotic livers. Isolated hepatocytes were cast in agarose gel threads and perfused with Krebs-Henseleit bicarbonate buffer. Cell viability was determined by Trypan Blue (TB) exclusion; cell injury was determined by lactate dehydrogenase (LDH) release; and superoxide anion (O2.-) was determined by lucigenin-enhanced chemiluminescence (LCL). During the pre-anoxic basal perfusion the following occurred: viability was 86% +/- 1% and 85% +/- 1%; LDH release was 16 +/- 3 and 15 +/- 3 mU/min; and LCL was 4 +/- 1 and 5 +/- 1 nA in steatotic and nonsteatotic hepatocytes, respectively. Cell viability decreased slightly under 4 hours of aerobic perfusion without differences between the two groups. In contrast, fatty hepatocytes died much faster than did control hepatocytes during anoxia; after 3 hours viability was 17% +/- 8% vs. 60% +/- 2% (P < .001), respectively. With reoxygenation following 2 hours of anoxia, the changes in viability, in LDH release, and in LCL were similar in both groups. These results indicate that in hepatocytes isolated from alcohol-fed rats when compared with control hepatocytes: 1) cell viability under aerobic conditions is not influenced; 2) anoxic injury is significantly increased; 3) a reduction in the hepatic glycogen stores, which may contribute to the enhanced sensitivity to anoxia, can be demonstrated; and 4) O2.- generation and cell injury occurring immediately after reoxygenation do not appear to be affected.

Animals↗
PubMed1997

Daily profile of plasma endothelin-1 and -3 in pre-ascitic cirrhosis: relationships with the arterial pressure and renal function.

BACKGROUND/AIMS: Measurements of plasma endothelin-1 and -3 in pre-ascitic cirrhosis have provided controversial results. Similarly, the role of the endothelin system in the pathogenesis of volume and hemodynamic disturbances of cirrhosis is still debated. To provide a further insight into this issue, we assessed the daily fluctuations of plasma endothelins and their relationship with arterial pressure and renal function in pre-ascitic cirrhosis. METHODS: Endothelin-1 and -3, plasma renin activity, atrial natriuretic peptide, noradrenaline and mean arterial pressure were measured at 11 pm, 7 am, 9 am and 6 pm in 10 patients with pre-ascitic cirrhosis and in 10 healthy subjects on normal sodium diet and carrying on their usual activities (supine from 10 pm to 7 am, standing and mobile after 7 am). Glomerular filtration rate and daily renal sodium excretion were assessed during the supine period, and from 7 am to 12 am and from 12 am to 10 pm during the standing period. RESULTS: Endothelin-1 was higher in patients than in control subjects (p=0.000) and did not change during the study. Endothelin-3 was also higher in patients (p=0.002) and showed slight fluctuation in control subjects. The mean daily level of plasma renin activity was lower (p=0.016) and that of atrial natriuretic peptide higher (p=0.000) in patients with cirrhosis. Norepinephrine and mean arterial pressure did not differ significantly between the two groups. No correlations were found between endothelins and either hemodynamic or neuro-hormonal and renal function parameters in the two groups. CONCLUSIONS: Despite the presence of increased effective volemia (as suggested by the reduced plasma renin activity and elevated atrial natriuretic peptide) and normal adrenergic tone, patients with pre-ascitic cirrhosis show elevated levels of endothelin-1 and endothelin-3 throughout the day. In early cirrhosis circulating endothelins, although elevated, do not appear to play a more prominent role in setting arterial pressure than in normal subjects, and endothelin elevation is not detrimental to renal function.

Adult↗
PubMed1997

Proteins but not nucleic acids are molecular targets for the free radical attack during reoxygenation of rat hepatocytes.

Isolated rat hepatocytes generate large amounts of reactive oxygen species and suffer a significant cell injury during postanoxic reoxygenation. The aim of this study was to determine whether oxidation of proteins and nucleic acids occurs during reoxygenation and whether their damage is related to the development of hepatocyte injury. Isolated perfused rat hepatocytes were exposed sequentially to 1 h of aerobic control, 2.5 h of anoxia, and 2 h of reoxygenation. Protein oxidation was determined by measuring the hepatocyte protein carbonyl content. DNA and RNA oxidation was assessed by measuring the 8-hydroxydeoxyguanosine and 8-hydroxyguanosine adducts, respectively. The control preanoxic carbonyl content was 6.48 +/- 1.03 nmol/mg protein. The preanoxic 8-8 hydroxydeoxyguanosine and 8-hydroxyguanosine levels were 4.76 +/- 1.22 pmol/ml and 14.19 +/- 2.17 pmol/ml, respectively. During anoxia, protein and nucleic acid oxidation did not change significantly. With reoxygenation, the protein carbonyl content increased significantly within 30 min, reaching a value of 10.25 +/- 1.58 nmol/mg. The nucleic acid oxidation level remained stable. Perfusion with 100 muM of during reoxygenation abolished protein oxidation. These results indicate that in rat hepatocytes during the early phase of reoxygenation: (1) the protein oxidation level increased significantly above the preanoxic aerobic values; (2) DNA and RNA oxidation does not appear to occur; and (3) free metal-mediated free radical reactions are involved in the oxidative protein damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Oxygen free radical content and neutrophil infiltration are important determinants in mucosal injury after rat small bowel transplantation.

Mucosal injury is an immediate event following revascularization of small intestinal grafts in the context of transplantation (SBTx). The generation of oxygen free radicals (OFR) and tissue infiltration by activated neutrophils are consequences of ischemia and reperfusion and known causative factors of tissue injury; to delineate their role in the reperfusion injury occurring after cold preservation of the intestine and subsequent transplantation was the aim of this study. Prior to orthotopic SBTx in Sprague-Dawley rats, grafts were stored in cold (4 degrees C) Ringer's lactate solution for 1 (n=6), 2 (n=7), and 4 hr (n=7). Small bowel biopsy specimens were obtained before harvesting, at the end of the (cold) ischemic period and immediately before unclamping (i.e., before revascularization) and 30, 60, 120 min, and 24 hr after transplantation to evaluate tissue injury by histology, OFR production, (measured by luminol-enhanced chemiluminescence [LCL]), and the degree of neutrophil infiltration by myeloperoxidase staining. Reperfusion of the graft significantly worsened the histologically graded mucosal injury compared with that seen before unclamping. However, 24 hr after engraftment, mucosal morphology was restored almost completely. OFR production increased significantly during the early phases of reperfusion (30, 60, and 120 min) and returned to control values after 24 hr. Reperfusion of the graft was associated with a marked increase in the number of mucosal neutrophils. The present study indicates that OFR production and neutrophilic infiltration commence and progressively increase with graft reperfusion. These changes parallel the mucosal injury. Ischemic intervals of 4 hr were not associated with a statistically significant greater ischemic-injury patterns compared with 1- and 2-hr intervals. The profound changes associated with reperfusion probably overshadow the minor, yet likely, progressive injury patterns associated with longer ischemia times.

Animals↗
PubMed1996

Clinical and pathologic features of hepatocellular carcinoma in young and older Italian patients.

BACKGROUND: It is not known whether putative etiologic factors and clinical and pathological features of hepatocellular carcinoma (HCC) differ between young adult and older white patients. METHODS: We examined the characteristics of 498 consecutive patients with HCC age < 50 years (Group 1: 54 patients) and age > or = 50 (Group 2: 444 patients), an age beyond which the tumor occurrence rate briskly increases. RESULTS: Demographic characteristics, alcohol and coffee intake, and cigarette smoking did not differ between the two groups. Group 1 had a greater prevalence of the hepatitis B surface antigen (HBsAg) carriers (P = 0.006), while the prevalence of either past hepatitis B virus infection (P = 0.008) or antivirus C antibodies (P = 0.016) was higher in Group 2. The lack of both hepatitis B and C virus serologic markers was more common in Group 1 (P = 0.018). In these patients, HCC was less frequently superimposed on cirrhosis (P = 0.002) and was more advanced at the time of diagnosis. In fact, despite a better histologic differentiation grade (P = 0.019), monofocal (solitary and massive) tumors were larger (P = 0.012), small lesions (< or = 5 cm) less frequent (P = 0.028), and either diffuse (P < 0.001) or massive (P = 0.011) types more common. An elevation of serum alpha-fetoprotein was less frequent in group 1 (P = 0.016), but this difference disappeared when the "diagnostic" cut-off of 400 ng/mL was considered. Albeit the prevalence of presenting symptoms did not significantly differ between the two groups, the clinical stage was more advanced in young patients (P = 0.004). The 9-year cumulative rate of survival was similar in the 2 groups. CONCLUSIONS: An early exposure to the virus and/or an accelerated hepatocarcinogenesis in HBsAg carriers can be inferred. Moreover, in the period of life at low risk for hepatoma: (1) the impact of nonalcoholic chemical carcinogenesis seems to be greater; (2) the tumor occurrence is less dependent on cirrhosis development; (3) although histologically better differentiated, the neoplasm is more advanced at the time of diagnosis; and (4) the long term survival is similar to that of the patients age 50 years or older.

Adolescent↗
PubMed1996

Effect of ethanol on adenosine triphosphate, cytosolic free calcium, and cell injury in rat hepatocytes. Time course and effect of nutritional status.

The events implicated in the early phases of acute ethanol-induced hepatocyte injury and their relation with the nutritional status of the liver are not clearly defined. We aimed to determine the effect of ethanol on ATP and cytosolic free Ca2+ in hepatocytes isolated from fed or fasted rats. Cell injury was assessed by LDH release and trypan blue uptake, ATP by [31P]NMR spectroscopy, and cytosolic free Ca2+ with aequorin. In control conditions, cells from fasted animals had a lower ATP level (-52%) and a higher cytosolic free Ca2+ (+101%) than did those isolated from fed animals. Ethanol caused a dose-dependent cell injury in both groups. At all ethanol doses, greater, damage occurred when using hepatocytes isolated from fasted rats. In both groups, a dose-dependent decrease in ATP content and a rise in cytosolic free Ca2+ were seen. The magnitude of these changes were significantly greater in the fasted group. In conclusion, these data showed that fasting affects the energy status and cytosolic free calcium level in hepatocytes; ethanol causes a dose-dependent cell injury that occurs in association with a fall in ATP and a rise in cytosolic free Ca2+ levels. The nutritional status of an animals is an important determinant of the severity of ethanol-induced damage to liver cells.

Adenosine Triphosphate↗
PubMed1996

Biochemical and 31P-NMR spectroscopic evaluation of immobilized perfused rat Sertoli cells.

Cell immobilization and perfusion are used for physiologic studies of Sertoli cells with phosphorus 31 nuclear magnetic resonance (NMR) spectroscopy and biochemical methods. In this study the 31P NMR spectra of Sertoli cells isolated from 18-to 21-day-old rats and immobilized in agarose threads continuously perfused with oxygenated Dulbecco's modifed Eagle medium were obtained at 81 MHz on an NMR system. Cytosolic Ca2+, intracellular Mg2+, lactate and pyruvate, and oxygen consumption were measured with standard biochemical methods. Perfused Sertoli cells maintain a stable intracellular adenosine triphosphate concentration for more than 10 hours. Sertoli cells placed in cold storage overnight and then subjected to perfusion partially regenerate cellular adenosine triphosphate levels. Sertoli cells consume an average of 4.8 +/- 0.4 nmol O2/min/10(6) cells and maintain average ambient lactate and pyruvate levels of 7.1 +/- 0.8 mg/dl and 0.65 +/- 0.05 mg/dl, respectively, with a lactate/pyruvate ratio in the range 8 to 12. The basal Ca2+(i) of Sertoli cells is 98 +/- 0.7 nmol/L (n = 58), which declines to a level less than 10 nmol/L when the Sertoli cells are perfused with a calcium-free medium. Perfusion of Sertoli cells with a sodium-free medium, with 10(-6) mol/L carbonyl cyanide P-trifluoromethoxy-thenylhydrozone, or with Ca2+ ionophore A23187 at a concentration of 10(-6) mol/L increases the Ca2+(i) to a level of 426 +/- 107 nmol/L, 274 +/- 29 nmol/L, or 282 +/- 57 nmol/L, respectively. A bioreactor for physiologic studies of Sertoli cells in real time with NMR spectroscopy has been developed. These data demonstrate that isolated, immobilized, and perfused Sertoli cells are stable for prolonged periods. In addition, these data suggest that Sertoli cells possess a functional Na+-Ca2+ antiporter and that they sequester extracellular Ca2+ in one or more intracellular compartments.

Animals↗
PubMed1996

[Natural course and physiopathology of ascites in the cirrhotic patient].

Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death.

Ascites↗
PubMed1995

Source of oxygen free radicals produced by rat hepatocytes during postanoxic reoxygenation.

The aim of this study was to determine the cellular source of oxygen free radicals generated by isolated hepatocytes during post-anoxic reoxygenation. Superoxide anions (O2.-) were detected by lucigenin chemiluminescence. Cell damage was assessed by LDH release. During anoxia, the chemiluminescence decreased to background levels while LDH release increased 8-fold. During reoxygenation, O2.- formation increased 15-fold within 15 min then declined towards control levels. LDH release increased from 161 to 285 mU/min in the first 30 min of reoxygenation, then declined toward the control rate. Allopurinol, an inhibitor of the xanthine-xanthine oxidase system, did not inhibit O2.- formation nor LDH release. Antimycin, a mitochondrial complex III inhibitor that does not block O2.- formation, increased both O2.- generation and LDH release 82 and 133% respectively. Diphenyleneiodonium (DPI), a mitochondrial and microsomal NADPH oxidase inhibitor, reduced O2.- and LDH release 60-70%. SOD, which catalyzes the dismutation of O2.- to H2O2, was without effect on O2.- and LDH release, but TEMPO, a stable nitroxide which mimics SOD and easily penetrates the cell membrane, decreased O2.-86% without affecting LDH. These results suggest that mitochondria or microsomes are the principal sites of O2.- production during reoxygenation of isolated hepatocytes, whereas the cytosolic xanthine/xanthine oxidase system is apparently not involved.

Allopurinol↗
PubMed1995

Etiologic factors and clinical presentation of hepatocellular carcinoma. Differences between cirrhotic and noncirrhotic Italian patients.

BACKGROUND: It is not known whether the prevalence of hepatocarcinogenic factors differs between cirrhotic and noncirrhotic patients with hepatocellular carcinoma (HCC) or whether the clinical presentation of HCC in these two groups differs. METHODS: The prevalence of the putative etiologic factors of HCC and its clinical presentation in 373 patients with cirrhosis and 102 without cirrhosis seen from 1981 to 1992 were evaluated. RESULTS: Hepatitis C virus infection (76 vs. 48%, P = 0.003) and both current (22.5 vs. 10%, P = 0.007) and past (50.5 vs. 34.5%, P = 0.045) hepatitis B virus infections were more common in cirrhotic than in noncirrhotic patients with HCC. The absence of exposure to both viruses was much less frequent in the former (7 vs. 40%, P < 0.001). Heavy alcohol intake prevailed in patients with cirrhosis (30 vs. 16.5%, P = 0.01). Alpha-fetoprotein elevation was more common in cirrhotic patients (63% vs. 31%, P < 0.001); however, the prevalence of diagnostic (> 400 ng/ml) levels did not differ significantly (24 vs. 17%) between the two groups. Extrahepatic extension of HCC was more common in noncirrhotic patients (20.5 vs. 6.5%, P < 0.001) and its independent predictors were poor cancer differentiation and absence of cirrhosis. "Asymptomatic" cancers were more frequently encountered with cirrhosis. Abdominal pain was the most common presenting symptom in both groups. Signs of hepatic decompensation prevailed in cirrhotic patients, whereas a "toxic syndrome" dominated the clinical picture of the noncirrhotic patients. CONCLUSIONS: Hepatitis viruses are associated more with carcinogenesis of the cirrhotic than of the noncirrhotic liver. Alpha-fetoprotein is not a sensitive neoplastic marker, particularly in noncirrhotic patients. In the latter, HCC appears more advanced at diagnosis and symptoms of neoplastic toxicity are prominent.

Abdominal Pain↗
PubMed1995

Chronic hepatitis C in patients with normal or near normal alanine aminotransferase levels: the role of interferon alpha 2b therapy.

BACKGROUND/AIMS: Interferon is the only approved therapy for chronic hepatitis occurring as a consequence of an infection with the hepatitis C virus. Because interferon is expensive, has a large number of untoward effects and its efficacy is not guaranteed, many physicians limit their use of this therapy to those with histologically advanced but not end-stage cirrhotic disease. Moreover, most cases are biopsied only after 6 months or more of abnormal alanine aminotransferase levels have been documented. The rationale for this approach to patients with hepatitis C virus infection has not been demonstrated. METHODS: In the present study, a total of 37 patients with alanine aminotransferase levels < 1.5 upper limits of normal (59 IU/l or less) who were HCV-RNA positive by reverse transcriptase polymerase chain reaction, were selected for interferon treatment, having been identified as having hepatitis C virus disease as the result of a screening Ab-HCV test confirmed with a positive radio immune blotting assay. Once identified, each subject underwent a percutaneous liver biopsy and was tested for the presence of HBsAg, Ab-HBs and HBV-DNA. All liver biopsies were read and graded according to the criteria of Knodell et al. Each subject was treated with interferon a2b at a dose of 5 MU administered daily until a response was achieved (a minimum period of 6 months) or until a full year had elapsed. A response was defined as HCV-RNA negativity in serum on three consecutive monthly determinations. The study population consisted of 21 males and 16 females ranging in age from 17 to 72 years (mean 46.7 +/- 2.2 years). Their mean serum alanine aminotransferase level at the initiation of therapy was 37.5 +/- 2.1 IU/l with a range of 10-59 (normal values being 40 IU/l or less). 54% of the subjects were presumed to have acquired their hepatitis C virus infection as a result of a blood transfusion; 32% as a result of prior intravenous drug abuse; and 13% had no identifiable risk factor for hepatitis C virus. Despite having normal or near normal serum alanine aminotransferase levels, 9 subjects had chronic persistent hepatitis, 13 had chronic active hepatitis and 15 had chronic active hepatitis + cirrhosis documented by histopathologic assessment of their liver biopsies. RESULTS: An interferon response was achieved in 5/9 with chronic persistent hepatitis, 11/13 with chronic active hepatitis and 8/15 with chronic active hepatitis + cirrhosis for an overall response rate of 65%. CONCLUSIONS: This study has demonstrated that individuals who: 1) are hepatitis C virus positive with serum alanine aminotransferase levels < 1.5 x upper limits of normal can have histologically advanced liver disease; 2) can respond to interferon therapy defined as clearance of detectable HCV-RNA in serum; and, 3) should be considered for interferon treatment.

Adult↗
PubMed1995

Cryoglobulinemia: a cause for false negative polymerase chain reaction results in patients with hepatitis C virus positive chronic liver disease.

With the introduction of interferon therapy for liver disease due to chronic viral hepatitis, it has become important to test individuals thought to have hepatitis C virus disease for the presence of the virus. Moreover, the current goal of therapy for hepatitis C virus-positive liver disease is to render the individual patient HCV-RNA negative. Recently, it has been reported that as many as one-third of the patients with hepatitis C virus liver disease test positive for the presence of mixed cryoglobulins. Few of these cryoglobulin-positive patients have overt disease manifestations of cryoglobulinemia, such as nephropathy, peripheral neuropathy and vasculitis. Because the cryoglobulins in patients with hepatitis C virus-positive disease are directed at hepatitis C virus epitopes, the precipitation of cryoglobulins from serum samples also effectively removes virus. When the viral carriage rate is low in terms of the number of genomes/unit serum, as occurs in cases that are partially treated, the serum can test negative for hepatitis C virus even by polymerase chain reaction, despite the presence of persistent viremia, if precautions preventing the precipitation of cryoglobulins prior to the removal of the sample for polymerase chain reaction testing are taken. From a group of 75 patients with hepatitis C virus-positive hepatitis seen at our institution in the last year (all HCV-RNA positive), 35% were found to test positive for the presence of cryoglobulins. Importantly, in all cases, the cryoglobulins collected tested strongly positive for HCV-RNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1995

Hemodynamic and renal effects of ascites apheresis, concentration and reinfusion in advanced cirrhosis.

BACKGROUND/AIMS: We studied the effects of ascites apheresis, concentration and reinfusion, a new form of treatment for tense or refractory ascites, on systemic hemodynamics and renal function. METHODS: Twelve patients with advanced cirrhosis (two belonging to Child-Pugh's class B and the remainder to class C) were monitored. They were evaluated under baseline conditions, just after the treatment, and 24 and 48 h after baseline assessment. In addition to systemic hemodynamics--as evaluated by Doppler echocardiography--and renal function, indirect markers of effective volemia, such as atrial natriuretic factor, plasma renin activity and aldosterone concentration, and plasma norepinephrine were also measured. RESULTS: The technique led to significant changes in systemic hemodynamics, such as an increase in stroke volume and cardiac output. However, due to a striking reduction in peripheral vascular resistance, mean arterial pressure also declined. The hemodynamic changes were associated with a parallel increase in atrial natriuretic factor. Despite the reduction in arterial pressure, plasma renin activity also significantly declined, while plasma norepinephrine did not undergo significant changes. Although an improvement in glomerular filtration rate and renal sodium excretion occurred, neither change reached statistical significance. All the hemodynamic, renal and neuro-humoral changes described above subsided almost entirely after 48 h, when no significant changes with respect to baseline values were any longer detectable with the exception of a slight reduction in mean arterial pressure. CONCLUSIONS: In advanced cirrhosis ascites apheresis, concentration and reinfusion enhance central volemia, but an exaggerated peripheral vasodilation largely wastes the potential favourable effect on arterial volemia. As a result, no significant improvement in renal perfusion and sodium excretion can ensue.

Adult↗