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Biomedical subjects

F Durand

Publications and source records attributed to F Durand.

At least 91 records · Page 5Linked to original sources
PubMed1995

Transplantation for fulminant and subfulminant hepatic failure with preservation of portal and caval flow.

This article describes experience with preservation of portal and caval flow during orthotopic liver transplantation (OLT) for fulminant or subfulminant hepatic failure (FSHF) as an alternative to venous bypass. As a modification of the standard procedure, hepatectomy and graft implantation were performed with preservation of caval patency in combination with a temporary portocaval shunt. From July 1991 to March 1994, 25 consecutive patients with FSHF underwent OLT with preservation of portal and caval flow. All patients had severe confusion (n = 9) or coma (n = 16) with a mean(s.d.) clotting factor V of 13(5) per cent and a mean(s.d.) serum bilirubin level of 408(151) mumol/l. During the anhepatic phase, haemodynamic data showed a preservation of cardiac filling pressure, mean arterial pressure, and renal perfusion pressure, while the mean(s.d.) urine flow was maintained at 182(120) ml/h. Venous bypass was not required. There were three (12 per cent) deaths after the operation, and all survivors made a full neurological recovery. Normal postoperative creatinine values allowed the early use of baseline immunosuppression. The authors conclude that, in patients with FSHF, successful liver transplantation can be achieved with this technical procedure.

Adult↗
PubMed1995

Preservation of renal perfusion and postoperative renal function by side-to-side cavo-caval anastomosis in liver transplant recipients.

Postoperative renal failure is common after liver transplantation (LT). The aim of this study was to investigate peroperative renal perfusion and postoperative renal function in 12 patients who underwent LT with side-to-side cavo-caval anastomosis (SSCCA). Three phases were considered during the procedure: hepatectomy, the anhepatic phase, and the postreperfusion phase (phases 1, 2, and 3, respectively). Mean arterial pressure, IVC pressure, and renal perfusion pressure were significantly higher during phase 2 than during phases 1 and 3. Cardiac index and pulmonary capillary wedge pressure did not differ significantly during the three phases. Creatinine clearance did not significantly decrease postoperatively. We conclude that SSCCA is associated with both the preservation of renal perfusion pressure during the entire procedure and the preservation of postoperative creatinine clearance. It is, moreover, a technique that results in a low rate of postoperative renal failure after LT.

Adult↗
PubMed1995

Immunostaining for membrane attack complex of complement is related to cell necrosis in fulminant and acute hepatitis.

BACKGROUND/AIMS: Complement activation is one of the mechanisms involved in inflammatory lesions. Initiation of the complement terminal pathway at a cell surface leads to the formation of a cytolytic membrane attack complex. Our study assess whether a membrane attack complex-associated mechanism is involved in liver cell necrosis of fulminant and subfulminant hepatitis. METHODS: Immunostaining for membrane attack complex was compared with immunostaining for cytokeratin and complement inhibitory proteins such as membrane cofactor protein, decay-accelerating factor, and homologous restriction factor in 15 patients with fulminant hepatitis and 5 patients with nonfulminant acute hepatitis. RESULTS: In all patients, hepatocytes surrounding necrotic areas, but not those at a distance, were stained for membrane attack complex, whereas the opposite staining pattern for membrane cofactor protein was observed. In controls, no hepatocyte staining for membrane attack complex was observed, whereas membrane cofactor protein, but not decay-accelerating factor or homologous restriction factor, was detected on hepatocytes. CONCLUSIONS: Complement activation by antibody-dependent or non-antibody-dependent mechanisms might be involved in the pathogenesis of either fulminant or acute hepatitis. Modulation of membrane cofactor protein expression on hepatocytes might contribute to the sensitivity of hepatocytes to membrane attack complex and subsequent cell lysis.

Acute Disease↗
PubMed1995

Ischemic hepatitis due to obstructive sleep apnea.

The case of an obese patient who developed massive centrilobular liver cell necrosis, severe coagulopathy, acute renal failure, and encephalopathy is presented. Hypovolemia and heart failure were absent, but the acute liver disease was associated with severe arterial hypoxemia due to obstructive sleep apnea that was shown by the nocturnal blood oxygen desaturation, the results of the polysomnographic study, and normal baseline pulmonary function tests. In this obese patient, liver cell necrosis was caused by severe liver cell hypoxia secondary to severe arterial hypoxemia as a consequence of obstructive sleep apnea associated with a Pickwickian syndrome. This observation is consistent with the hypothesis that liver ischemia was directly related to severe arterial hypoxemia.

Female↗
PubMed1995

[Development of a control method for sample distributors].

The use in routine of distribution automations in Blood Bank laboratories should imply regular testing of the equipment by users. This work was carried out on Microlabs as well as on an IEMS. We used a coloured solution (Alizarine Red in pH9 buffer). We applied the Beer-Lambert law, knowing that any volume modification induces a change in optical density. After testing the linearity of the photometers used in the laboratory, we set up 4 distribution programmes so as to simulate classic distribution of diluted or undiluted serum: 1) for large volume dispensing, 2) for small volume distribution in a small amount of buffer, 3) for distribution of small volumes in large buffer volumes, 4) a specific IEMS programme. Results, expressed as coefficients of variation (CV) for each volume, varied from 9.8 to 0.7% according to the programme. These results show that large volume distribution does not pose any problem (CV < 5%). When dilution occurs, the error observed in serum distribution adds up to that of the thinner, and the smaller the two volumes, the greater is the error. It therefore appears necessary to find the best compromise between serum volume and thinner volume to obtain a CV < 5%. This error may appear negligible in semi-quantitative tests, but it may be important in quantitative tests. Lastly, this programme can easily be adapted in routine to monitor the dispensers efficiently.

Blood Specimen Collection↗
PubMed1995

[Development of a validation method for readers of ELISA microplates].

The results, either positive or negative, of the ELISA tests performed on blood donors to detect viral markers, are always validated by reading microplates on photometers. In Rennes, these microplates can be read on MR 7000 (Dynatech) or IEMS (Labsystems) photometers. This step, the last one in the technical sequence, conditions the results. Regular checking of the photometers therefore may enhance the quality of the testing sequence. To check the quality of the photometers, we use a 96-well microplate, the "Universal Calibration Test Plate" marketed by BIO-TEK Instruments USA. The plate includes 8 blank wells, 6 wells equipped with glass filters (3 stained and 3 unstained). This plate comes with a table showing the optical density in relation to the wavelength. We first verify the repeatability of each photometer, and secondly, verify accuracy. The plate also permits verifying the linearity of each photometer. In view of the results, we were able to state that both photometers were accurate, since the results obtained were compatible with an optical density of +/- 0.024 +/- 1%. Do. The tests are repeatable, with a variation coefficient below 0.5%, linearity was verified (r: 0.999 for both photometers). Reading the plate only takes a few minutes and permits daily control of the photometers. It only requires that the test results be reported on a control card to follow-up possible deviations, and technical maintenance can thus be carried out immediately.

Calibration↗
PubMed1995

Hemodynamics after orthotopic liver transplantation: study of associated factors and long-term effects.

Among 68 liver transplant recipients, 190 hemodynamic studies were performed to evaluate the role of sepsis, anemia, acute graft rejection, and persistent portosystemic shunts. The hemodynamic outcome after orthotopic liver transplantation (OLT) in stable patients was also determined. Patients with sepsis showed a significant increase in cardiac index (5.1 +/- 0.9 vs. 3.4 +/- 0.7 L/min m2) and hepatic venous pressure gradient (6.3 +/- 2.9 vs. 3.3 +/- 2.1 mm Hg), compared with patients without sepsis. Cardiac index was higher in patients with, than in patients without, anemia (4.1 +/- 0.6 vs. 3.0 +/- 0.6 L/min m2). The hepatic venous pressure gradient was higher in patients with than in patients without acute graft rejection (5.1 +/- 2.9 vs. 2.6 +/- 1.2 mm Hg). Among patients with acute rejection, the hepatic venous pressure gradient was higher in patients with severe rejection than in those with moderate or mild rejection (7.2 +/- 3.3 vs. 4.6 +/- 2.4 and 2.8 +/- 0.9 mm Hg). In the postoperative period, in patients undergoing transplantation for acute liver failure, the hepatic blood flow was normal and significantly lower than in patients receiving transplant for cirrhosis (1.15 +/- 0.37 vs. 1.96 +/- 0.71 L/min). In patients undergoing transplantation for cirrhosis, cardiac index, azygos, and hepatic blood flows significantly decreased after 1 year compared with the first 6 postoperative months. Multivariate analysis showed that sepsis, anemia, and time after OLT were independent variables influencing cardiac index. Sepsis, time after OLT, and the existence of portosystemic shunts were independent variables influencing hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Deleterious influence of pyrazinamide on the outcome of patients with fulminant or subfulminant liver failure during antituberculous treatment including isoniazid.

Isoniazid and pyrazinamide are well-known hepatotoxic drugs, often used in combination. The aim of this study was to assess the prognostic influence of pyrazinamide on the outcome of fulminant or subfulminant liver failure caused by antituberculous therapy. Eighteen patients with fulminant or subfulminant liver failure due to antituberculous therapy were studied. Nine patients received isoniazid and rifampicin without pyrazinamide (group 1), and nine patients received isoniazid and rifampicin together with pyrazinamide (group 2). The severity of fulminant and subfulminant liver failure, as judged by the prevalence of coma and the lowest level of factor V, was similar in the two groups. Spontaneous survival was greater in group 1 (eight of nine) than in group 2 (two of nine) (P < .02). The authors conclude that pyrazinamide co-administration was associated with an increased mortality in patients with fulminant or subfulminant hepatitis occurring during antituberculous therapy. In these patients, pyrazinamide administration and an interval of more than 15 days between the onset of antituberculous treatment and jaundice, combined with grade III encephalopathy and factor V below 20%, predicted death without liver transplantation.

Adolescent↗
PubMed1994

Systemic release of interleukin-10 during orthotopic liver transplantation.

Experimental and clinical observations indicate that the liver allograft is less immunogenic than other organ transplants and can promote immune tolerance. Because interleukin-10 recently emerged as a macrophage and T-cell-derived cytokine with potent immunosuppressive properties, we studied its production in 28 patients undergoing orthotopic liver transplantation. Plasma levels of immunoreactive interleukin-10 dramatically increased within 2 hr after liver allograft reperfusion, with peak levels ranging between 214 and 4998 pg/ml (median = 677 pg/ml). This systemic release of interleukin-10 was transient because it returned to low levels by 48 hr (range = 26 to 51 pg/ml). The higher interleukin-10 levels measured in right atrial blood as compared with portal blood indicated that interleukin-10 was most likely synthesized within the liver graft. To get insight into the cellular origin of interleukin-10, we also measured serum levels of interleukin-4 and interferon-gamma, both produced by T cells, and interleukin-8, a cytokine secreted by macrophages, in eight patients. Interleukin-4 and interferon-gamma levels remained undetectable in most of the patients, whereas interleukin-8 levels paralleled those of interleukin-10. Portal endotoxemia was probably not involved in interleukin-10 production because endotoxin levels remained low (< 20 pg/ml) before and after liver allograft reperfusion. Interleukin-10 plasma levels did not correlate either with cold ischemia time or with the occurrence of rejection episodes. We conclude that orthotopic liver transplantation is associated with a massive release of interleukin-10 and interleukin-8, most likely produced by allograft macrophages.

Adult↗
PubMed1994

Expression of complement-regulatory proteins in normal and UW-preserved human liver.

BACKGROUND/AIMS: Somatic cells are protected against complement-mediated injury by specialized membrane proteins, known as complement-regulatory proteins (CRP). The knowledge of the pattern of CRP expression in the liver is important to evaluate the role of complement-mediated injury in graft rejection. METHODS: We determined the distribution of four main CRP: membrane cofactor protein (MCP), decay accelerating factor (DAF), protectin, and complement receptor 1 (CR1) in 30 histologically normal livers, 13 samples from University of Wisconsin cold-storage solution (UW)-preserved tissue and 17 postoperative biopsies of UW-preserved allografts. RESULTS: In normal liver, hepatocytes expressed only MCP. Bile duct cells were reactive for MCP and protectin. Sinusoidal endothelial cells expressed MCP and protectin but displayed no or faint expression of DAF. Endothelial cells of portal vessels and centrilobular veins expressed high levels of DAF, MCP, and protectin. No expression of CR1 was observed. No change in CRP expression was usually detected after UW preservation, except for protectin, induced on hepatocytes in 9 samples of UW-preserved liver tissue and in 9 allografts. CONCLUSIONS: Hepatocytes and sinusoidal endothelial cells, which have a defective expression of CRP, might be at risk for complement-mediated injury. However, this risk is not aggravated after UW preservation.

Adenosine↗
PubMed1994

Expression of cytokine-dependent adhesion molecules in postreperfusion biopsy specimens of liver allografts.

BACKGROUND/AIMS: Allogeneic recognition of donor cells by host T lymphocytes requires the expression of cytokine-dependent molecules, such as class II major histocompatibility antigens, intracellular adhesion molecule 1 (ICAM-1), and lymphocyte function-associated antigen 3 (LFA-3). In the liver, activation of Kupffer cells after ischemic injury during the transplantation procedure may result in an early induction of cytokine-dependent molecules. METHODS: The pattern of induction of ICAM-1, HLA-DR, HLA-DQ, and LFA-3 was investigated in 30 postreperfusion surgical biopsy specimens of liver allografts by an immunohistochemical technique. RESULTS: Two patterns of induction were observed: focal or diffuse. On hepatocytes, ICAM-1 was induced in 22 cases (11 focal, 11 diffuse), HLA-DR in 18 cases (13 focal, 5 diffuse), HLA-DQ in 13 cases (3 focal, 10 diffuse), and LFA-3 in 1 case (focal). On bile duct cells, HLA-DR was expressed in 19 cases, associated with HLA-DQ in 7 cases. No induction of ICAM-1 and LFA-3 was detected. Compared with the other patients, the group of patients with diffuse postoperative hepatocellular induction of ICAM-1 was characterized by higher preharvesting serum transaminase levels in the donor (P < or = 0.001), suggestive of preoperative ischemic injury, and increased incidence of acute graft rejection (P = 0.04). CONCLUSIONS: Preoperative warm ischemia may modify the immunogenicity of liver allografts.

Adult↗
PubMed1994

Interleukin-6: an early marker of bacterial infection in decompensated cirrhosis.

Fifty-seven patients with decompensated cirrhosis were studied prospectively to assess the sensitivity and specificity of early clinical or biological signs of bacterial infection. Among them, 19 had proven infection on admission (7 spontaneous bacterial peritonitis, 5 bacteraemia, 3 urinary tract infections, 2 pneumonia, 1 dental abscess and 1 cholangitis). Fever, polymorphonuclear cell count, fibrinogen and C-reactive protein levels were found to be of little or no help in diagnosing bacterial infection on admission. Interleukin-6 plasma levels were, however, significantly different between infected (median: 1386 pg/ml, range: 237-20,000) and non-infected patients (median: 34 pg/ml, range: 0-4500, p < 0.00001). Levels above 200 pg/ml were always found in infected patients, giving a sensitivity of 100% and a specificity of 74%. C-reactive protein correlated weakly with interleukin-6 levels, indicating a defective acute-phase response in cirrhosis. Tumor necrosis factor alpha plasma levels were less sensitive (95%) and specific (68%) for the diagnosis of bacterial infection at a threshold of 50 pg/ml, but were more closely related to a poor patient outcome. In decompensated cirrhosis, interleukin-6 plasma levels on admission provided the most sensitive and specific tool for the diagnosis of bacterial infection.

Adult↗
PubMed1994

[Hyperthyroidism: a possible factor of cholestasis associated with hyperemesis gravidarum of prolonged evolution].

We report two cases of hyperemesis gravidarum with hyperthyroidism and jaundice. The cessation of vomiting associated with supportive care was followed by complete recovery in 5 weeks. Hyperthyroidism occurs in 60% of hyperemesis gravidarum, but jaundice is uncommon. The association of jaundice and hyperthyroidism suggests that hyperthyroidism is a possible factor of cholestasis in patients with hyperemesis gravidarum.

Adult↗