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Biomedical subjects

D Valla

Publications and source records attributed to D Valla.

At least 127 records · Page 7Linked to original sources
PubMed1991

[Venous thrombosis in gastroenterology].

Venous thrombosis involving the digestive tract affects the suprahepatic veins and the terminal part of the inferior vena cava, the portal vein and its roots. The etiology and diagnosis of this condition have made considerable progress. A thrombogenic disease can now be recognized in 90% of cases of involvement of the suprahepatic veins, and 75% of portal involvements. The most frequent causes are primary myeloproliferative syndromes, paroxysmal nocturnal hemoglobinuria, hereditary deficiency in coagulation proteins and circulating anticoagulants. The cause of involvement of the portal vein also include insults during biliary surgery and abdominal infections, particularly those caused by Bacteroides fragilis. Mechanical involvement due to compression finally plays a minor role in the etiology. Noninvasive techniques of diagnosis are now available, including ultrasound, computed tomography and magnetic resonance imaging. The expression of obstruction of the suprahepatic veins predominantly consists in ascites and hepatomegaly. Thrombosis of the portal vein preserving the mesenteric arches usually remains asymptomatic until the intrahepatic block is revealed by a digestive hemorrhage caused by portal hypertension. Isolate involvement of the splenic vein exceptionally causes the rupture of gastric or esophageal collateral veins. The treatment should combine the prevention of further thromboses by anticoagulants and the specific treatment of the venous obstruction. In case of suprahepatic obstruction, there are several methods of restoring a canal of drainage for hepatic blood. Their indications depend on the patency of the inferior vena cava and of the portal vein. In case of portal obstruction, portal-systemic bypass is feasible only if one of the major roots of the portal vein still is patent.(ABSTRACT TRUNCATED AT 250 WORDS)

Budd-Chiari Syndrome↗
PubMed1990

Protein F. A novel F(ab)-binding factor, present in normal liver, and largely released in the digestive tract during hepatitis.

Significant percentages of patients suffering from non-A non-B hepatitis (43%) and B hepatitis (35%) were found to release an Ig-binding factor in their stools. This factor, which we called "protein F" was less frequently observed (20%) in patients suffering from other liver disorders, and was found in only 6.7% of healthy subjects (p less than 10(-7), less than 10(-4), and less than 0.03, respectively). The specificity of the detection test (a nonimmune ELISA-like assay) was confirmed by inhibition experiments. Binding was located on the F(ab) fragment of Ig, irrespectively of their isotype. Protein F was inactivated by pepsin, neuraminidase, and high concentrations of subtilisin, whereas it was resistant to trypsin and chymotrypsin. Molecular sieving by HPLC indicated an apparent molecular mass of 175 kDa. In preparative SDS-PAGE, the molecular mass was 85 kDa in favor of a dimer disrupted under dissociating conditions. Preparative IEF showed the isoelectric charge to lie between 3.9 and 4.1. Analysis of liver extracts from two patients suffering fron non-A non-B hepatitis, and from a transplant donor, revealed the presence of the factor in the three cases.

Carrier Proteins↗
PubMed1990

[Portal hypertension of extrahepatic origin].

Portal hypertension may be due to a suprahepatic or infrahepatic block. Suprahepatic blocks result in Budd-Chiari syndrome. Their principal cause is myeloproliferative syndromes and invasion of the hepatic veins by a tumour. Their main manifestations are ascites and liver enlargement. Treatment consists of re-establishing the hepatofugal drainage. Infrahepatic blocks are due to obstruction of the portal vein, either by thrombosis facilitated by thrombogenic diseases, or by a tumour. Their main consequences are gastrointestinal hemorrhages. Treatment consists of preventing the rupture of oesophageal varices.

Budd-Chiari Syndrome↗
PubMed1990

Predictive value of whole blood chemiluminescence in patients with alcoholic hepatitis.

Recent reports suggest that ethanol metabolism leads to reactive oxygen intermediates that may be responsible for the lesions observed in alcoholic hepatitis. This study investigated the production of reactive oxygen intermediates in peripheral blood phagocytes of patients with alcoholic hepatitis and attempts to evaluate its predictive value. Using a luminol-dependent chemiluminescence method, reactive oxygen intermediate production was measured directly within microamounts of whole blood, both in the absence (basal chemiluminescence production) and in the presence of phagocyte-stimulating agents including latex, zymosan, phorbol myristate acetate and N-formyl-methionyl-leucyl-phenylalanine. Thirty patients with well-documented and histologically proven alcoholic hepatitis were studied. Pugh's and Child's classification, Orrego's composite clinical and laboratory index and Maddrey's discriminant function were used to assess the prognosis of the liver disease. Patients were followed up monthly for 6 mo. Results were compared with those obtained in 17 patients with nonalcoholic liver disease and in 78 normal control subjects. Basal chemiluminescence production was significantly higher in patients with alcoholic hepatitis than in those with nonalcoholic liver disease and in normal subjects (p less than 0.001). Chemiluminescence responses to latex, zymosan and phorbol myristate acetate were significantly lower in alcoholic hepatitis patients than in normal subjects (p less than 0.001); however, when compared with nonalcoholic liver disease patients, these responses were significantly decreased only in the presence of zymosan (p less than 0.05). Both basal chemiluminescence production (p less than 0.001) and zymosan-induced chemiluminescence responses (p less than 0.02) were closely related to alcoholic hepatitis prognosis indices (i.e., Pugh's and Child's classification, Orrego's composite clinical and laboratory index and Maddrey's discriminant function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Interferon alpha-2a treatment of 26 patients with chronic non-A non-B hepatitis. Predictive factors of response].

The type and predicting factors of response to alpha interferon therapy have been studied in 26 patients with chronic non-A non-B hepatitis. Interferon was administered three times weekly during 6 months at a dose of 3 millions units/day. Eleven patients (42 percent) had serum alanine aminotransferase levels below 1.5 times the upper limit of normal range at the end of treatment. Only eight (31 percent) patients had persistent normalization of seric alanine aminotransferase value, 6 months after the end of the interferon treatment. The main factors involved in the response to therapy were age, apparent duration of the disease, and mode of contamination: patients who responded to interferon were younger, had a shorter duration of hepatitis and a parenterally transmitted disease.

Adolescent↗
PubMed1990

[Epidemiologic aspects of viral hepatitis at a Parisian university hospital. Apropos of 130 cases].

One hundred and thirty adults with viral hepatitis were hospitalized in the Department of Hepatology-Gastroenterology at the Hospital Salpètrière between October 1984 and October 1986. Eighty had acute hepatitis and 50 suffered from chronic hepatitis. Among the former, 15 had hepatitis A, 40 had hepatitis B and/or delta and 25 had non A-non B hepatitis. The latter group was divided into 32 hepatitis B and/or delta and 18 non A-non B. The results of clinical, biological, serological and histological analyses were comparable to those reported in the literature for hepatitis A and B. Hepatitis non A-non B was more prevalent in males (72%). This predominance seems to be associated with the high number of heart transplant patients (12, 11 of them were men) in our study population. A liver biopsy was performed on 19 out of the 25 acute and on 32 of the chronic non A-non B hepatitis patients. Persistent chronic hepatitis was the most commonly found lesion. Transfusion was implicated in 53.8% of the patients, drug addiction in 18.6% of the cases and intramuscular injection or acupuncture in 5% of them. No risk factor was found in 23.2% of the patients. Seventy-two percent of the acute non A-non B hepatitis cases evolved towards a chronic form. We have attempted to find the factors involved in progression to chronicity. No correlation was found for age or the means of contamination. In contrast, immunodepression was significantly correlated. This study reflects the prevalence of non A-non B hepatitis infection post-transfusion in a hospitalized population including many transplant recipients.

Acute Disease↗
PubMed1989

Portal hypertension and ascites in acute hepatitis: clinical, hemodynamic and histological correlations.

We attempted to ascertain the mechanism of portal hypertension and ascites complicating acute hepatitis in 66 patients who underwent transvenous liver biopsy and measurement of hepatic venous pressure gradient. Increase in hepatic venous pressure gradient was related to the severity of acute hepatitis, as indicated by the significant correlation between the values for hepatic venous pressure gradient and serum bilirubin, serum albumin or coagulation factor V, and by its higher value in patients with, than in patients without, encephalopathy. Hepatic venous pressure gradient was higher in patients with, than in patients without, ascites (12.5 +/- 3.4 vs. 8.4 +/- 3.6 mmHg, respectively; p less than 0.001). No ascites was clinically detectable in the patients in whom hepatic venous pressure gradient was below 6 mmHg. We tested the hypothesis that sinusoidal collapse due to liver cell dropout was a major factor in portal hypertension. Semiautomatic determination of the fractional area of sinusoidal collapse on chromotrope-stained sections and automatic measurement of Sirius red-stained collagen fiber density were performed. Hepatic venous pressure gradient significantly correlated with fractional sinusoidal collapse area (r = 0.61, p less than 0.001) and with Sirius red-stained collagen fiber density (r = 0.43, p less than 0.01). We conclude that portal hypertension in the course of acute hepatitis is related to the severity of liver damage and is a major factor in the development of ascites. Portal hypertension is mainly determined by intrahepatic vascular space being reduced by the collapse of sinusoids.

Acute Disease↗
PubMed1989

Successful endoscopic obturation of gastric varices with butyl cyanoacrylate.

In 27 patients who had bled from esophagogastric varices, large-sized and/or actively bleeding gastric varices were endoscopically obturated with the tissue adhesive butyl cyanoacrylate. Active bleeding was stopped in six patients. Rebleeding occurred in 10 patients; in four patients, rebleeding was due to ruptured gastric varices, occurred early and was successfully treated by reinjection of gastric varices; in one patient, rebleeding was attributed to ulceration on an injected gastric varix. Eight patients died: two of rebleeding (from esophageal varices or undetermined source), four of sepsis and/or liver failure and two at home of undetermined cause. No specific complication due to injection of gastric varices was observed. The results obtained in this series of patients with gastric varices obturated by injection of butyl cyanoacrylate are much more satisfactory than those obtained in previously published series of patients with gastric varices treated by injection of sclerosants.

Adult↗
PubMed1989

[Electroencephalographic study of the effect of a benzodiazepine antagonist in hepatic encephalopathy].

Observing animal models of fulminant hepatic failure lead to the hypothesis of a GABAergic origin of the comatose state in hepatic encephalopathy (HE). The hypothesis of hyperstimulation of gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptors in HE has been tested with a BZ antagonist (flumazenil, Anexate) on 7 patients suffering from severe HE. The standard EEG has been recorded 30 min before and after slow IV perfusion of 1 mg flumazenil. Although we did not observe a complete EEG normalization, a significant improvement of EEG was observed after only a few minutes in 6 out of the 7 cases studied. Modification of the reactivity parallels clinical improvement of encephalopathy. These effects persist mostly 4 h after perfusion. The results are consistent with the hypothesis of hyperstimulation of GABA-BZ receptors in HE. The positive effect of flumazenil on vigilance level should encourage its use in chronic hepatic encephalopathy.

Adult↗
PubMed1988

Etiology of portal vein thrombosis in adults. A prospective evaluation of primary myeloproliferative disorders.

In a prospective study of 33 adults with portal vein thrombosis unrelated to a liver tumor, we have assessed the prevalence of primary myeloproliferative disorders using conventional criteria and cultures of bone marrow progenitor cells. A primary myeloproliferative disorder was documented in 14 patients investigated at the time of recognition of portal vein thrombosis. Among these 14 patients, the main clue to the presence of the myeloproliferative disorder was (a) the observation of suggestive abnormalities of peripheral blood cell counts in 4 patients; (b) characteristic findings at bone marrow biopsy or determination of total red cell volume in 3 patients; and (c) formation of "spontaneous" erythroid colonies in cultures of bone marrow progenitor cells in erythropoietin-poor medium in 7 patients. In 2 other patients, agnogenic myeloid metaplasia with myelosclerosis of apparently recent onset developed 5 yr after recognition of portal vein thrombosis. In conclusion, primary myeloproliferative disorders--in a full-blown or latent form, or at an early stage--are a major cause of portal vein thrombosis.

Blood Cell Count↗
PubMed1988

Drug-induced vascular and sinusoidal lesions of the liver.

Drugs can induce various vascular and sinusoidal lesions of the liver, in particular hepatic vein thrombosis, veno-occlusive disease, sinusoidal dilatation, peliosis hepatis, hepatoportal sclerosis and angiosarcoma. None of these lesions is specific of drug-induced injury and all of them can be determined by causes other than drugs. However, for one of these lesions, veno-occlusive disease, chemotherapy (and/or irradiation) represents the main aetiology.

Budd-Chiari Syndrome↗
PubMed1988

Portal vein thrombosis with ruptured oesophageal varices as presenting manifestation of hereditary protein C deficiency.

The protein C system is essential in limiting the activation of coagulation in vivo. We report the case of a 45 year old man with portal vein thrombosis complicated by ruptured oesophageal varices. Low concentration of plasma protein C was found in the patient and subsequently in one brother with a history of venous thromboembolism, and also in one son and one nephew who were asymptomatic. Hereditary protein C deficiency should be considered in patients with portal hypertension due to portal vein thrombosis.

Esophageal and Gastric Varices↗