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Biomedical subjects

M Doffoël

Publications and source records attributed to M Doffoël.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Primary sclerosing cholangitis and autoimmune cochlear deafness: a new syndrome?].

Association of autoimmune cochlear hearing loss with primary sclerosing cholangitis is reported in two patients. Endocochlear sensorineural hearing loss was associated with the presence of anti-cochlear antibodies in the serum directed against the walls of vessels in the stria vascularis. The hearing loss appeared at the same time or shortly after the diagnosis of cholangitis. This association, which has never been described, may reinforce the theory of the role of immunologic factors in the pathogenesis of primary sclerosing cholangitis, possibly linked to or initiated by vasculitis.

Adult↗
PubMed1991

[Pseudo-alcoholic cirrhosis].

Alcohol-like liver disease may be observed in patients with obesity or non insulin-dependent diabetes, or after treatment with such antianginal drugs as amiodarone and perhexiline maleate. In such cases cirrhosis is associated, at histology, with foci of acidophilic necroris, Mallory's bodies and inflammatory neutrophilic infiltrates. Alcohol-like liver disease is rare. It affects mostly women in their fifties and usually is clinically latent. Abnormalities of liver function tests mainly consist of increased serum aminotransferase levels. Complications of portal hypertension are uncommon. The pathogenesis of the disease remains purely hypothetical. In practice, in the absence of antianginal therapy the finding of cirrhosis in an obese and/or diabetic patient should prompt a search for excessive alcohol consumption before ascribing the cirrhosis to obesity and/or diabetes.

Angina Pectoris↗
PubMed1989

[In vitro demonstration of a deficit in suppressor T-cell function in alcoholic cirrhosis. Role of hepatitis B virus infection].

The T lymphocyte suppressor cell activity has been evaluated in 33 alcoholic patients compared with 16 normal controls, using an in vitro test. Suppressor T cells were activated with concanavalin A, and suppressor effect was quantified by the inhibition of an autologous B cell culture response to Pokeweed Mitogen. When compared with controls, cirrhotic patients showed a significant defect of suppressor cell activity on B cell production of IgG (20 +/- 3 vs 46 +/- 5 p. 100, p less than 0.001) and IgM (26 +/- 4 vs 56 +/- 8 p. 100, p less than 0.05). In cirrhotic patients, defect of T cell suppressor function was independent of sex and severity of the cirrhosis (Child's staging). This defect was more marked in cirrhotics with serological markers of hepatitis B virus (HBV) infection (n = 11) than in cirrhotics without markers (n = 22) (9 +/- 5 vs 25 +/- 3 p. 100, p less than 0.05; 16 +/- 6 vs 30 +/- 5 p. 100, p less than 0.05 respectively for IgG and IgM production suppression). These results suggest that HBV and lymphocytes interact directly. This interaction could increase the T suppressor cell defect, and explain the promoting role of HBV infection in the constitution of the cirrhosis in alcoholics even when viral replication is not serologically apparent.

Female↗
PubMed1988

[Study of insulin resistance in cirrhosis by the hyperinsulin euglycemia clamp].

To explore the insulin resistance state in liver cirrhosis and to assess the respective role of insulin sensitivity and cellular metabolism alterations, an euglycemic glucose clamp was performed in 12 cirrhotic patients and 6 healthy volunteers with 3 successive hyperinsulinemic periods of 90 mn (infusions of 7, 20 and Iu/h). An artificial beta-cell model allowed to quantify the amount of glucose needed to keep glycemia at 4.70 mmol/l. In 7 cirrhotic patients, insulin secretion was tested by an intravenous glucose tolerance test. The dose-response curves showed a significant (p less than 0.01) decrease of the theoretical maximal metabolic clearance rate of glucose (capacity). The insulin concentration corresponding to the half-maximal response (ED50) did not differ between cirrhotic and control subjects because of a very important dispersion of individual values in cirrhotics. The ED50 value was lower than the values of control subjects in five cirrhotic patients and normal or enhanced in seven other patients; the former showed the most reduced values for capacity, and the latter a more marked hyperinsulinemia during the intravenous glucose tolerance test. The two subgroups of patients did not differ for clinical or biological parameters of cirrhosis, or for glucose tolerance. These results 1) show a constant and marked impairment of glucose metabolism capacity in liver cirrhosis, 2) and suggest that the insulin resistance inconstantly observed in this state is a consequence of chronic hyperinsulinemia.

Adult↗
PubMed1987

[Determination of sub-populations of circulating T lymphocytes in alcoholic cirrhosis using monoclonal antibodies OKT3, 4, 5, Leu 2 and Leu 15. Effect of hepatitis B virus infection].

Peripheral T lymphocyte subpopulations were quantified in 24 alcoholic cirrhotic patients, 11 of them having anti-HBs and/or anti-HBc antibodies, and were compared with 35 healthy control subjects, 10 of them having anti-HBs and/or anti-HBc antibodies. The monoclonal antibodies utilized (OKT3, OKT4, OKT8 in simple staining, Leu 2 and Leu 15 in double staining) are considered as markers of mature (CD3), helper (CD4), cytotoxic/suppressor (CD8, Leu 2), suppressor (Leu [2+ 15+), and cytotoxic (Leu 2+ 15-) T cells. In cirrhotics, when compared to controls, the number of CD3 cells was reduced (p less than 0.01); the proportion of CD4 cells was within normal range, and that of CD8 cells diminished (p less than 0.001), contrasting with an increased proportion of Leu 2+ cells (p less than 0.01), related to an increased proportion of Leu 2+ 15+ cells. Leu 2+ 15- lymphocytes were within normal range. In control subjects, a decreased proportion of Leu 2+ 15+ cells was found (p less than 0.05) when Ac HBs and/or Ac HBc were present. In cirrhotics having at least one serologic marker of hepatitis B virus infection, when compared with negative ones, increased proportions of Leu 2+ (p less than 0.05) and Leu 2+ 15+ (p less than 0.05) cells were found. These results show that data concerning T lymphocyte subpopulations are conflicting when various types of antibodies are used. However, they suggest abnormalities of immune regulation, possibly a defect of T suppressor cell function. Hepatitis B virus infection probably modifies immune regulation in alcoholic cirrhosis, and perhaps in normal subjects.

Antibodies, Monoclonal↗
PubMed1987

[Hyperammonemia induced by propranolol in cirrhotic patients. Role of the kidney and influence of the severity of the cirrhosis].

The effect of the intravenous injection of 0.1 mg/kg of propranolol on arterial ammonemia was studied in 30 patients with alcoholic cirrhosis comparatively with 10 healthy volunteers. Moreover, in 20 patients in the cirrhotic group (10 were Pugh's grade A or B and 10 others were grade C), left renal vein catheterization was performed to follow the changes in ammonemia and glutaminemia levels simultaneously with those occurring in arterial blood. After 30 min, arterial ammonemia was significantly increased in the controls (p less than 0.02) and in the cirrhotic patients (p less than 0.001). The renal venous ammonemia was also significantly increased in all of the cirrhotic patients (p less than 0.01). In the grade A and B patients, the increase in ammonemia was more marked in the renal vein as compared with that in arterial blood (p less than 0.001). In contrast, in the grade C patients, the increase in ammonemia did not differ significantly between the two sectors. The difference in ammonia concentration between arterial and renal venous blood increased significantly after 30 min in the grade A and B patients (p less than 0.001) whereas it was stable in the grade C patients. The changes of glutaminemia in arterial and renal venous blood were not significantly different in the two groups of cirrhotic patients. These data show that, in our experimental conditions, propranolol induces arterial hyperammonemia in cirrhotic patients and that the kidney could interfere with the mechanism of hyperammonemia, at least in grade A and B patients.

Ammonia↗
PubMed1986

[Malnutrition and deficiency of insulin secretion in alcoholic cirrhosis. Study by the assay of urinary C-peptide].

In order to evaluate the relationship between nutritional status and insulin secretion in cirrhosis, the following parameters of caloric (tricipital skin fold, prealbumin) and proteic (arm muscle size, transferrin, 24 h-urinary creatinine excretion) nutritional status were compared in 20 alcoholic cirrhotics and 10 normal subjects. Insulin secretion was evaluated in both groups by insulin and C-peptide response to an intravenous glucose tolerance test and by 24 h urinary excretion of C-peptide. When compared to normals, cirrhotics have lower values for all nutritional status parameters and individually for at least three of those in 14 (70 p. 100) patients. In cirrhotics there is a significant decrease of the 4-min poststimulative response of insulin and C-peptide, contrasting with higher basal and late poststimulative values than in normals. This contrast could be explained by a reduced metabolic clearance rate of insulin (consistent with insulin resistance) and of C-peptide (the urinary clearance of which is 2.5 times lower in cirrhotics than in normals). The 24-h urinary excretion of C-peptide, probably weakly dependent of this reduced clearance, is 50 p. 100 lower in cirrhotics: 12.9 +/- 1.6 nM/24 h than in normals: 26.0 +/- 2.4 nM/24 h (p less than 0.001). In cirrhotics there is a significant linear correlation between 24 h urinary C-peptide excretion and all the nutritional status parameters but one (prealbumin). These results indicate that in cirrhosis: 1) urinary C-peptide excretion rate is a good index of insulin secretion; 2) urinary C-peptide indicates a marked deficit in insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗