[Iproniazid-induced hepatitis. The diagnostic value of a new antimitochondrial antibody anti-M6]. / Hépatite à l'iproniazide. Intérêt diagnostique d'un nouvel anticorps antimitochondrial, l'anti-M6.

The authors report the observations of four patients with iproniazid hepatitis. Three of these patients died. An antimitochondrial antibody was found in the 4 patients at a high titer. This antibody differed from the antimitochondrial antibodies which have been described previously (anti-M1, anti-M5). This new antibody was called anti-M6. The evolution of the anti-M6 titer has been studied in the patient who survived. This titer progressively decreased; the antibody was no longer detectable 6 months after the withdrawal of iproniazid. Anti-M6 has not been found in other hepatic diseases. It was not detected in 15 patients receiving iproniazid without hepatitis or in 6 patients receiving isoniazid. Anti-M6 appears as a useful serologic marker for the diagnosis of iproniazid hepatitis.

[Acute hepatitis caused by isaxonine phosphate (Nerfactor)]. / Hépatite aiguë due au phosphate d'isaxonine (Nerfactor).

We report the cases of four adult patients suffering from acute hepatitis due to isaxonine phosphate (Nerfactor), a drug recently proposed for the treatment of the lesions of peripheral nerves. Hepatitis developed 14 to 166 days after the beginning of the administration of the drug. In all the patients, predominantly centrilobular hepatocytic necrosis was present. In two of our patients, the course of hepatitis was fatal. Hepatitis induced by isaxonine phosphate is likely to be due to an immuno-allergic mechanism.

Acute intravascular hemolysis and acute liver failure associated as a first manifestation of Wilson's disease.

In three patients, the first manifestation of Wilson's disease was a syndrome in which acute intravascular hemolysis and acute liver failure were associated. This syndrome developed in three periods; the first, lasting 3 to 14 days, was characterized by fatigue, fever, and jaundice; the second, lasting 1 or 2 days, by severe intravascular hemolysis; and the third, lasting 2 to 6 days, by hepatic encephalopathy. All of the patients died from liver failure 7 to 21 days after the onset of the syndrome. The association of acute intravascular hemolysis and acute live failure is a characteristic manifestation of Wilson's disease; it is rarely associated with other liver diseases. This association might result from hepatic cell necrosis due to accumulation of copper, the consequences being acute liver failure and destruction of erythrocytes by the large amounts of copper released from the necrotic hepatic cells to the plasma.

[Acute fatty infiltration of the liver in pregnancy. One case (author's transl)]. / Stéatose hépatique aiguë gravidique. Une observation.

Acute fatty infiltration of the liver in pregnancy is characterised by microvacuolar fatty infiltration, without necrosis, occuring at the end of pregnancy. This syndrome, defined by Sheehan in 1940, remains rare. The authors were able to find 62 authentic cases in the french, english and german literature. The course is fatal in 75% of cases for the mother and 70% for the child. The gravity is related to hepatocellular failure, but also to extra-hepatic complications (renal failure, haemorrhagic syndrome, infectious complications, acute haemorrhagic and/or necrosing pancreatitis). When the course is favourable, the hepatic lesions disappear in a few weeks and there is no recurrence during subsequent pregnancies. The histological lesions of acute fatty infiltration of the liver in pregnancy are identical to those of fatty infiltration of the liver induced by cyclines and of Reye syndrome.

Intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy. An unusual but favorable association?

During the 26th week of a first pregnancy, a 25-year-old woman presented with pruritus suggesting an intrahepatic cholestasis of pregnancy. The pruritus, however, persisted despite the premature delivery of a normal newborn at the 35th week. Moreover, aspartate aminotransferase activity increased, reaching a maximum of 38 times normal level on the 17th day after the delivery. Thus, an acute fatty liver of pregnancy was suspected and confirmed by liver biopsy. This patient appeared to have both intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy, an association not previously reported. It is suggested that intrahepatic cholestasis of pregnancy caused premature delivery, which in turn may have prevented the onset of severe maternal and fetal complications caused by acute fatty liver of pregnancy.

Abnormal tissue oxygenation in patients with cirrhosis and liver failure.

Systemic haemodynamic and hepatic venous pressures, arterial and mixed venous gases and arterial lactate concentration were measured in 35 patients with histologically proven alcoholic cirrhosis who had been classified into three groups (A, B and C). Eight alcoholic patients without cirrhosis on liver biopsy were also studied. Compared with group A patients, group C patients had significantly higher hepatic venous pressure gradient, cardiac index, O2 transport and arterial lactate concentration and significantly lower systemic vascular resistance, arteriovenous O2 content difference and O2 uptake. In group B patients, corresponding values fell between those of groups A and C. Group A patients, unlike group C patients, were not significantly different from patients without cirrhosis with respect to cardiac index, systemic vascular resistance, O2 uptake and arterial lactate concentration. Our results suggest that in patients with cirrhosis, liver failure-associated hyperdynamic circulation may be accompanied by an abnormal tissue oxygenation.

[Cushing's syndrome caused by a bilateral adrenal adenoma (author's transl)]. / Syndrome de Cushing par adénome bilatéral des surrénales.

An unusual of bilateral adrenal benign adenoma with Cushing's syndrome is reported. Nine months after bilateral adrenalectomy, no more sign of hyperadrenocorticism was present. An adenoma was found in each gland with adjacent tissue atrophic. Physiopathology is not clear even if suppression test by dexamethasone and stimulation test by lysin-vasopressin are compatible with a central origin.

[Benign postoperative intrahepatic cholestasis]. / Cholestase intra-hépatique postopératoire bénigne

The authors report the clinical, biochemical, histological and etiologic characteristics of 24 patients with the syndrome of benign intra-hepatic post-operative cholestasis. Jaundice appeared early in the post-operative period, from the first to the 12th post-operative day. All patients had received blood transfusions. In 23 patients, the post-operative course was complicated, chiefly by local infection or septicemia. Hyperbilirubinemia ranged from 2 to 28 mg per 100 ml and was mainly conjugated; serum alkaline phosphatase activity was normal or moderately elevated; in 3 patients, it was markedly elevated; serum glutamic-pyruvic transaminase activity was normal on 7 patients, moderatly increased in 15, and markedly increased in one. Liver histology was normal in 6 patients, and showed minimal lesions (cholestasis and slight portal inflammatory changes) in 3. Jaundice did not appear to modify the final outcome. It appears to be due both to increased production of bilirubin (as a result of blood transfusions) and to decreased excretion of bilirubin by the liver (as a result of the surgical operation and of infection).

[Postoperative intraabdominal suppurations due to Ristella. Clinical, bacteriological and therapeutic characteristics]. / Suppurations intra-abdominales post-opératoires Ristella. Particularités cliniques, bactériologiques et thérapeutiques

From 1972 to 1974, 8 intraabdominal postoperative suppurations due to Bacteroides have been observed at Hospital Beaujon. Three characteristic features of such infections have been analysed: the high frequency of associated jaundice; the difficulty of isolation of the Bacteroides; their specific sensitivity to some antibiotics. In 5 patients, jaundice related to the bacterial infection has been observed; jaundice was of the cholestatic type; it was mainly due to conjugated hyperbilirubinemia; in approximately 50 p.cent of the cases, serum alkalin phosphatases activity and serum glutamic-pyruvic transaminase activity were moderately elevated; the presence of jaundice did not seem to have any influence on the prognosis. The frequent association to Bacteroids of enterobacteria makes isolation of the Bacteroides difficult. The necessity of some precautions in the handling (storage at 4 degrees C or immediate inoculation in anaerobic conditions) is emphasized. Bacteroides are always resistant to penicillin and to the other broad spectrum antibiotics usually effective enterobacteria. They are sensitive to tetracyclins (5/8), lincomycin (2/4), clindamycin (2/3), rifampicin (8/8), pristinamycin (7/7), carbenicillin (3/3), erythromycin (8/8) and chloramphenicol (8/8).

Abnormal pressor response to vasopressin in patients with cirrhosis: evidence for impaired buffering mechanisms.

In patients with cirrhosis, vasopressin infusion induces sustained vasoconstriction and elevation of arterial pressure. The vasopressor effect could be caused by impairment of mechanisms normally aimed at buffering increases in arterial pressure (reflex bradycardia and decreases in arteriolar resistance). We studied the acute effects of continuous vasopressin infusion (0.4 IU/min) on systemic hemodynamics in seven patients with cirrhosis and in six patients without cirrhosis (controls). Vasopressin effects on systemic O2 consumption were also studied. In both groups, vasopressin infusion induced similar peak increases in arterial pressure, followed by similar decreases in heart rate and cardiac output. However, cirrhotic patients and controls differed 30 min after the start of vasopressin infusion. At 30 min, mean arterial pressure, diastolic arterial pressure and systemic vascular resistance remained significantly higher than preinfusion values in patients with cirrhosis. No decrease in systemic O2 consumption occurred in cirrhotic patients. In controls, at 30 min, mean arterial pressure and diastolic arterial pressure had returned to baseline. Systemic vascular resistance was not significantly higher than the preinfusion value and systemic O2 consumption had significantly decreased to below preinfusion values. We conclude that the vasopressor effect of vasopressin is abnormally sustained in patients with cirrhosis. This might be caused by insufficient buffering of vasopressin-induced arteriolar constriction rather than by abnormal vagal control of heart rate. In turn, as suggested by the lack of a decrease in systemic O2 consumption, persistent arteriolar constriction might be related to abnormally sustained sympathetic vascular tone in patients with cirrhosis.

Arterial and mixed venous acid-base status in patients with cirrhosis. Influence of liver failure.

Although it has been established that liver failure is associated with arterial hypocapnia and alkalaemia (i.e., respiratory alkalosis), the influence of liver failure on mixed venous acid-base status has not yet been studied. Thus, arterial and mixed venous acid-base status were simultaneously measured in controls and in a large series of patients with cirrhosis. Grade B patients (n = 28) or Grade C patients (n = 21) had significantly lower arterial and mixed venous carbon dioxide tensions than controls (n = 29). Grade B or Grade C patients also had significantly higher arterial, mixed venous pH, and lower mixed venous bicarbonate concentrations than controls. Among Grade A patients (n = 27), those with the lowest Pugh's score (i.e., equal to five) had significantly lower mixed venous carbon dioxide tension than controls. The other arterial and mixed venous acid-base values did not differ significantly between Grade A patients with the lowest Pugh's score and controls. Grade A patients with a Pugh's score equal to six and Grade B patients had similar acid-base disorders. No significant differences were found between groups concerning the anion gap and plasma chloride concentrations. In conclusion, this study shows that in Grade B or C patients, respiratory alkalosis was responsible for mixed venous hypocapnia, alkalaemia and hypobicarbonataemia. In addition, in Grade A patients with the lowest Pugh's score (equal to five), analysis of arterial and mixed venous blood revealed that mixed venous hypocapnia was the sole anomaly of the acid-base status. This last finding suggests that mixed venous hypocapnia might be an early event preceding the onset of arterial hypocapnia.