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Biomedical subjects

E Pisi

Publications and source records attributed to E Pisi.

At least 109 records · Page 6Linked to original sources
PubMed1982

Myofibrillar protein catabolic rates in cirrhotic patients with and without muscle wasting.

1. The urinary excretion of 3-methylhistidine and creatinine was measured in 15 controls and in two groups of 15 patients with liver cirrhosis, with and without severe muscle wasting. All subjects were on a meat-free diet. The values obtained were used to calculate the fractional catabolic rate of myofibrillar protein. 2. In patients without muscle wasting 3-methylhistidine excretion was high in the presence of normal urinary creatinine. The fractional breakdown rate was significantly increased as compared with that of controls. 3. In patients with severe muscle wasting 3-methylhistidine excretion was normal and urinary creatinine was remarkably reduced. The myofibrillar catabolic rate was further increased compared with that of controls and of the other group of patients. 4. 3-Methylhistidine and creatinine excretion allow a complete evaluation of myofibrillar protein degradation, which appears to be remarkably increased in cirrhotic patients. The relevance of increased myofibrillar protein turnover in muscle wasting of subjects with advanced cirrhosis remains to be determined.

Adult↗
PubMed1981

Plasma amino acids as markers of liver dysfunction in cirrhotics.

To determine the role of liver dysfunction in the plasma amino acid profile of cirrhotic patients, we correlated basal plasma amino acids and several biochemical and functional hepatic variables in 29 cirrhotics with normal mental state or mild encephalopathy. Increased levels of aromatic amino acids and free tryptophan correlated positively with the extent of portosystemic shunt, as assessed by the ammonia tolerance test (r = 0.758 and r = 0.589, respectively). There was a negative correlation between these amino acids and liver function, as evaluated by the galactose elimination capacity test (r = -0.657 and r = -0.551), thus suggesting that phenylalanine, tyrosine, and free tryptophan may be considered indexes of liver dysfunction in non-comatose cirrhotics.

Adult↗
PubMed1981

HBsAg-induced hypertrophic smooth endoplasmic reticulum as a target for liver-kidney microsomal (LKM) antibodies.

To test the hypothesis that LKM antibodies are directed against antigen(s) of the smooth endoplasmic reticulum, liver biopsies from patients with HBsAg chronic hepatitis, rich in liver cells with HBsAg-induced hypertrophic SER, were used. A close correspondence was seen between cells with HBsAg-positive cytoplasm by immunoperoxidase and cells with a stronger and more homogeneous fluorescence by indirect immunofluorescence with LKM-positive sera. These results point to antigenic components of SER as reacting with LKM antibodies. The relevance of antigens present in the ribosomes and membranes of rough endoplasmic reticulum needs further evaluation.

Antibodies↗
PubMed1981

Binding of tryptophan to albumin in liver cirrhosis: a reappraisal of the problem.

The competition of free fatty acids and bilirubin in the binding of tryptophan to albumin was studied in 12 controls and 36 cirrhotics at various stages of hepatic encephalopathy. Total tryptophan was not significantly altered in cirrhotics, while free tryptophan progressively increased with the deterioration of their mental state. Bound tryptophan levels were consequently reduced in patients with cirrhosis, mainly in the presence of hepatic encephalopathy, and strictly correlated with albumin (r = 0.80). The ratio bound tryptophan/albumin, which represents the muMoles of tryptophan bound by 1 gram of albumin, did not show significant difference in the various groups of patients. No correlation was found between this ratio and the levels of free fatty acids and bilirubin, which were raised in cirrhotics. Our data suggest that the fall in albumin levels, but not the increase in free fatty acids or bilirubin, may play a role in increasing free tryptophan levels in cirrhotics. Thus, marked hypoalbuminemia may be a risk factor of hepatic encephalopathy in patients with cirrhosis.

Albumins↗
PubMed1981

Abnormal cardiovascular reflexes in juvenile diabetics as preclinical signs of autonomic neuropathy.

The prevalence of abnormalities of cardiovascular reflexes as a marker of autonomic neuropathy was studied in a group of juvenile diabetics with long-standing disease, aged 20-58 years (mean 36). No patient had clinical evidence of autonomic failure. The study was carried out employing the most simple techniques and routine equipment. Resting heart rate, beta-to-beat variation, Valsalva ratio, systolic blood pressure in supine position and immediately after standing were measured. The results were compared with those determined in an age and sex-matched population. Beat-to-beat variation test appeared to be the most sensitive technique in detecting an impaired autonomic function (12/54 = 22.2%). Resting tachycardia was found in 10 patients and postural hypotension in 6. Only 1 patient had an abnormal Valsalva ratio associated with postural hypotension and reduced beta-to-beat variation. In agreement with previous studies our data confirm that autonomic dysfunction is frequent in asymptomatic diabetics. The methods to detect these abnormalities are easy to perform. Therefore they may be routinely used as screening tests in the diabetic population.

Adult↗
PubMed1980

Smooth-muscle antibodies in children with neuroblastoma.

Smooth-muscle antibodies (SMA) were detected in 16 of 18 (89%) children with neuroblastoma and in 43 of 172 (25%) pediatric hospital patients without malignancies. The SMA were mainly of the IgG class. The most common immunofluorescence pattern was SMA-V (vessel) and titers did not exceed 1:160. Absorption and immunodiffusion tests with action (from rabbit skeletal muscle) showed that the SMA associated with neuroblastoma are mainly directed against actin, although different antigen specificities (myosin, meromyosin) are probably involved in some cases. In both chronic active hepatitis and neuroblastoma, SMA would represent a specific response to intracellular contractile proteins (mainly actin) induced by tissue damage. A feedback role in controlling cellular proliferation has been postulated for experimentally raised SMA. This would be relevant in cases of malignancy.

Antibodies↗
PubMed1980

Prevalence of subclinical hepatic encephalopathy in cirrhotics and relationship to plasma amino acid imbalance.

Neuropsychological status, as assessed by trailmaking test; plasma amino acids, and ammonia, were studied in 54 cirrhotics without clinical evidence of encephalopathy to determine the prevalence of subclinical mental dysfunction and its relationship to metabolic abnormalities. Control values for psychometric performance were established in 54 normal subjects matched for age, sex, educational level, and employment status. Of these subjects, 16 were also used as controls for fasting ammonia and plasma amino acids. Eighteen cirrhotics (33%) showed impaired performances of the psychometric test; free tryptophan and the ratio free tryptophan to neutral amino acids were increased in 37% and 62% of cases and correlated with the psychometric scores (r = 0.45 and r = 0.70, respectively). In eight cirrhotics with mild encephalopathy, psychometric and metabolic evaluations were repeated several times during the infusion of amino acid solutions rich in branch-chain amino acids. Again significant correlations were observed between the psychometric scores and plasma amino acids. We conclude that a considerable proportion of clinically normal cirrhotics have neuropsychological deficits. The severity of impairment may be related to the plasma amino acid imbalance, namely to an increased passage of tryptophan across the blood-brain barrier.

Adult↗
PubMed1979

Insulin and glucagon levels in liver cirrhosis. Relationship with plasma amino acid imbalance of chronic hepatic encephalopathy.

Alterations in insulin and glucagon levels might account for the plasma amino acid imbalance of cirrhotics. In order to verify this hypothesis we evaluated basal insulin, glucagon, branched-chain amino acids, aromatic amino acids, and free tryptophan in 13 controls and 37 cirrhotics divided on the basis of their mental state; in 4 patients the hormonal and amino acid patterns were sequentially studied during various stages of encephalopathy. Glucagon is high in cirrhotics and progressively increases with the worsening of the mental state. Free tryptophan and aromatic amino acids show a similar behavior and significantly correlate with glucagon levels (r = 0.67 and r = 0.81, respectively). On the other hand insulin levels, which are high in cirrhotics without encephalopathy, fall in the presence of deep coma. Insulin did not correlate with any of the plasma amino acids considered. Our data suggest that the catabolic state associated with increased glucagon levels may account for some of the alterations in the plasma amino acid profiles of cirrhotics. Portal-systemic shunting does not seem to be the common cause of both hyperglucagonemia and hyperaminoacidemia. Decreased branched-chain amino acid levels may be related to factors different from those involved in the alterations of carbohydrate homeostasis.

Adult↗
PubMed1979

Oral glucose in cirrhotics. Effects on plasma aminoacid patterns and the role of insulin and glucagon.

Changes in the plasma aminoacid (AA) profile present in hepatic encephalopathy were related to a catabolic state characterized by a reduced insulin/glucagon molar ratio (IRI/IRG). Oral glucose is able to suppress the hyperglucagonemia and further to increase the elevated insulin levels of cirrhotics leading to a rise of IRI/IRG. We evaluated the plasma AAs in ten controls and twelve cirrhotics following the ingestion of oral glucose. At 180 min we demonstrated a similar fall (about 35%) of plasma AAs both in cirrhotics and in controls, with the exception of free tryptophan, which fell more markedly in cirrhotics (about 60%), possibly secondary to the fall in plasma free fatty acids. After the oral glucose load, the levels of aromatic AAs and free tryptophan, as well as the molar ratio free tryptophan/branched-chain + aromatic AAs returned to normal in cirrhotics. High levels of both aromatic AAs and free tryptophan have been implicated in the pathogenesis of hepatic coma. Our data support the hypothesis that the administration of oral glucose might be relevant in the management of cirrhotic patients with hepatic encephalopathy, possibly improving their mental state.

Adult↗