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Biomedical subjects

J M Paz

Publications and source records attributed to J M Paz.

At least 19 recordsLinked to original sources
PubMed1991

Abnormal serum immunoglobulin concentrations in patients with diabetes mellitus.

Since the recently reported relationship between serum fructosamine and IgA concentrations appears to throw doubt on the clinical utility of fructosamine as a measure of hyperglycemic status if IgA concentration is not taken into account, we studied serum immunoglobulin concentrations in 169 diabetics and their relationship with various clinical and analytical parameters. Over 41% of the patients studied had abnormal serum IgA concentrations. Serum IgA concentration was negatively correlated with serum albumin, and among IDDM patients was positively correlated with age (so that the prevalence of abnormal IgA was 57.7% among IDDM patients aged over 30 years). Among NIDDM patients, abnormal IgA concentrations were especially prevalent among those being treated with oral hypoglycemics. Abnormal IgA was also more frequently found in both IDDM and NIDDM patients, who had been under treatment for 10 years or more. Abnormal IgG concentrations were found in 11.8% of the diabetics, and the mean IgM concentration found in the patients was 41.6% lower than in the normoglycemic group. We conclude that abnormal serum IgA concentrations are very common in diabetic patients and that further research should be carried out to verify whether the determination of serum immunoglobulins, IgA in particular, is of clinical use for monitoring diabetes or evaluating its secondary effects.

Adolescent↗
PubMed1991

Short-term effects of administration of anticonvulsant drugs on free carnitine and acylcarnitine in mouse serum and tissues.

1. The short-term evolution of concentrations of free carnitine and acylcarnitine was studied in the serum, liver, kidney, heart and skeletal muscle of mice after administration of single therapeutic doses of the anticonvulsant drugs, valproic acid (VPA), carbamazepine (CBZ), phenytoin (PHT) and phenobarbitone (PHB). 2. The effects of the drugs were immediate but transitory, control levels of free carnitine and acylcarnitine having been recovered or almost recovered in serum and in all tissues 8 h post administration (p.a.). 3. VPA was the only drug that significantly reduced free carnitine concentration in serum, which recovered control levels by 4 h p.a. 4. All the drugs studied brought about marked deficits of serum acylcarnitine, which had disappeared 2 h p.a. in the case of VPA and not until 8 h p.a. for CBZ, PHT or PHB. 5. The minimum concentrations of free carnitine and acylcarnitine in serum were invariably associated with the maximum concentration of drug in serum. 6. Free carnitine concentration was not affected by VPA in any tissue, PHT and PHB brought about significant deficits in heart and kidney, and CBZ a significant deficit in muscle. 7. Acylcarnitine concentration was significantly reduced in heart, kidney and muscle by CBZ, PHT and PHB, but in liver the effects of all drugs were very small. 8. These results are compatible with the hypothesis that the primary cause of anticonvulsant-induced alteration of carnitine metabolism is interference with renal reabsorption of carnitine.

Animals↗
PubMed1991

Alteration of renal carnitine metabolism by anticonvulsant treatment.

We administered therapeutic doses of valproic acid (VPA), carbamazepine (CBZ), phenytoin (PHT), and phenobarbital (PHB) to mice for 7 days, and 8 hours after the final dose we measured the concentrations of carnitine in serum, liver, kidney, skeletal muscle, and heart, and in the 7 days' accumulated urine. The results for serum and urine show that VPA induced a significant increase in renal clearance of acylcarnitine without affecting that of free carnitine, whereas CBZ, PHT, and PHB significant increased clearance of free carnitine but not that of acylcarnitine. Thus, VPA appears to reduce tubular resorption of acylcarnitine, and CBZ, PHT, and PHB appear to reduce tubular resorption of free carnitine.

Ammonia↗
PubMed1990

Effects of acute valproate administration on carnitine metabolism in mouse serum and tissues.

Carnitine concentrations in serum, liver, kidney, muscle and heart were determined 30 min, 2 hr and 4 hr after administration of single 50 mg/kg doses of valproic acid (VPA) or octanoic acid (OTA) of fasting mice. Half an hour post-administration (p.a.) of VPA, free carnitine concentrations were smaller than in controls in serum, liver, kidney and heart. Four hr p.a., the effects of VPA had disappeared from all the carnitine sources, which now had concentrations that were not significantly different from those of controls. The effects of OTA are different from, and sometimes the opposite of, those of VPA, showing that the effects of VPA are specific to it. Hyperammonemia, on the other hand, was greatest 4 hr p.a. of VPA. These findings show that the effect of VPA on carnitine metabolism is immediate but transient, and accordingly suggest that the carnitine deficiency observed in patients under prolonged treatment with VPA-containing anticonvulsants must be due to a more complex mechanism than direct interaction between carnitine and VPA.

Ammonia↗
PubMed1990

Free carnitine and acylcarnitine levels in sera of alcoholics.

We report the free, acyl-, and total carnitine contents of 49 clinically healthy volunteers and 167 chronic alcoholics with various clinically and/or anatomopathologically identified degrees of hepatic affection. There was a gradual upward trend in carnitine levels as the degree of hepatic affection increased. In cirrhotic patients, both free and acylcarnitine levels were significantly higher than normal, but there was no systematic hypercarnitinemia in other stages of alcoholism; on the contrary, noncirrhotic alcoholic patients accounted for 82.6% of all hypocarnitinemia cases. Hypercarnitinemia among cirrhotic alcoholics was due chiefly to increased free carnitine concentrations. Acylcarnitine levels in patients with hepatic steatosis were significantly higher than those in normal subjects (P less than 0.001), but there were no other statistically significant differences in either acyl- or free carnitine levels between normals on the one hand and, on the other, patients with hepatic steatosis, alcoholic hepatitis, slight hepatopathy, or chronic hepatopathy without portal hypertension.

Acetylcarnitine↗
PubMed1990

Evaluation of determination of lactate dehydrogenase isoenzyme 1 by chemical inhibition with perchlorate or with 1,6-hexanediol.

We have evaluated the determination of lactate dehydrogenase (EC 1.1.1.27) isoenzyme 1 activity by chemical inhibition of the other isoenzymes with perchlorate and with 1,6-hexanediol. In the hexanediol method, we studied the effect of the duration of incubation with the inhibitor; a 5-min incubation yielded results closest to those of an immunochemical technique (Isomune-LD). The perchlorate method was the most precise, and the hexanediol method the least, although for none of the techniques did the coefficient of variation exceed the medically acceptable limit prescribed by the College of American Pathologists. Pairwise correlation among the immunoprecipitation, electrophoretic, and chemical inhibition methods was good (r greater than 0.991), although the differences between means were statistically significant (except for the comparison of the two chemical inhibition methods). Because of its ease, low cost, and precision, we recommend the perchlorate method for routine use.

Adult↗
PubMed1989

Carnitine deficiency associated with anticonvulsant therapy.

Valproic acid therapy is known to be associated with carnitine deficiency in adult as well as young epileptic patients. In a study of the possible existence of such side-effects with other anticonvulsants, 76.5% of adult patients treated with valproate were deficient in serum free carnitine, with acylcarnitine levels significantly higher than in controls (p less than 0.01), while the carnitine deficiency rate in a group of patients treated with anticonvulsants other than valproate was 21.5%. Since in clinical practice only about one fifth of patients are treated with valproate, this means that about 15% of epileptics are carnitine deficient because of valproate treatment and 17% because of other anticonvulsants. The mechanisms and clinical and biological consequences of the carnitine deficiency associated with antiepileptic drugs other than valproate are not known.

Adolescent↗
PubMed1989

Serum and plasma ceruloplasmin in humans.

In a group of 76 clinically healthy human volunteers, we found a high correlation (r = 0.997, p less than 0.001) between the ceruloplasmin oxidase activities in serum (mean 127.2 U/l) and plasma (mean 124.0 U/l). Similarly high correlation was observed for immunoreactive ceruloplasmin, which was assayed in 65 samples (r = 0.993, p less than 0.001), with means of 306.1 mg/l in serum and 296.4 mg/l in plasma. Although the difference between the means measured in serum and plasma is in both cases statistically significant, it is clinically irrelevant according to the criteria of the College of American Pathologists. Finally, a high correlation between serum and plasma concentrations (r = 0.970, p less than 0.001, N = 32) was also found for acid alpha 1-glycoprotein, whose sialic acid content is greater than that of ceruloplasmin; in this case there was no statistically significant difference between the means. These results suggest that in humans, ceruloplasmin does not bind to erythrocyte and/or platelet membranes via sialyl groups during clotting, which disagrees with the hypothesis of Paynter (Aust. J. Biol. Sci. (1982) 35, 353--361) in cows and sheep.

Adult↗
PubMed1989

Effects of various serum proteins on quantification of fructosamine.

We determined fructosamine concentrations with the CentrifiChem 600 centrifugal analyzer and the Hitachi 737 discrete analyzer. Reference intervals agreed with the most recently published results, and values in fasting patients were significantly correlated with glycated hemoglobin, plasma glucose, albumin, beta- and gamma-globulins, IgG, IgA, IgM, and total protein. Partial correlation analysis showed that only fructosamine and IgA were dependently related. In a group of nondiabetic patients with pathological values for IgA concentrations, 79.4% had pathological values for fructosamine. These results throw doubt on the clinical value of fructosamine determinations if serum IgA is not taken into account.

Adult↗
PubMed1988

Urinary D-glucaric acid and serum hepatic enzyme levels in chronic alcoholics.

Urinary D-glucaric acid (DGA) and the activities of gamma-glutamyl transferase (GGT) and other hepatic enzymes in serum were determined in 33 noncirrhotic male alcoholics who had continued to consume alcohol until at least 24 h prior to the taking of samples. DGA excretion was significantly greater in them than in a group of 30 healthy controls (p less than 0.001), exceeding the upper reference level in 38% of the alcoholic cases (as compared with 88% for GGT). In the alcoholic patients, there was highly significant correlation between urinary DGA and serum GGT (r = 0.613, p less than 0.001), suggesting that in both cases the increased levels are due to enzyme induction. None of the biochemical variables studied were significantly correlated with estimated daily alcohol consumption. Urinary DGA levels fell off rapidly with abstinence, and in 31 alcoholic patients who had consumed no alcohol for 5 days, there was no statistically significant correlation between DGA excretion and serum GGT (r = 0.158, p congruent to 0.4).

Adult↗
PubMed1987

Cord serum gamma glutamyltransferase in newborns.

This article reports correlations among gamma-glutamyltransferase (GGT), fetal haemoglobin (fH), alpha-fetoprotein, 5'-nucleotidase, ceruloplasmin, and direct, indirect, and total bilirubin in the serum of blood taken from the umbilical cords of 128 newborns delivered after 37-42 weeks of gestation. GGT was significantly correlated with alpha-fetoprotein, but not with direct bilirubin, indirect bilirubin, total bilirubin, fH, or %fH. Neither fH nor %fH were correlated with alpha-fetoprotein, but there was highly significant negative correlation between both fH and %fH on the one hand, and gestational age and weight at birth on the other. The %fH was also correlated negatively with ceruloplasmin, which in turn exhibited negative correlation with alpha-fetoprotein. The predominant forms of GGT in umbilical cord and adult sera were, respectively, those with alpha 1 and alpha 2 mobility. In cord sera, delipidation with n-butanol brought about loss of GGT activity and a shift from an alpha 1 to an alpha 2 position, whereas no significant effect of this kind was observed in adult sera. Affinity chromatography through Concanavalin A-Sepharose showed cord sera to contain a proportion of bound-GGT (68.5 +/- 5.5%) that was significantly greater (p less than 0.001) than that found in adult sera (59.8 +/- 10.2%). It is concluded that the high GGT activity of cord sera is probably due to hepatic immaturity rather than maternal sources, enzymatic induction or microsomal lesions; that the predominant form of GGT in cord serum may be a complex with HDL and less sialized than the adult enzyme; and that, of the factors examined, the best indicator of neonatal maturity is fetal haemoglobin.

5'-Nucleotidase↗
PubMed1986

Carnitine deficiency in haemodialysed patients.

Free carnitine, acylcarnitine and total carnitine concentrations have been determined in the sera of chronic renal insufficiency patients undergoing regular haemodialysis treatment and in those of healthy controls. The most striking difference was found to be the high proportion of acylated carnitine (23.4 mumol/l) in the haemodialysed patients. Free carnitine and acylcarnitine levels were not completely restored between successive dialysis treatments, making levels measured immediately before the third weekly sessions significantly lower than those measured before the first session (p less than 0.01). In patients monitored throughout 25 wk of treatment, there was an exponential decay of both total serum carnitine levels (Spearman's r = -0.993, p less than 0.001) and free carnitine levels (Spearman's r = -0.972, p less than 0.001). It is suggested that in the absence of exogenous supplies of carnitine, endogenous synthesis is unable to make up for losses due to dialysis treatment, and that carnitine deficiency consequently ensues.

Adolescent↗
PubMed1985

Determination of L-carnitine in serum, and implementation on the ABA-100 and CentrifiChem 600.

Deproteinization of serum samples by heating to 100 degrees C, then freezing, allows up to 60% of the volume of the sample to be recovered. Concentrations of L-carnitine in samples so treated are comparable with those obtained by more sophisticated and expensive methods, and precision and accuracy are similar to those of other available techniques. There is no medically significant difference between results obtained in the ABA-100 and CentrifiChem 600, and the method is suitable for screening studies. Concentrations in the serum of presumably healthy adults ranged from 29.3 to 66.1 mumol/L. As little as 3 mumol of L-carnitine per liter can be determined.

Carnitine↗
PubMed1982

Serum copper concentration and hepatic enzyme induction during long-term therapy with anticonvulsants.

We evaluated hepatic enzyme induction by measuring urinary D-glucaric acid and serum gamma-glutamyltransferase in a group of 40 adult epileptics of both sexes who were receiving long-term treatment with phenobarbital and (or) phenytoin. Total concentrations of copper and ceruloplasmin in their serum and the oxidase activity of ceruloplasmin were significantly greater than in the control group. However, non-ceruloplasmin copper and specific oxidase activity of the ceruloplasmin (activity per gram) were unchanged. A highly significant relationship was found between gamma-glutamyltransferase and (a) copper (r = 0.682, p less than 0.001), (b) ceruloplasmin (r = 0.523, p congruent to 0.001), and (c) the oxidase activity of the ceruloplasmin (r = 0.598, p less than 0.001). There is also a significant correlation of hemopexin with ceruloplasmin (r = 0.531, p congruent to 0.001) and the oxidase activity of the ceruloplasmin (r = 0.598, p less than 0.001). These results suggest that hypercupremia in patients undergoing long-term anticonvulsant therapy is a direct result of hepatic enzyme induction caused by the drugs that induce synthesis of ceruloplasmin.

Adult↗