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Biomedical subjects

M Mattioli

Publications and source records attributed to M Mattioli.

At least 91 records · Page 5Linked to original sources
PubMed1981

Intravenous labetalol in severe hypertension. Effects on blood pressure, plasma renin activity and catecholamines.

2-Hydroxy-(1-hydroxy-[(1-methyl-3-phenylpropyl)amino]-2-ethyl)-5-benzamide (labetalol), a new alpha- and beta-adrenergic blocking agent, was employed in 21 patients with severe hypertension by slow (6 patients) and rapid (15 patients) i.v. infusion. A marked and significant fall of blood pressure was observed in both groups, though more gradual in patients treated by slow infusion. A rapid blood pressure fall with cardiac output decrease was observed by passing from supine to standing position in the first hours after infusion. Therefore, it is advisable to keep a supine position for a few hours. Plasma renin activity decreased after labetalol infusion, but basal plasma renin levels were not related to hypotensive effect of labetalol. In slow infusion patients, plasma noradrenaline levels increased and no changes of plasma adrenaline levels were observed during infusion. The most likely explanation of these variations is an increase of sympathetic activity secondary to hypotension, caused by labetalol, whereas a technical interference seems to be excluded. The simultaneous blockade of alpha- and beta-receptors can inhibit, in this case, the pressor effects of the sympathetic reflex.

Adult↗
PubMed1979

Kidney 15-hydroxy-prostaglandin-dehydrogenase activity during the development of experimental hypertension in the rat.

15-hydroxy-prostaglandin-dehydrogenase (PGDH) activity was studied in rat kidney homogenates during the development of hypertension, within 20 days after left renal artery constriction by a solid silver clip. In the ischemic kidney PGDH activity increased at day 6, reached maximum at day 10, then progressively at day 15 and returned to normal levels at day 20. No difference was found between contralateral kidneys and kidneys of normotensive control rats. Variations of PGDH activity did not seem to be related to either renal perfusion pressure or renin production. Increased PGDH activity may be a consequence of an enzyme induction following increased PG-synthetase activity, or it could be viewed as a defence mechanism, according to the hypothesis of a prohypertensive effect of PG in the rat.

Animals↗
PubMed1977

Ferritin distribution and synthesis in sex-linked anemia.

The ferritin concentration of duodenum, liver, and spleen and the incorporation of L-leucine-3H into immunoprecipitated duodenal and liver ferritin was measured in genotypically normal (+/Y) mice and mice with sex-linked anemia (sla/Y), an X-linked recessive trait determined by a defect in intestinal iron absorption. Liver and splenic ferritin concentration was lower in sla/Y animals than in +/Y animals. Parenteral iron administration produced an increase in the duodenal, liver, and splenic ferritin concentration in both sla/Y and +/Y animals that was most striking in the case of the liver. Duodenal ferritin synthesis, both in vivo and in vitro, was increased in iron-deficient sla/Y animals and decreased in iron-deficient +/Y animals. In contrast, liver ferritin synthesis was decreased in both sla/Y and +/Y iron-deficient animals. In sla/Y animals fed an iron-deficient diet, duodenal ferritin synthesis decreased to near normal levels. These results indicating a high level of duodenal ferritin synthesis in standard-fed mice with sex-linked anemia suggest that the primary genetic defect is more likely a disorder of intramucosal iron transport than a primary disturbance of ferritin metabolism.

Anemia↗
PubMed1976

Antinuclear antibodies (ANA): immunologic and clinical significance.

The methods currently used for the detection of ANA have been analyzed, with emphasis on their practical application to the diagnosis of the CTD. The use of the indirect IF-ANA test was recommended as a screening procedure to detect ANA. The need to standardize the technique using a single substrate and fluorescent conjugates with uniform F/P ratios was stressed. Most importantly, the value of titrating ANA for the diagnosis of the CTD was discussed. ANA titers higher than 1/500 are usually very significant clinically, often found in spontaneous or drug-induced SLE and few other CTD. The immunologic aspects of ANA and their potential value as aids in the diagnosis and management of the CTD were discussed. Anti-nDNA antibodies have been found to have a high degree of specificity for SLE and high titers of these antibodies correlate well with low levels of serum complement and severity of kidney involvement. The spectrum of ANA in the sera from patients with SLE has been expanded with the finding of anti-Sm antibodies which, when detected by gel precipitation with prototype serum, have been found so far only in SLE. Some of these antibodies have been found to have prognostic significance. Patients with MCTD and a group of patients with SLE have high titers of serum ANA with specificity for an RNase-sensitive component of ENA. The group of SLE patients defined by the presence of these antibodies (anti-Mo) have a better prognosis and in general develop only mild nephritis or have no kidney involvement at all. High titers of pure antinucleolar antibodies probably are found almost exclusively in the sera of patients with scleroderma. Some ANA have organ specificity, and GS-ANA have been found in all patients with Felty's syndrome and in a large proportion of patients with RA. One of the great advances in the field has been the recognition that ANA can be induced in the human and in experimental animals by the use of a number of therapeutic agents. Some of these agents can also induce a clinical picture resembling spontaneous SLE, though kidney involvement does not occur or is extremely mild. It is interesting that the whole spectrum of ANA can be found in drug-induced LE except anti-nDNA antibodies which have been associated to the pathogenesis of immune complex nephritis in spontaneous SLE. There is no doubt that research on ANA has contributed a great deal to the understanding of the CTD and will continue to be a valuable tool for the clinician and the investigator.

Animals↗
PubMedDate not supplied

Mutations in the HFE gene and their interaction with exogenous risk factors in hepatocellular carcinoma.

The possible role of iron in facilitating the development of liver cancer is still debated. The aims of this study were to define the prevalence of the mutations 845G --> A and 187C --> G (C282Y and H63D) in the HFE gene associated with hereditary hemochromatosis in Italian patients with hepatocellular carcinoma occurring in cirrhosis and to analyze the interaction between these mutations and other established risk factors for hepatocellular carcinoma. The HFE gene mutations, performed by polymerase chain reaction, were analyzed in 81 patients (63 males, 18 females) with hepatocellular carcinoma. None of the patients had a phenotype compatible with homozygous hereditary hemochromatosis. Interaction between HFE mutations and exogenous risk factors was analyzed by collecting information on alcohol consumption, hepatitis B and C virus infections, and iron status at the time of diagnosis of chronic liver disease. This analysis was performed only in males to rule out gender influence on patients' iron status by using the case-only approach specifically designed to estimate departure from multiplicative risk ratios under the assumption of independence between genotype and environmental exposure. The prevalence of the C282Y mutation was significantly higher in patients with hepatocellular carcinoma than in normal controls (8.6% vs 1.6%, P < 0.03). At univariate analysis, iron overload was significantly associated with both HFE mutations (P < 0.0001), whereas ongoing hepatitis B virus infection was associated with the C282Y mutation (P < 0.05). By multivariate analysis, a trend for an increased risk of being positive for hepatitis virus markers (OR 2.9, CI 95% 0.9-9.5) and of having been alcohol abusers (OR 3, CI 95% 0.7-14) was observed in patients heterozygous for the HFE mutations. These data indicate that the prevalence of the main mutation associated with hereditary hemochromatosis is significantly higher in cirrhotic Italian patients with hepatocellular carcinoma compared to a normal population and suggest that heterozygotes for HFE mutations exposed to hepatitis virus infections or who had been alcohol abusers could have an increased risk of developing cirrhosis and later liver cancer than people without the mutations exposed to the same risk factors.

Carcinoma, Hepatocellular↗