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Biomedical subjects

R Cuomo

Publications and source records attributed to R Cuomo.

33 records · Page 2Linked to original sources
PubMed1999

Manometric study of hiatal hernia and its correlation with esophageal peristalsis.

The pathogenesis of gastroesophageal reflux disease (GERD) is considered multifactorial, but alterations of the esophagogastric junction (EGJ) and hiatal hernia play a prominent role. The correlations between hiatal hernia and the other pathogenetic factors are as yet unclear, and they need to be investigated by a methodological approach based on new anatomic and functional criteria. Our aim was to study, by stationary manometry, the relationships between small reducible hiatal hernia, identified by endoscopy, and esophageal peristalsis, in patients with and without GERD. According to the absence or presence of esophagitis (E), and the absence or presence of hiatal hernia (H), 58 subjects were divided into four groups: controls 10; H 14; E 10; and HE 24. Stationary manometry was performed by the rapid pull-through (RPT) technique, with catheter water perfused, to study the lower esophageal high pressure zone [lower esophageal sphincter (LES) and diaphragmatic crura] and the parameters of esophageal peristalsis. In patients with hiatal hernia, the various combinations of peak and/or deflection of manometric line pressure identified five EGJ profiles, only one of which reveals (by one-peak profile due to superimposed LES and diaphragmatic crura) the reducibility of the hernia. The frequency of the five profiles was calculated in the HE and H groups: a two-peak profile was significantly more prevalent in these patients, although less so in the group with esophagitis. In E patients the distal amplitude and the distal propagation of esophageal waves were significantly lower than in the other three groups (P < 0.05 vs controls and group HE; P < 0.01 vs group H). Furthermore, the distal amplitude was significantly higher in the group H than in the HE (P < 0.01). Our results show a better definition of hiatal hernia morphology, via the RPT technique, disclosing five pressure profiles. In addition, a significant link was found between small reducible hiatal hernia without GERD and wave amplitude of the distal esophagus. The amplification of peristaltic clearing may be considered the initial protective process against acid reflux; the breakdown of this mechanism may trigger the pathological sequence of GERD.

Adult↗
PubMed1996

Intravenous load of fructose and fructose 1,6-diphosphate: effects on uricemia in patients with nonalcoholic liver disease.

OBJECTIVES: The i.v. load of fructose causes a significantly higher adenosine triphosphate (ATP) degradation and uric acid production in cirrhotic patients than in healthy controls. Resynthesis of ATP from adenosine diphosphate (ADP) may be facilitated by the phosphorylated compound fructose 1,6-diphosphate, which is used as energy support in parenteral nutrition. The aim of our research was to evaluate: 1) The 1-h uricemic effect of i.v. fructose (0.5 g/kg body weight) in 10 healthy controls and in 78 patients with differenct stages of non-alcoholic chronic liver damage associated or not with malnutrition or hepatocellular carcinoma; and 2) the effect of fructose 1,6-diphosphate (5 g/50 ml) administered i.v. after fructose infusion on the induced uricemia in a subgroup of 13 patients with well compensated cirrhosis. RESULTS AND CONCLUSIONS: The increase of uricemia above the basal level after fructose infusion was significantly higher (p < 0.01) in cirrhotics (3 mg/dl) than in controls (1.2 mg/dl) and in patients with chronic hepatitis (1.9 mg/dl) and was completely reversed by fructose 1,6-diphosphate in the patients tested. Neither Child-Pugh classes of cirrhosis nor malnutrition (present in about 50% of the patients) or hepatocarcinoma significantly affected the fructose-induced uricemia. Therefore, the fructose test efficiently differentiates cirrhotics from chronic hepatitis patients and healthy subjects, but it does not distinguish the various stages of the progression of cirrhosis or its complications.

Adult↗
PubMed1995

Nicotinamide methylation and hepatic energy reserve: a study by liver perfusion in vitro.

BACKGROUND/AIMS: The synthesis of pyridine nucleotides from nicotinamide requires adenosine triphosphate. In man when exogenous nicotinamide is poorly utilized in this synthesis, the excess follows a dissipative metabolic pathway and is excreted in urine as N-methylnicotinamide. In human cirrhosis N-methylnicotinamide serum levels are higher than normal, in basal condition and after nicotinamide oral load. The aim of this study was to verify N-methylnicotinamide production in relation to hepatic content of adenosine triphosphate during in vitro perfusion of rat liver, in normal conditions and after adenosine triphosphate depletion by metabolic stress. METHODS: "Stress" was obtained by pre-washing with saline for 15 min before the perfusion with nutritive medium. RESULTS: The adenosine triphosphate decrease in the stressed liver was 38% after pre-washing with saline and 80% at the end of nutritive perfusion. In control liver the corresponding decreases were 1% after pre-washing with nutritive medium and 65% at the end of perfusion with the same medium. The total nicotinamide adenine dinucleotide decreases were 44% and 56% in the stressed liver, and 19% and 52% in the control liver. The output levels of N-methylnicotinamide at 90 min of rat liver nutritive perfusion were 31.50 +/- 4.72 nmol/g for normal liver and 66.40 +/- 13.17 for stressed liver (p<0.001). Liver adenosine triphosphate was inversely related to N-methylnicotinamide production (r=0.93; p<0.001). CONCLUSIONS: These data suggest that nicotinamide methylation may be enhanced when there is hepatic adenosine triphosphate decrease and energy failure induced by hypoxia or metabolic stress, similar to that obtained in vitro by saline washing before perfusion with nutritive medium. This study shows that the evaluation of N-methylnicotinamide production in man (before and after nicotinamide load) might be useful to explore the energy state of diseased liver.

Adenosine Triphosphate↗
PubMed1994

Nicotinamide methylation in patients with cirrhosis.

Methylation reactions play an important role in the transformation of endogenous and exogenous substances. Up to 85% of all transmethylation reactions occur in the liver. Several studies have shown that these metabolic processes are greatly influenced by the presence of hepatic diseases. We investigated the methylation of nicotinamide in 16 control subjects and in 29 patients with cirrhosis (19 Child A, 10 Child B). The basal serum value of N-methyl-nicotinamide was measured in all subjects. In seven controls and in nine patients with cirrhosis (5 Child A and 4 Child B), the serum levels and urinary excretion (5 and 24 h) of N-methyl-nicotinamide were also evaluated after oral administration of nicotinamide (1.5 mg/kg body weight). The basal serum levels of N-methyl-nicotinamide were significantly (p < 0.05) higher in patients with cirrhosis (Child A: median 34 ng/ml, 16th percentile 24, 84th percentile 61; Child B median 45, 16th percentile 34, 84th percentile 81) than in controls (median 22, 16th percentile 13, 85th percentile 28). After the nicotinamide load the urinary excretion and the time course of serum N-methyl-nicotinamide in cirrhosis were also higher (p < 0.05) than in controls (24 h urinary excretion = 66.2 mg +/- 5 S.D. in cirrhosis; 47.2 +/- 10.3 in controls) (area under the serum concentration versus time curve = 68 micrograms.ml-1.min-1 +/- 22 S.D. in cirrhosis; 32 +/- 15 in controls). In conclusion, our results show that cirrhosis does not impair the efficiency of nicotinamide methylation.

Female↗
PubMed1991

Bile and biliary lipid secretion in rats with hexachlorobenzene-induced porphyria. Effect of S-adenosyl-L-methionine administration.

We investigated liver morphology and biliary function in vivo in rats made porphyric by hexachlorobenzene (HCB). In one group of HCB rats we also evaluated whether S-adenosyl-L-methionine (SAMe), administered during the last 15 days of HCB treatment, attenuated liver injury and the accumulation of porphyrins (HCB + SAMe group). In HCB rats we found: (a) a 100% increase in liver weight; (b) a 500-fold increase in total liver porphyrins (TLP); (c) significantly increased serum bilirubin and cholesterol levels; (d) unchanged total bile flow (TBF) but enhanced levels of the bile acid independent fraction (BAIF); and (e) decreased excretion in bile of bile acids (BA), phospholipids (PL) and cholesterol (CHO) (58, 65 and 47%, respectively, expressed as mmol/min per kg liver). SAMe was found to partially reverse HCB-related effects. TLP levels were about 65% lower in HCB + SAMe treated rats than in HCB rats. However, while SAMe restored bile CHO excretion to control values, it did not influence bile excretion of BA, PL, or BAIF. In conclusion, HCB-induced porphyria was characterized by a complex derangement of liver morphology and biliary function that was unrelated to the extent of porphyrin accumulation in the liver.

Animals↗
PubMed1990

Bile acids reversible effects on small intestinal permeability. An in vitro study in the rabbit.

To define the action of deconjugated bile acids on the small intestinal permeability in an in vitro system, we investigated the effects of chenodeoxycholic acid and ursodeoxycholic acid on the rate of transmural flux of lactulose in jejunal and ileal mucosa of rabbits, stripped of their muscle layers and mounted in Ussing chambers. In a series of experiments, tissue samples from small intestinal segments either exposed to bile acids or not also were examined by scanning and transmission electron microscopy to study the integrity of the tight junctions. Results show that chenodeoxycholate, starting at the concentration of 0.1 mM, enhanced in a dose-related manner the transepithelial flux of lactulose in the ileum. Both chenodeoxycholate (0.5 mM) and ursodeoxycholate (0.5 mM) significantly increased mucosal permeability to lactulose in jejunum and ileum; the effect of chenodeoxycholate was also shown to be reversible, as it completely disappeared within 40 min after its withdrawal and it did not result in permanent changes of epithelial transport function. Finally, the tight junctions appeared loosened by the addition of 1 mM chenodeoxycholate, suggesting that this is the major site of the transient bile acid increase of small intestinal permeability to compounds such as lactulose, having a molecular radius wider than 0.5 nm.

Animals↗
PubMed1990

Jejunal bacterial overgrowth and intestinal permeability in children with immunodeficiency syndromes.

Seventeen paediatric patients with immunodeficiency syndromes (10 with selective IgA deficiency, four with panhypogammaglobulinaemia, and three with selective T cell deficiency) were investigated for bacterial overgrowth of the small intestine and gut permeability to macromolecules. Five of 12 patients showed viable bacterial counts of more than 2 x 10(5)/ml in jejunal fluid. Bacterial overgrowth was also confirmed indirectly by breath hydrogen determination, which was higher than 10 ppm in four of the five patients with positive jejunal culture. Gut permeability to lactulose and L-rhamnose was abnormal in 16 of the 17 immunodeficient patients, who also had higher mean urinary excretion ratios than control subjects-mean (SD) values were 0.216 (0.160) and 0.029 (0.002), respectively. These studies indicate that bacterial overgrowth of the small intestine is a common feature in immunodeficient patients, regardless of the immunological abnormality. Moreover, these patients have an increased gut permeability to macromolecules.

Adolescent↗
PubMed1990

Protective effect of S-adenosyl-L-methionine in hepatic uroporphyria. Evaluation in an experimental model.

The potential use of S-adenosyl-L-methionine (SAMe) as therapy for human porphyria cutanea tarda was investigated in an experimental model of hepatic porphyria--that is, chronic treatment of female rats with 0.2% hexachlorobenzene (HCB) in the diet. Administration of SAMe (25 mg/kg subcutaneously twice daily) during the last 15 days of HCB administration halved porphyrin accumulation in the liver but did not alter HCB-induced massive inhibition of uroporphyrinogen decarboxylase. Equally unaffected were inhibition of glutathione peroxidase and stimulation of lipid peroxide formation induced by HCB. Hypothetically, the beneficial effect of SAMe on hepatic porphyrin accumulation might be linked to modifications of the cellular availability of adenosine triphosphate.

Animals↗
PubMed1989

Effects of anthracycline therapy on intestinal absorption in patients with advanced breast cancer.

Although cytotoxic chemotherapy for human cancer has been reported to induce alterations in intestinal permeability, its effects on the absorptive process are still controversial. We have studied mediated and nonmediated absorption in 10 patients with metastatic breast cancer before and after treatment with Adriamycin by the use of specific test sugars given orally and their subsequent urinary recovery, as measured by chromatography. Mediated absorption was investigated by the use of D-xylose and 3-O-methylglucose, while lactulose and L-rhamnose were used to study nonmediated permeation. Lactulose is considered a marker of unmediated paracellular (tight junction) permeation, while L-rhamnose explores passage across cell membranes. The test was performed on patients before and on the second and the eighth days after Adriamycin administration, and only once in 22 age-matched healthy women. Under basal conditions, as well as 2 and 8 days after chemotherapy, D-xylose and 3-O-methylglucose absorption was 35% lower in patients than in controls (P less than 0.001). Lactulose absorption was significantly higher in patients than in controls under basal conditions (P less than 0.001); it reached levels three times higher the second day after chemotherapy, and returned to basal levels by the eighth day. The data suggest an early reversible effect of Adriamycin on cellular tight junctions with resulting increased permeabilization. This effect seems of a toxic nature rather than due to increased cell loss. It is interesting that both nonmediated absorption and mediated absorption were already altered before chemotherapy in cancer patients, suggesting a preexisting functional damage of the intestine. The significance of this alteration as a potential mechanism of cancer cachexia is discussed.

3-O-Methylglucose↗
PubMed1987

Investigation of intestine function during acute viral hepatitis using combined sugar oral loads.

One fifth of all cases of A virus hepatitis (AVH) have symptoms of gastroenteritis at the onset. This study investigated the mediated intestinal absorption of D-xylose (D-xyl) and 3-o-methyl-D-glucose (3-omG) and the non-mediated permeation of lactulose (Lacl, mol wt 342) and L-rhamnose (L-rh, mol wt 164) during acute and remission phases of AVH. Ten patients with AVH were given an oral load containing these sugars (5 g D-xyl: 2.5 g 3-omG, 1 g L-rh, 5 g lacl in 250 ml water) once during the acute phase and again during remission. The same load was given once to a group of 22 healthy controls. The mean concentration of D-xyl in urine and the ratio of D-xyl to 3-omG in plasma and urine were normal in both the AVH phases, ruling out intestinal malabsorption even in the acute phase. This study showed a significant increase in non-mediated permeation to Lacl, but not to L-rh, during the acute phase. These data indicate that the barrier function of the intestine is compromised in AVH infection while the absorptive function is not. An abnormally low concentration of D-xyl and 3-omG in plasma at one hour was found in all patients during the acute phase. This finding cannot be explained by alterations in intestinal absorption, but could be accounted for by increased space distribution of the sugars because of increased diffusion into tissue cells and/or expansion of the extracellular space by fluid retention.

3-O-Methylglucose↗
PubMed1985

Investigation of intestine and liver function in cirrhosis using combined sugar oral loads.

Active and passive intestinal absorption and the efficiency of hepatic galactose clearance were studied in 12 patients with liver cirrhosis and 8 healthy control subjects using differential absorption techniques in which paired sugar markers were ingested simultaneously. Such differential absorption procedures overcome the effects of variation in gastric emptying, intestinal transit, distribution space and renal clearance which could invalidate tests incorporating a single marker only. In the cirrhotic group, active absorption of D-xylose (D-xyl) compared with that of 3-O-methyl-D-glucose (3-OMG), indicated by the ratio of D-xyl/3-OMG concentration in plasma, showed no reduction in respect to the control group. The passive intestinal permeability to lactulose (lac) compared with that of L-rhamnose (rham), indicated by urinary lac/rham excretion ratio, was not raised. These findings indicate no dysfunction of small intestinal mucosa in cirrhotic patients in spite of the clinical evidence of portal hypertension. Urinary galactose (gal) excretion after oral load was 10 times higher in the cirrhotic group (P less than 0.001). The gal/3-OMG excretion ratio correlated well with galactose elimination capacity as assessed by an intravenous method. Estimation of plasma D-xyl/3-OMG concentration and both urinary lac/rham and gal/3-OMG excretion ratios after appropriate oral loads provided a convenient and simultaneous evaluation of intestinal absorption, permeability and hepatic galactose elimination.

Adult↗
PubMedDate not supplied

Endoscopic ultrasound localization of a solitary insulinoma of pancreatic tail misdiagnosed as epilepsy: case report.

A 17-year-old female patient with features of epilepsy was treated with valproic acid. Two years later, hypoglycemia and hyperinsulinemia appeared. Transabdominal ultrasonography, spiral computed tomography, and indium-111 Octreoscan were performed without positive results. Endoscopic ultrasonography identified an oval tumor in the pancreatic tail with a color Doppler hypervascular pattern. Surgical enucleation decreased levels of insulin and C-peptide within 20 min, and the patient became free of symptoms and medications.

Adolescent↗
PubMedDate not supplied

Gastrointestinal peptide hormones in acute viral hepatitis.

Liver affects the release and clearance of many hormones, but the interactions between gastrointestinal peptides and liver function are obscure. Aim of this study was to evaluate plasma concentrations of gastrointestinal peptides during acute hepatic cytonecrosis and during liver regeneration in man. The study was performed in ten patients with viral hepatitis (8 virus A, 2 virus B) in the acute phase (alanine transaminase = 3073 +/- 739 U/L; mean +/- SEM), and at days 7, 45 and 52 after the initial evaluation, during clinical and biochemical recovery (52nd day, alanine transaminase = 77 +/- 26). Plasma concentrations of the following hormones were evaluated by radioimmunoassay: glucagon, insulin, gastrin, vasoactive intestinal peptide, bombesin, neurotensin, cholecystokinin, secretin and motilin. Only serum bombesin and cholecystokinin were significantly (p < 0.01) increased in the acute phase of hepatitis (bombesin: 138 +/- 21 pg/ml; cholecystokinin: 57 +/- 7 pg/ml); they returned to normal values during convalescence (bombesin: 60 +/- 8; cholecystokinin: 31 +/- 4). During hepatocellular necrosis, plasma concentrations of cholecystokinin and bombesin, which are both cellular growth factors and regulatory signals of food introduction and satiety state, were increased by 83% and 130%, respectively. Increase of these hormones may cause the dyspepsia and lack of appetite that characterizes the initial phase of acute viral hepatitis.

Acute Disease↗