Search PubMed⌕ Search

Biomedical subjects

G Gasbarrini

Publications and source records attributed to G Gasbarrini.

At least 469 records · Page 26Linked to original sources
PubMed1989

Cytophilic antibodies cause leucocyte migration inhibition in coeliac disease.

Leucocyte migration inhibition in response to challenge with gluten fraction III was prevented by pretreatment of coeliac leucocytes with pronase, an enzyme that removes cytophilic antibodies. Leucocytes from healthy volunteers preincubated with serum from untreated and treated coeliac patients showed marked migration inhibition when incubated with gluten fraction III. No migration inhibition was observed with leucocytes from healthy volunteers preincubated with serum from patients with small bowel diseases other than coeliac disease and from other healthy volunteers. Untreated and treated coeliac patients who were leucocyte migration inhibition negative in the direct assay had migration indices in the sensitized range in the serum induced assay. This work is in keeping with a previous suggestion that in coeliac disease leucocyte migration inhibition induced by gluten fraction III is caused by cytophilic antibodies.

Adult↗
PubMed1989

"Low T3 syndrome" in cirrhosis: effect of beta-blockade.

The so-called "low T3 syndrome" has frequently been reported in patients with cirrhosis. In this study, we aimed to determine whether administration of propranolol to such patients leads to further changes in plasma thyroid hormones, since it can affect their peripheral metabolism. Twenty cirrhotics (11 with ascites) whom we investigated showed no clinical evidence of thyroid dysfunction. The free fractions of plasma T3 and T4 (FT3, FT4) were determined by radioimmunoassay before and after the achievement of an effective beta-blockade by propranolol. The activity of the sympathetic nervous system also was evaluated by measuring plasma norepinephrine concentration. Under basal conditions, cirrhotics showed a reduced FT3 (2.45 +/- 0.11 SEM vs 3.55 +/- 0.16 pg/ml; p less than 0.001) and comparable FT4 (7.62 +/- 0.79 vs 9.2 +/- 0.42 pg/ml) and FT3/FT4 ratio (0.38 +/- 0.04 vs 0.42 +/- 0.013) with respect to healthy controls. When patients with ascites were considered apart, a reduction of FT4 was also found (6.78 +/- 0.74 pg/ml; p less than 0.01). In these patients, many of whom showed an increased plasma norepinephrine concentration, an inverse correlation between log FT3/FT4 and log plasma norepinephrine concentration was found (r = -0.79; p less than 0.01). The effective beta-blockade did not lead to significant changes in either FT3 or FT4 or FT3/FT4, whether the patients were considered as a whole (2.52 +/- 0.19 pg/ml, 9.3 +/- 1.41 pg/ml, and 0.36 +/- 0.04, respectively), or were split into groups according to the presence of ascites. When administered to cirrhotics, propranolol did not worsen thyroid hormone abnormalities, thus appearing to be safe in this respect. This may result from an impaired influence of the sympathoadrenergic system on thyroid hormone metabolism.

Adult↗
PubMed1988

Endoscopic demonstration of loss of duodenal folds in the diagnosis of celiac disease.

Among 873 patients undergoing upper gastrointestinal endoscopy for various reasons over a two-year period, four had a loss of Kerckring's folds in the descending duodenum. Endoscopic duodenal biopsy in all four patients revealed subtotal villous atrophy due to celiac disease. We undertook a prospective study to evaluate the extent to which this finding predicted celiac disease in 65 consecutive patients referred for intestinal biopsy. Duodenal folds were absent or markedly decreased in 15 of 17 patients with subtotal villous atrophy and in 8 of 48 patients with partial villous atrophy or normal duodenal mucosa, giving a sensitivity of 88 percent and a specificity of 83 percent for this endoscopic finding with respect to celiac disease. We recommend that all patients undergoing upper gastrointestinal endoscopy be examined for the loss or reduction of duodenal folds and, should this be found, that the examination include duodenal biopsy. The value of this procedure as an aid in the diagnosis of celiac disease should be particularly great in patients with minimal, transient, or unrelated symptoms.

Adult↗
PubMed1988

Decreased plasma postheparin diamine oxidase levels in celiac disease.

The highest diamine oxidase activity is contained in small-bowel mucosa and, after heparin administration, the enzyme is released by the intestine into the plasma. Previous experimental studies showed that measurement of plasma postheparin diamine oxidase activity is a sensitive test for quantitating the length and severity of small-bowel mucosal injury. On this basis, we measured plasma diamine oxidase activity in celiac disease, a condition characterized by a loss of mature enterocyte mass. Twenty-five untreated celiac patients, 21 celiac patients on a gluten-free diet, 16 patients with small-bowel diseases other than celiac disease (abnormal controls), and 18 healthy controls were studied. Diamine oxidase activity was measured using [14C]putrescine as substrate and expressed as units per milliliter of plasma. Basal diamine oxidase levels in controls and patients were too low for significant differences between the groups to be detected. After preliminary experiments in which, on separate occasions, heparin was intravenously administered at doses of 75 and 150 units/kg and in which the second blood sample was taken 10 and 30 min after heparin injection, it was decided to use the 150 unit/kg dose and to measure plasma diamine oxidase activity in the blood sample taken 10 min after heparin stimulation in all the remaining subjects taking part in the study. Postheparin diamine oxidase levels were significantly lower in untreated celiac patients (mean 1.53 units/ml) than in healthy controls (mean 5.85), treated celiac patients (mean 4.82), and abnormal controls (mean 2.62). Except in three patients, no overlap between healthy controls and untreated celiac patients was observed. No significant difference was detected between healthy controls and treated celiac patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis.

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.

Adult↗
PubMed1988

Acute phase proteins in chronic and malignant liver diseases.

Six acute phase proteins (haptoglobin, alpha 1-acid glycoprotein, alpha 1-antitrypsin, alpha 2-macroglobulin, C reactive protein and transferrin) have been measured in the sera of chronic liver disease (CLD) patients with different aetiology (viral, autoimmune and alcoholic) and histology (steatosis, chronic persistent hepatitis, chronic active hepatitis, cirrhosis), and in patients with liver cancer. 1) The most striking changes concerned alpha 2-macroglobulin (increased) and haptoglobin (decreased) levels. 2) Transferrin was lower in alcoholic liver disease than in viral CLD, CRP was lower in autoimmune than in viral or alcoholic CLD, and alpha 1-acid glycoprotein was lower in viral and alcoholic CLD than in autoimmune CLD. Acute phase protein assay may prove useful in differential diagnosis, particularly when specific markers are not available (autoimmune, non A, non B, alcoholic liver diseases). 3) No significant differences related to aetiology (B, non A non B, D viruses) were observed in viral CLD. 4) Patients who progressed to CLD after acute viral hepatitis type B or non A non B did not show different APP levels from those who had recovered when tested 8-12 months after the acute phase. 5) The pattern of APP changes observed in primary liver cell carcinoma was different from both the cirrhotic pattern and the pattern presented by other tumours with or without liver metastasis.

Acute-Phase Proteins↗
PubMed1988

Sorbitol malabsorption in normal volunteers and in patients with coeliac disease.

Sorbitol is a hexahydroxy alcohol used as a sugar substitute in many dietetic foods and as a drug vehicle. Previous studies have suggested that sorbitol ingestion may be an additional cause of non-specific gastrointestinal distress. We evaluated sorbitol malabsorption in 30 healthy volunteers, seven patients with untreated coeliac disease and nine patients with coeliac disease on a gluten free diet, using a four hour H2 breath test. After ingestion of test solutions containing sorbitol 10 and 20 g and of four sweets (6.8 g sorbitol), 90%, 100%, and 62% of healthy volunteers, respectively had significantly raised H2 excretion, indicating malabsorption of sorbitol. Of all healthy subjects tested, 45% after 10 g, 100% after 20 g, and 50% after four sweets complained of symptoms of carbohydrate intolerance during the eight hours after sorbitol. After a 5 g dose given at concentrations of 2%, 4%, 8%, 16%, malabsorption was shown in 10%, 12%, 22%, and 43% of the healthy volunteers. Symptoms of intolerance at 5 g were experienced only at concentrations of 8% and 16%. Unlike healthy volunteers and coeliac patients on a gluten free diet, 100% of untreated coeliacs malabsorbed a 2% solution of 5 g sorbitol. These results show that malabsorption and intolerance of sorbitol may result from ingestion of doses and/or concentrations usually found in many foods and drugs; they underline the need to consider this as a possible and hitherto underestimated cause of gastrointestinal symptoms.

Adult↗
PubMed1988

Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis.

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.

Adult↗
PubMed1987

Chronobiological evaluation of sympathoadrenergic function in cirrhosis. Relationship with arterial pressure and heart rate.

Intraday activity of the adrenergic system was investigated in 7 healthy controls and in cirrhotic patients without ascites (group 1, 7 cases) and with ascites (group 2, 9 cases) by determining the urinary norepinephrine and vanillylmandelic acid excretions at 4-h intervals for 24 h. Mean arterial pressure and heart rate were also recorded. In controls, the statistical evaluation by the cosinor method showed a circadian rhythm of such variables, with zenith in the morning and nadir at night. Intraday changes of urinary excretion of norepinephrine were closely related to arterial pressure and heart rate in most subjects. The most important change in cirrhotic patients was the achronia [no detection of a statistically significant (p greater than 0.05) rhythm] in urinary excretion of norepinephrine and arterial pressure. This occurred not only in group 2 patients, who had lower arterial pressure and higher NE mesors than controls (p less than 0.05), but also in group 1 patients, whose mesors were comparable to controls. The statistical significance of heart rate rhythmicity was preserved in patients, but its zenith was progressively displaced toward evening (group 1) and night hours (group 2, whose mesor was increased). Changes in urinary excretion of vanillylmandelic acid roughly paralleled those of norepinephrine both in controls and patients, but they did not significantly increase even in the group with ascites. In both groups of cirrhotic patients, the correlation between urinary excretion of norepinephrine, arterial pressure, and heart rate within the same subject was lost in most cases. This chronobiological study showed that the sympathoadrenergic activity can be deranged also in the early stages of cirrhosis, and suggested that an altered control of cardiovascular homeostasis is present even under steady state conditions. This alteration might blunt adrenergic responses to stress conditions.

Adrenergic Fibers↗
PubMed1987

Fasting breath hydrogen in celiac disease.

We studied the possible clinical significance of high basal levels of H2 by analyzing the breath excreted by the following fasting subjects: 50 healthy volunteers, 149 subjects with functional bowel disorders, 16 patients with small bowel bacterial overgrowth proven by bacteriology, 34 patients with untreated celiac disease, 40 patients with celiac disease on a gluten-free diet, and 40 patients with disorders of the small intestine other than celiac disease (disease controls). The fasting levels of H2 in untreated celiac patients (mean 22.5 +/- 19.3 ppm) were significantly higher than those in healthy volunteers (5.8 +/- 3.1 ppm), patients with functional bowel disorders (6.6 +/- 4.4 ppm), treated celiac patients (9.9 +/- 8.1 ppm), and disease controls (7.0 +/- 6.7 ppm). No significant difference was found between patients with untreated celiac disease and bacterial overgrowth (mean 14.7 +/- 14.0 ppm). The percentage of patients with elevated H2 fasting levels in untreated celiac disease (58.8%) was significantly higher than that in the other groups, except for the patients with bacterial overgrowth (43.7%). In 14 celiac patients, studied before and after a gluten-free diet, fasting H2 levels decreased from 26.6 +/- 18 to 11.6 +/- 10 ppm, becoming normal only in those patients with healing of intestinal lesions. Our results show that high fasting H2 levels are a frequent feature of untreated celiac disease and that the return to normal of these levels is predictive of villous regrowth.

Adult↗
PubMed1987

A possible cytotoxicity inducer role of 5/9 positive lymphocytes infiltrating the liver in CAH patients.

The presence, in chronic active hepatitis (CAH) patients, of an inflammatory infiltrate basically composed of T lymphocytes suggested the hypothesis that these lymphocytes could play a role in the pathogenesis of the disease. The aim of this study has been to characterize, in a group of carefully selected CAH patients, the liver-infiltrating T lymphocyte, utilizing commercial monoclonal antibody (anti-Leu 1, anti-Leu 2a, anti-Leu 3a) and 5/9 monoclonal antibody that recognizes a further lymphocyte subset within T4 cells. Our data show that both T4 positive subpopulation and T8 positive subpopulation are represented in the infiltrate in the same ratio; furthermore the distribution of 5/9 positive lymphocytes is prevalent where the infiltrate is mainly composed of T8 positive lymphocytes. Moreover, there is a positive correlation between 5/9 positive cells in the liver and GPT and the patients with high percentages of infiltrating 5/9 positive lymphocytes show a low T4/T8 ratio with respect to patients with low percentages of 5/9 positive cells. These data support the hypothesis that 5/9 positive lymphocytes may present an inducer role on cytotoxic cells.

Adult↗
PubMed1987

Expression of major histocompatibility complex class II antigens on bile duct epithelium in patients with hepatic graft-versus-host disease after bone marrow transplantation.

We studied the expression of major histocompatibility complex (MHC) class II antigens in liver biopsies taken from ten patients with clinical and biochemical evidence of liver damage after bone marrow transplantation. In all six patients who had histologically confirmed graft-versus-host disease, MHC class II antigens were detected on intrahepatic bile ducts. In four patients with no histological features of graft-versus-host disease, MHC class II antigens were not detected. In controls, a positive reaction for bile duct MHC class II antigens was only detected in the patients with primary biliary cirrhosis. Characterisation of the lymphocytes surrounding the bile ducts showed a prevalence of Leu 3+ cells in graft-versus-host disease and primary biliary cirrhosis. We propose that the aberrant expression of class II antigens on bile duct epithelium cells may play a role in the pathogenesis of graft-versus-host disease. A similar pattern in primary biliary cirrhosis may suggest a common pathogenetic mechanism.

Adult↗
PubMed1987

Alterations in helper-specific circulating T lymphocytes and in the autologous mixed lymphocyte reaction in chronic hepatitis B.

Defects in T lymphocyte subpopulations and in the functional characteristics of such cells have been thought to play a role in the evolution of chronic hepatitis B, but the precise nature of the alterations and their significance remains unresolved. We studied lymphocyte subsets in 27 patients with chronic hepatitis B utilizing standard monoclonal antibodies including Leu 1,2a,3a,7 and D1/12 (against the common determinant of the Dr molecule), as well as a newly described monoclonal antibody, "5/9," which is thought to characterize a unique subpopulation of T4 cells with specific helper/inducer function. These results were compared with those obtained using the autologous mixed lymphocyte reaction assay for the same patients in order to further delineate the lymphocyte alterations in chronic hepatitis B. A significant reduction in the mean number of Leu 3a (T4) positive cells was observed as well as a reduction in the number of 5/9 positive cells. These changes were most evident in those positive for HBeAg in serum. Reduction in Leu 3a cells was associated with a reduced autologous mixed lymphocyte reaction assay response, and was most marked in the HBeAg-positive individuals. These findings suggest that HBeAg-positive patients in whom active viral replication is occurring have a defect in T lymphocyte number and function, which may be due in part to reduced 5/9 positive cells. These alterations may be related to the persistence of virus in chronic active hepatitis B patients.

Antibodies, Monoclonal↗