We describe the case of a 58-year-old woman with autoimmune enteropathy associated with thyroiditis, gastritis, transitory neutropenia, sicca syndrome and severe axonal polyneuropathy of autoimmune origin. Enterocyte autoantibodies were not detected. However, predisposition to autoimmune disease was indicated by the presence of high titres of anti-gastric parietal cell, anti-thyroglobulin, anti-thyroid peroxidase and anti-neutrophil antibodies. CD4+ and CD8+ lymphocytes were equally distributed in the lamina propria of the small intestine, but CD8+ cells were highly represented among intraepithelial lymphocytes.

The purpose of this study was to identify the cis-acting elements and the trans-acting factors involved in the iron-induced expression of the collagen alpha1(I) (COL1aI) gene. Rat hepatic stellate cells were cultured in the presence of 50 microM ferric chloride, 50 microM ascorbic acid, and 250 microM citric acid (Fe/AA/CA), and the effects on collagen gene expression and the binding of nuclear proteins to the COL1aI promoter were measured. The Fe/AA/CA treatment induced a time- and dose-dependent increase in the cellular levels of COL1aI mRNA that was abrogate by pretreating cells with cycloheximide, antioxidants, and inhibitors of aldehyde-protein adduct formation. Transient transfection experiments showed that Fe/AA/CA exerted its effect through regulatory elements located between -220 and -110 bp of the COL1aI promoter. Gel retardation assays showed that Fe/AA/CA increased the binding of nuclear proteins to two elements located between -161 and -110 bp of the COL1aI promoter. These bindings were blocked by unlabeled consensus Sp1 oligonucleotide and supershifted with Sp1 and Sp3 antibodies. Finally, Fe/AA/CA increased cellular levels of the Sp1 and Sp3 proteins and Sp1 mRNA. Treatment with Fe/AA/CA stimulates COL1aI gene expression by inducing the synthesis of Sp1 and Sp3 and their binding to two regulatory elements located between -161 and -110 bp of the COL1aI promoter.

Acute pancreatitis due to ascaris lumbricoides infestation is extraordinarily uncommon in Europe. The diagnosis can be difficult because of the low index of suspicion in our area, and this may lead to death. The case of a Columbian patient living in Spain who developed an acute pancreatitis is discussed. He had no history of alcohol abuse, gallstones, or drug abuse. The sonography showed a longitudinal structure with inner parallel linear bands and undulant movements inside the gallbladder and a hypoechogenic pancreas. These features are compatible with acute pancreatitis secondary to Ascaris lumbricoides infestation. The patient was treated with mebendazole and his evolution was excellent. Sonography was useful as an assessment modality during follow-up. We conclude that Ascaris lumbricoides should be recalled as a rare cause of acute pancreatitis in Western countries. Sonography allows early diagnosis and prompt treatment.

Objective. To assess in a multicenter double blind clinical trial the gastroenteroprotective effect of zinc acexamate (ZAC).Methods. 276 patients with rheumatic disease and history of peptic ulcer or intolerance to nonsteroidal antiinflammatory drugs (NSAID), and requiring treatment with these drugs were included. An initial normal endoscopy was needed for inclusion. Patients were treated with one NSAID (diclofenac, piroxicam, naproxen or ketoprofen) and one capsule (300 mg) of either ZAC (141 patients) or placebo (135 patients) at single nocturnal dose. After 28 days, patients underwent a clinical and endoscopic control.Results. 26 patients withdrew from the trial (10 of ZAC and 16 of placebo) and 41 were lost to followup (22 of ZAC and 19 of placebo). Gastroduodenal mucosal damage was graded according to a modified Lanza score. The incidence of gastric ulcer was null with ZAC and 6.0% with placebo (6 cases) (p < 0.05). The incidence of duodenal ulcer was 0.9% with ZAC (1 case) and 6.0% with placebo (6 cases) (p < 0.05). Overall ulcer incidence was 0.9% with ZAC (1 case) and 12% with placebo (12 cases) (p < 0.001). Nine patients of ZAC group (8%) and 25 of placebo (25%) presented some gastric damage (p < 0.001), and 5 (5%) and 19 (19%) respectively presented some duodenal damage (p < 0.005). After treatment, 88% of patients treated with ZAC and 66% with placebo had a completely normal endoscopy (p < 0.0005). No major side effects were reported through the study.Conclusion. ZAC has shown to be effective and well tolerated for the prevention of NSAID induced gastroduodenal damage in patients with rheumatic disease at risk. The incidence of gastric and duodenal ulcers decreased in 92% (13 times the risk), when compared to placebo.

Background/Aims: Hepatic osmoreceptors are sensitive to changes in portal blood osmolity and cause variations in plasma antidiuretic hormone and water diuresis, which prevent major systemic osmotic changes. Insensitivity of hepatic osmoreceptors might contribute to maintaining increased plasma levels of antidiuretic hormone and negative free water clearance after oral hydration in some cirrhotic patients. Methods: We measured free water clearance and plasma arginine vasopressin levels in basal conditions and after oral, intravenous, and intragastric water overload in control subjects (group I) and patients with cirrhosis (some with a positive [group II] and some a negative [group III] free water clearance). Results: In groups I and II, no significant differences in plasma arginine vasopressin levels were found regardless of the route used for hydration. In group III, plasma levels were significantly higher between 0 and 75 minutes after intragastric hydration than after oral or intravenous hydration. No significant changes in plasma osmolality were detected between minute 0 and 20 after the end of oral or intragastric hydration, although plasma arginine vasopressin decreased significantly only 5 minutes after the oral hydration. Group III patients showed evidence of autonomic neuropathy. However, this dysfunction was unrelated to the insensitivity to gastric hydration. Conclusions: Hepatic osmoreceptors seem to be disturbed in some cirrhotic patients, although this dysfunction may be compensated for by normally functioning oropharyngeal and hypothalamic osmoreceptors.

The validity of brush cytology of the gastric mucosa with Diff-Quik rapid staining was studied in 69 samples, and its effectiveness was compared with two other techniques (culture and urease test). Brush cytology is the method of choice for detecting Helicobacter pylori since it is rapid, easy to perform and has good sensitivity and specificity.

BACKGROUND The aims of the present study were to 1) compare the serum levels of the aminoterminal peptide of procollagen type III (PIIIP) in patients with different chronic liver diseases, 2) correlate their concentrations with histologic features in liver biopsy and 3) evaluate their use in the diagnosis of liver diseases and in recognition of fibrosis. METHODS With these aims PIIIP was determined in 57 patients with different chronic liver diseases and in 50 healthy donors. RESULTS PIIIP was significantly elevated in patients with chronic active hepatitis (18.3 +/- 5.5 ng/ml; p less than 0.01) and with liver cirrhosis (27.8 +/- 11.7 ng/ml; p less than 0.001). The serum levels of this peptide related significantly with the severity of liver disease (p less than 0.001) in addition to the degree of morphometric liver fibrosis (Rs: 0.736; p less than 0.001) and with the degree of histologic activity (Rs: 0.78; p less than 0.001). The correlation between PIIIP and fibrosis was due to the relation between the same and inflammation. The levels of this peptide which were higher than 15 ng/ml were a sensitive test for the diagnosis of active liver disease (0.80) and cirrhosis (0.87) permitting differentiation between chronic and persistent active hepatitis. The differentiation between chronic active hepatitis and cirrhosis was only possible when 24 ng/ml were taken as a discriminative level. CONCLUSIONS The comparison of serum levels of the aminoterminal peptide of procollagen type III (PIIIP) in patients with different chronic liver diseases can predict moderate or high degrees of inflammatory activity when PIIIP are higher than 15 ng/ml. This test is of use for evaluating chronic hepatopathies although the levels reflect the activity of inflammation better than the degree of hepatic fibrosis.

We report a patient with common variable hypogammaglobulinemia and diffuse nodular lymphoid hyperplasia of the small intestine complicated by a jejunal malignant lymphoma. Immunopathological and histological studies showed a polymorphous centroblastic lymphoma with intracytoplasmatic IgM immunoglobulin and lambda light chains. Some mucosal nodules separate from the tumor mass showed atypical lymphoid cell populations similar to lymphoma cells, suggesting a transition between hyperplastic nodules and lymphoma nodules. Four similar cases, and six other patients with malignant lymphoma of the small intestine, associated with diffuse nodular lymphoid hyperplasia, but without immunodeficiency, have already been described. All these cases suggest that nodular lymphoid hyperplasia increases the risk of small intestine lymphoma.

Renal function and plasma antidiuretic hormone (ADH) levels were studied basally and after oral water load in four groups of subjects: 15 healthy controls (group I), 15 cirrhotics without ascites (group II), 15 cirrhotics with ascites (group III), and 10 decompensated cirrhotics with hyponatremia (group IV). Renal function and ADH levels were normal in group II. In groups III and IV water diuresis and fractional proximal sodium excretion were significantly decreased, whereas fractional distal sodium resorption and fractional excretion of potassium did not differ from those of controls. Basal ADH was significantly increased only in patients of group IV. In these patients ADH remained abnormally high after water loading. ADH did not correlate with water diuresis, plasma osmolality, mean arterial pressure, and plasma renin activity. We conclude that impaired water excretion in decompensated cirrhotics without hyponatremia cannot be ascribed to high serum levels of ADH. On the contrary, it seems to be related mainly to a reduced delivery of filtrate to the diluting segment of the nephron. In cirrhotic patients with hyponatremia high levels of ADH may play an additional role.

Plasma arginine vasopressin concentration (pAVP) was determined in 47 patients during the insufflation stage of laparoscopy. Laparoscopy was performed under local anesthesia in 39 patients, and under general anesthesia in 8. Pneumoperitoneum was induced with 3-4 1 nitrous oxide to a maximum intra-abdominal pressure of 10 mm Hg. Induction of pneumoperitoneum resulted in a prompt and significant increase in pAVP in every case. In 34% of cases, pAVP increased two- to fivefold as compared with preinduction levels; in 44.7% of cases, elevations of more than fivefold were seen. Increased arginine vasopressin secretion was not related to underlying liver disease, degree of anxiety, changes in blood pressure, heart rate, pCO2, pO2, serum bicarbonate or plasma osmolality. Elevated pAVP was associated with a significant increase in right atrial pressure. In conclusion, abdominal distension during laparoscopy was accompanied by an increase in pAVP. It seems likely that arginine vasopressin response could be due to a decrease in the left atrial transmural pressure gradient.

The Budd-Chiari syndrome due to membranous obstruction of the hepatic blood outflow tract is a rare condition in western countries, and its association with nodular regenerative hyperplasia of the liver has never been described. We present the case of a 34-year-old woman with membranous obstruction of hepatic veins and nodular regenerative hyperplasia of the liver. Although webs have been difficult to demonstrate by sonography, we were able to image a structure in the hepatic vein near the junction with the inferior vena cava, suggesting a membranous nature.

We studied the effects of unilateral lumbar sympathetic block on kidney function in eight patients with cirrhosis and hepatorenal syndrome. In five patients with basal glomerular filtration rate (GFR) below 25 ml/min, sympathetic block induced a significant increase in GFR, osmolal clearance, urinary sodium excretion, fractional excretion of filtered sodium (FENa) and effective renal plasma flow (ERPF) and a decrease in plasma renin activity. In the three patients with basal GFR greater than 25 ml/min, sympathetic block produced no significant change in renal function. We conclude that sympathetic block might improve renal function in cirrhotics with hepatorenal syndrome, particularly those with more impaired GFR.

The clinical and biochemical evolution of hepatic lesions in 124 patients with toxic oil syndrome from 1981 to 1986 has been reviewed. Most patients became asymptomatic during the early phase of the disease and abnormal liver function tests gradually normalized. In 1981, liver injury resembled drug-induced cholestatic hepatitis in 31 patients, and in 1 patient chronic destructive nonsuppurative cholangitis was evident. From 1982 to 1986 serial liver biopsies demonstrated toxic cholestatic hepatitis in 14 patients, chronic active hepatitis in 13, and nonalcoholic cirrhosis in 4. Nineteen patients showed lesions suggestive of alcoholic liver disease, but only 8 had a history of heavy alcohol intake. One patient developed biliary cirrhosis, another liver cell adenoma, and 8 nodular regenerative hyperplasia of the liver. We conclude that although liver injury had subsided in most patients, a significant number developed a variety of different liver diseases after follow-up for 5 yr.

We studied the significance of urinary enzyme measurements in diagnosing proximal tubular damage in cirrhosis of the liver. Urinary excretion (u-enzyme) and fractional urinary excretion (FEenzyme) of gamma-glutamyltranspeptidase (GGT), leucine aminopeptidase (LAP), alkaline phosphatase (AP) and beta-glucuronidase (B-GLU) were quantified in 14 control subjects (group I), 12 cirrhotics with functional renal failure (group II), 13 cirrhotics with renal tubular damage (group III) and 7 non-liver patients with renal tubular damage (group IV). Urinary enzyme excretion and fractional enzyme excretion were significantly higher in the cirrhotics of group III than in the controls or group II. In group III, these tests usually reached values within the range of group IV. The sensitivity of urinary enzyme excretion was 0.92 and specificity ranged from 0.75 (u-LAP) to 1 (u-GGT; u-B-GLU). The sensitivity of fractional enzyme excretion was between 0.61 (FEB-GLU) and 0.84 (FEGGT; FELAP), while specificity was from 0.91 (FELAP; FEAP) to 1 (FEGGT; FEB-GLU). The results indicate that measurement of urinary enzymes may be very useful in diagnosing renal tubular damage in cirrhotic patients with impaired renal function.

We describe the laparoscopic findings in 5 patients with nodular regenerative hyperplasia of the liver (NRH). A nodular liver surface and signs of portal hypertension were observed, which in all cases gave rise to the laparoscopic diagnosis of liver cirrhosis. Multiple and single liver biopsies in 3 and 2 cases respectively, permitted the definitive diagnosis of the NRH lesion. The laparoscopic picture of NRH is indistinguishable from that of cirrhosis, and for this reason it is advisable to carry out liver biopsy even in cases where cirrhosis seems unquestionable.