Effect of oral anticoagulants on the outcome of faecal immunochemical test.

BACKGROUND: We aimed to evaluate whether oral anticoagulants (OACs) alter faecal immunochemical test (FIT) performance in average-risk colorectal cancer (CRC) screening. METHODS: Individuals aged 50-69 years were invited to receive one FIT sample (cutoff 75 ng ml(-1)) between November 2008 and June 2011. RESULTS: Faecal immunochemical test was positive in 9.3% (21 out of 224) of users of OAC and 6.2% (365 out of 5821) of non-users (P-trend=0.07). The positive predictive value (PPV) for advanced neoplasia (AN) in non-users was 50.4% vs 47.6% in users (odds ratio, 0.70; 95% CI, 0.3-1.8; P=0.5). The PPV for AN in OAC more antiplatelets (aspirin or clopidogrel) was 75% (odds ratio, 2; 95% CI, 0.4-10.8; P=0.4). CONCLUSIONS: Oral anticoagulant did not significantly modify the PPV for AN in this population-based colorectal screening program. The detection rate of advanced adenoma was higher in the combination OAC more antiplatelets.

Influence of Helicobacter pylori infection and eradication on blood lipids and fibrinogen.

BACKGROUND: An association between Helicobacter pylori infection and heart disease has been suggested. A potential mechanism may be inflammation-induced atherogenic changes of lipoproteins, but epidemiological studies have provided conflicting results. METHODS: In a prospective multicentre study, 830 patients submitted for endoscopy and H. pylori testing were evaluated. Of the 686 H. pylori-positive patients, 487 received and 199 did not receive eradication treatment. Serum lipids and plasma fibrinogen were measured at baseline in all patients and 3 months later in those initially positive for H. pylori. RESULTS: H. pylori had no influence on baseline lipid or fibrinogen levels. Increases in high-density lipoprotein cholesterol were observed in 368 patients who received eradication treatment and in 193 untreated patients: 0.06 mmol/L (P=0.000) and 0.07 mmol/L (P=0.009), respectively. Similar minor increases in total cholesterol and triglycerides occurred in both groups. Lipid changes were related to symptom relief and a reduction in smoking. Eradication therapy was associated with a minor decrease in plasma fibrinogen irrespective of the resolution of infection. CONCLUSIONS: H. pylori has no influence on blood lipids or fibrinogen. Both the eradication of infection and symptomatic treatment without eradication are associated with minor lipid changes related to symptom relief and lifestyle modifications. Thus, the inflammatory changes associated with H. pylori are unlikely to affect lipoprotein or fibrinogen metabolism.

Sp family of transcription factors is involved in iron-induced collagen alpha1(I) gene expression.

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.

Plasma arginine vasopressin concentration during laparoscopy.

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.

Helicobacter pylori infection. Rapid diagnosis with brush cytology.

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.

[Serum aminoterminal procollagen type-III peptide in the diagnosis of chronic hepatopathies]. / Péptido aminoterminal del procolágeno tipo III sérico en el diagnóstico de las hepatopatías crónicas.

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.

Mismatch repair status in the prediction of benefit from adjuvant fluorouracil chemotherapy in colorectal cancer.

AIM: Some retrospective studies have shown a lack of benefit of 5-fluorouracil (5-FU) adjuvant chemotherapy in patients with mismatch repair (MMR) deficient colorectal cancer. Our aim was to assess if this molecular marker can predict benefit from 5-FU adjuvant chemotherapy. A second objective was to determine if MMR status influences short term survival. METHODS: We included 754 patients with a median follow up of 728.5 days (range 1-1097). A total of 260 patients with stage II or III tumours received 5-FU adjuvant chemotherapy, according to standard clinical criteria and irrespective of their MMR status. A tumour was considered MMR deficient when either BAT-26 showed instability or there was loss of MLH1 or MSH2 protein expression. RESULTS: At the end of the follow up period, 206 patients died and 120 presented with tumour recurrence. Sixty six (8.8%) patients had MMR deficient tumours. There were no significant differences in overall survival (MMR competent 72.1%; MMR deficient 78.8%; p = 0.3) or disease free survival (MMR competent 61.3%; MMR deficient 72.3%; p = 0.08). In patients with stage II and III tumours, benefit from 5-FU adjuvant chemotherapy was restricted to patients with MMR competent tumours (overall survival: chemotherapy 87.1%; non-chemotherapy 73.5%; log rank, p = 0.00001). Patients with MMR deficient tumours did not benefit from adjuvant chemotherapy (overall survival: chemotherapy 89.5%; non-chemotherapy 82.4%; log rank, p = 0.4). CONCLUSIONS: Benefit from 5-FU adjuvant chemotherapy depends on the MMR status of tumours in patients with colorectal cancer. 5-FU adjuvant chemotherapy improves survival in patients with MMR competent tumours but this benefit from chemotherapy cannot be extended to patients with MMR deficient tumours.

Laparoscopy in fever of unknown origin - study of seventy cases.

Laparoscopy was performed on 70 patients with FUO after clinical review and when bacteriological, serological and radiological investigations had failed to reveal the diagnosis. Laparoscopy proved helpful in making the diagnosis in 68.4% of these patients; in 44.2% it provided a definite diagnosis, and in 24.2% it contributed significantly to the establishment of a diagnosis. Laparoscopy was of most use (76.6%) in those patients with physical signs or biochemical results suggestive of an abdominal disorder. In the absence of such sign laparoscopy was helpful in only 20.0% of patients. There was no mortality, and morbidity was insignificant. It is our conclusion that laparoscopy can be recommended in FUO, particularly in patients with signs of abdominal disease.

Plasma arginine vasopressin response to oral, gastric, and intravenous water load in patients with cirrhosis.

BACKGROUND/AIMS: Hepatic osmoreceptors are sensitive to changes in portal blood osmolality 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.

Clinico-biochemical evolution and late hepatic lesions in the toxic oil syndrome.

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.

The role of sonography in the early diagnosis of biliopancreatic Ascaris infestation.

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.

Reddish-purple areas on the liver surface: the laparoscopic picture of peliosis hepatis.

Reddish-purple areas occasionally found on the surface of the liver have been related to peliosis hepatis. The purpose of the present study was to determine: 1) the frequency of these changes in a total of 3035 laparoscopies and 2) the histological substrate of these laparoscopical changes. In 20 cases (0.65%), reddish-purple patches of round, triangular, star-shaped or net-work configuration were found on the liver surface. Liver biopsies taken from these areas showed: 1) dilatation of sinusoids; 2) blood-filled cavities, and 3) intralobular hemorrhages. These lesions were frequently combined. In three cases no lesions were found. The presence of these histological lesions was compared with those found in a group serving as controls, in whom no reddish-purple spots were seen at laparoscopy. Our study shows that there is a close statistical relationship (X2: 19.01; p less than 0.001) between the histological and laparoscopic changes. We conclude that: 1) Reddish-purple areas on the liver surface are caused by Peliosis hepatis or are Peliosis hepatis-related lesions, and 2) Peliosis hepatis is not an extremely rare condition in laparoscopy.

Budd-Chiari syndrome associated with nodular regenerative hyperplasia of the liver.

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.

Antidiuretic hormone and renal function after water loading in patients with cirrhosis of the liver.

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.

Effects of lumbar sympathetic block on kidney function in cirrhotic patients with hepatorenal syndrome.

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.

Malignant lymphoma of jejunum with common variable hypogammaglobulinemia and diffuse nodular hyperplasia of the small intestine. A case study and literature review.

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.

Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981).

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.

Autoimmune enteropathy in an adult with autoimmune multisystemic involvement.

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.

Laparoscopic and histological problems in the diagnosis of nodular regenerative hyperplasia of the liver.

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.