1.
Carlsson, Annelie, et al.
(författare)
Prevalence of IgA-antigliadin antibodies and IgA-antiendomysium antibodies related to celiac disease in children with Down syndrome
1998
Ingår i: Pediatrics. - : American Academy of Pediatrics (AAP). - 1098-4275 .- 0031-4005. ; 101:2, s. 5-272
Tidskriftsartikel (refereegranskat) abstract
OBJECTIVE: This study was undertaken to investigate the prevalence of celiac disease in children and adolescents with Down syndrome.MATERIAL AND METHODS: Forty-three children and adolescents with Down syndrome were screened for IgA-antigliadin antibodies (AGA) and IgA-antiendomysium antibodies (EMA). Patients found to be either AGA- or EMA-positive were investigated further with intestinal biopsy.RESULTS: None of the 43 patients had known celiac disease at entry into the study; 37% (16/43) were found to have AGA levels above normal, and 16% (7/43) to be EMA-positive. Of the 15 patients who underwent biopsy, 8 manifested villous atrophy. Villous atrophy was present in all 7 of the EMA-positive patients, whereas the villi were normal in 7 of the 13 AGA-positive patients who underwent biopsy.CONCLUSIONS: EMA is a good immunologic marker for use in screening for celiac disease, and screening is justified in patients with Down syndrome.
2.
Saalman, Robert, 1952, et al.
(författare)
Antibody-dependent cell-mediated cytotoxicity to gliadin-coated cells with sera from children with coeliac disease.
1998
Ingår i: Scandinavian journal of immunology. - 0300-9475. ; 47:1, s. 37-42
Tidskriftsartikel (refereegranskat) abstract
Antibody-dependent cell-mediated cytotoxicity (ADCC) has been suggested as a contributing immunological mechanism in the disease process of coeliac disease. In the present study, sera from coeliac children were examined for their capacity to mediate ADCC against gliadin-coated target cells. The ADCC-mediating efficacy of sera were tested using monocytes from healthy adults as effector cells and gliadin-coated erythrocytes from the same donor as targets. Using monocytes as effector cells, sera from children with active coeliac disease (untreated or challenged), demonstrated significantly higher ADCC-mediating capacity than sera from healthy and disease references as well as children with treated coeliac disease. A positive correlation was found between the ADCC-mediating capacity and serum IgG as well as IgA anti-gliadin antibody levels. The results suggest that an antibody-dependent monocyte/macrophage-induced cytotoxic reaction might be involved in the disease process of coeliac disease.
3.
Öberg, Åke, 1954-, et al.
(författare)
Are lymph node micrometastases of any clinical significance in Dukes' stages A and B colorectal cancer?
1998
Ingår i: Diseases of the Colon & Rectum. - : Wolters Kluwer. - 0012-3706 .- 1530-0358. ; 41:10, s. 1244-1249
Tidskriftsartikel (refereegranskat) abstract
PURPOSE: The aim was to investigate the significance of lymph node micrometastases in Dukes Stages A and B colorectal cancer.METHODS: Archival specimens were examined from 147 patients (96 colon, 51 rectum; 44 Stage A, 103 Stage B) who had surgery between 1987 and 1994. One lymph node section from each node (colon, 1-11; median, 4; rectum, 1-15; median, 3) was examined with use of an anticytokeratin antibody.RESULTS: Forty-seven (32 percent) patients had micrometastases. At follow-up in June 1996, 23 patients had died of cancer or with known tumor relapse, after a median time of 28 (range, 5-67) months; 8 of 47 (17 percent) patients had micrometastases, 15 of 100 (15 percent) did not. No statistically significant differences were observed according to micrometastases when the results were analyzed with respect to Dukes stage or survival time. The median survival time of living patients with micrometastases was 48 (range, 18-97) months, and for patients without micrometastases, 48 (range, 19-111) months. Six of 96 living patients had a tumor relapse; three of these displayed micrometastases.CONCLUSION: Lymph node micrometastases are not a useful prognostic marker in Dukes Stages A and B and do not imply different strategies for additional therapy or follow-up.
4.
Kölby, Lars, 1963, et al.
(författare)
Gastric carcinoid with histamine production, histamine transporter and expression of somatostatin receptors.
1998
Ingår i: Digestion. - 0012-2823. ; 59:2, s. 160-6
Tidskriftsartikel (refereegranskat) abstract
A case of sporadic, histamine-producing gastric carcinoid with liver metastases is reported. The patient was treated with somatostatin analogue (octreotide) combined with cortisone and blockade of histamine receptors prior to surgery, which included subtotal gastrectomy, excision of lymph node metastases and superficial liver metastases. Residual liver metastases were injected with ethanol. These interventions markedly reduced the urinary excretion of the main histamine metabolite (MelmAA). Eighteen months later combined immuno- and chemotherapy was initiated due to tumour progression and recurrent hormonal symptoms with good clinical results over 12 months. Scintigraphy, using 111In-DTPA-D-Phe1-octreotide, visualized somatostatin receptors (sstr) in primary tumour, lymph node metastases and liver metastases. The tissue/blood 111In concentration ratios of tumour biopsies were very high. Northern analyses confirmed expression of all subtypes of sstr1-5. Immunocytochemically, tumour cells were strongly positive for chromogranin A, histamine and vesicular monoamine transporter (VMAT) 2 (histamine transporter), but negative for VMAT 1, suggesting an origin from gastric enterochromaffin-like cells. In primary tumour cell cultures, histamine, 5-HTP and 5-HIAA, but not 5-HT, could be detected in conditioned culture medium, indicating a defective decarboxylation of the tryptamine precursor. This rare case of histamine-producing gastric carcinoid demonstrates that excellent symptom relief can be achieved despite disseminated disease, if active, multimodal treatment strategy is instituted. The presence of high numbers of sstr in tumour tissue also raises the possibility of receptor-guided radiotherapy.
5.
Ahrné, Siv, et al.
(författare)
The normal Lactobacillus flora of healthy human rectal and oral mucosa.
1998
Ingår i: Journal of applied microbiology. - 1364-5072. ; 85:1, s. 88-94
Tidskriftsartikel (refereegranskat) abstract
The Lactobacillus flora of the rectal and oral mucosa was sampled from 42 healthy volunteers. Species identification was carried out by numerically comparing API 50CH fermentation patterns with type strains, using an SJ-similarity cut-off level of 79%. For the largest groups, identity was further confirmed by DNA-DNA hybridizations against the type strain of the species. Seventeen lactobacilli clusters were defined, of which most were found both on rectal and oral mucosa. The largest taxa were Lactobacillus plantarum, Lact. rhamnosus and Lact. paracasei ssp. paracasei, which were isolated from 52%, 26% and 17% of the individuals, respectively. Most isolates were tested for their capacity to adhere to the human colonic cell line HT-29 in the absence and presence of methyl-alpha-D-mannoside. Mannose-sensitive adherence to HT-29 cells was encountered in two-thirds of the Lact. plantarum isolates, but infrequently among isolates of other taxa. The results suggest that Lact. plantarum is a major colonizer of the human gastrointestinal mucosa, and that its capacity to adhere to mannose-containing receptors may be of some ecological importance.
6.
7.
Appelros, Stefan, et al.
(författare)
Activation peptide of carboxypeptidase B in serum and urine in acute pancreatitis
1998
Ingår i: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 42:1, s. 97-102
Tidskriftsartikel (refereegranskat) abstract
The pathophysiology of acute pancreatitis involves activation of the pancreatic proenzymes. Levels of the trypsinogen activation peptide in urine in acute pancreatitis has been shown to correlate with the severity of disease. However, this peptide is unstable in urine and, because of its low molecular mass, difficult to measure. Procarboxypeptidase B has a larger activation peptide which could be more suitable for analysis in serum and urine.
8.
Raab, Y, et al.
(författare)
Eosinophil activation in ulcerative colitis : studies on mucosal release and localization of eosinophil granule constituents.
1998
Ingår i: Digestive Diseases and Sciences. - 0163-2116 .- 1573-2568. ; 43:5, s. 1061-70
Tidskriftsartikel (refereegranskat) abstract
Activation of eosinophil granulocytes (eosinophils) seems to contribute to the pathophysiology of several inflammatory conditions. This process was evaluated in 18 patients with ulcerative colitis and in 18 healthy controls using intraluminal segmental perfusion of the sigmoid colon and rectum and immunoanalysis for eosinophil cationic protein (ECP) in the perfusate. Immunohistochemistry for eosinophils and neutrophils was made in simultaneously taken biopsies and in biopsies from surgical specimens taken from additional 10 patients. The mucosal release of ECP was increased severalfold in patients with UC. The bowel biopsies demonstrated a lamina propria infiltrated with eosinophils. The degree of eosinophil activation/degranulation was related to the intensity of the inflammatory reaction. Activated eosinophils and extracellular deposits of ECP were, in particular, seen in crypt abscesses and in areas with damaged surface epithelium. Since ECP is highly cytotoxic, its release at the site of inflammatory bowel lesions might reflect a potential pathophysiological mechanism.
9.
Verbaan, Hans, et al.
(författare)
Factors associated with cirrhosis development in chronic hepatitis C patients from an area of low prevalence
1998
Ingår i: Journal of Viral Hepatitis. - : Wiley. - 1365-2893 .- 1352-0504. ; 5:1, s. 43-51
Tidskriftsartikel (refereegranskat) abstract
The aim of this study was to evaluate the importance of different endogenous and exogenous factors associated with cirrhosis development among hepatitis C virus (HCV)-positive individuals from an area of low prevalence. We studied 106 consecutive HCV RNA positive patients who had undergone liver biopsy. Each patient was assessed with special attention to risk factors for hepatitis C infection, average daily alcohol consumption and analysis of plasma levels of alpha1-antitrypsin (alpha1AT) and alpha1-antichymotrypsin (alpha1ACT). Viral RNA, amplified from serum with the polymerase chain reaction (PCR) technique, was used for genotyping. Liver biopsies were assessed according to conventional histopathological criteria, and for necroinflammatory activity (grade) and fibrosis (stage) according to a numerical scoring system. The presence of cirrhosis (stage 4) was used as the dependent variable in multivariate logistic regression analysis. Alcohol abuse (P = 0.007), age at entry (P < 0.001), immigrant status (P = 0.017) and a low alpha1ACT level (P = 0.008) were all independent determinants of progression to cirrhosis whereas HCV genotype 1, estimated duration of HCV infection and positivity for antibodies to hepatitis B core antigen (HBcAb) were not. Cirrhosis occurred at a significantly younger age (P = 0.00(5) among alcohol abusers. Hence, both endogenous and exogenous factors such as subnormal alpha1ACT levels and alcohol appear to contribute to the rate of progression to cirrhosis among HCV-positive patients.
10.
Verbaan, Hans, et al.
(författare)
Long-term outcome of chronic hepatitis C infection in a low-prevalence area
1998
Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 33:6, s. 650-655
Tidskriftsartikel (refereegranskat) abstract
BACKGROUND: Although hepatitis C virus (HCV) infection is recognized as an important causative factor in the development of liver cirrhosis and hepatocellular cancer (HCC), the strength of this correlation has been difficult to confirm in low-prevalence areas. METHODS: Stored serum samples from 987 consecutive (1978-88) patients with chronic liver disease were tested with an enzyme-linked immunosorbent assay for anti-HCV and further confirmed by immunoblot. To evaluate the long-term outcome, the cohort was followed up until 1995, for a median observation time of 10 years. RESULTS: Anti-HCV, confirmed by immunoblot, was found in 9.5% (94 of 987) of the patients, and at inclusion most patients were asymptomatic irrespective of anti-HCV status. Of the 445 patients who died during the study period, 44 were HCV-positive. A liver-related cause of death was far commoner and the age-adjusted survival shorter among HCV-positive patients than among HCV-negative ones. At death 68% (30 of 44) of the HCV-positive subgroup had developed cirrhosis, and 30% (13 of 44) had concurrent HCC, as compared with 36% (142 of 393) (P = 0.001) and 8% (31 of 393) (P = 0.001), respectively, of the HCV-negative subgroup. HCV infection (P < 0.001), alcohol abuse (P < 0.001), and immigrant status (P = 0.045) were independent factors with regard to the development of cirrhosis, whereas HCV infection (P = 0.040) and immigrant status (P = 0.012) were independent factors with regard to HCC. CONCLUSIONS: HCV infection is common among patients with chronic liver disease, even when clinical evidence of viral infection is sparse, and constitutes a significant cause of death even in a low-prevalence area.
