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Biomedical subjects

S Niemelä

Publications and source records attributed to S Niemelä.

At least 19 recordsLinked to original sources
PubMed2001

Genetic analysis in Finnish families with inflammatory bowel disease supports linkage to chromosome 3p21.

In inflammatory bowel diseases (IBD), certain chromosomal candidate loci have been repeatedly identified by independent studies in different populations. To investigate the contribution of the loci on chromosomes 1, 3, 7, 12, 14, and 16 to the susceptibility of IBD in Finnish population, where the predominant feature is the excess of ulcerative colitis (UC) families compared to Crohn's disease (CD) families, we carried out linkage analyses using 93 Finnish, multiply-affected IBD families. We observed nominal evidence for linkage to chromosome 3p21, consistent with earlier reports. The lod scores peaked at D3S2432, with a maximum two-point lod score of 1.68 (P=0.0027). In addition, we studied whether risk of IBD is associated with functional variants of two positional candidate genes; the chemokine receptor CCR5 gene on chromosome 3p21 and the interleukin-4 receptor alpha-subunit gene (IL4RA) on chromosome 16. We did not find any significant correlation between a 32-bp deletion variant of CCR5 or a single nucleotide change A1902G (Gln576Arg) of IL4RA, and IBD phenotypes, with the exception that in the UC group homozygosity for the G1902 allele of IL4RA was less frequent (0.019 vs 0.049, P=0.038). In conclusion, our study, carried out in a genetically homogenous population, suggests that chromosome 3 may contain a susceptibility gene for IBD.

Alleles↗
PubMed1999

Elevated pancreatic enzymes in inflammatory bowel disease are associated with extensive disease.

OBJECTIVE: Our aim was to perform a cross-sectional study to estimate the prevalence of elevated pancreatic enzymes in patients with inflammatory bowel disease and to correlate the enzyme activities with clinical, endoscopic, and histological findings. METHODS: Two hundred thirty-seven patients diagnosed with inflammatory bowel disease (IBD), including a subgroup with known hepatobiliary disease, were studied crosssectionally. Serum and urinary pancreatic enzymes were prospectively sampled and compared to endoscopic and histological findings obtained previously. RESULTS: Hyperamylasemia was found in 11% and hyperlipasemia in 7% of the total study group. The corresponding prevalences in patients with Crohn's disease were 17% and 9%, those in ulcerative colitis 9% and 7%, and those in indeterminate colitis 10% and 5%, respectively. High levels of serum amylase and pancreatic isoamylase were associated with extensive colonic disease (p < 0.005) and high histological activity (p < 0.05). Amylase, but not lipase, was significantly elevated in patients with primary sclerosing cholangitis. Smokers showed higher urinary amylase levels than non- and ex-smokers. The use of medication had no influence on the enzyme levels. CONCLUSIONS: Pancreatic enzymes are elevated in a significant proportion of patients with IBD, and the enzyme increase is associated with a more extensive and active disease, and in some cases with primary sclerosing cholangitis.

Adult↗
PubMed1998

Collagenous colitis and Yersinia enterocolitica infection.

Collagenous colitis is a rare clinical and pathological entity characterized by watery diarrhea and deposition of collagen beneath the surface epithelium of the colon. Its etiology is unknown. We present a careful retrospective clinicopathological analysis of six patients with collagenous colitis diagnosed at our hospital during a three-year period. Three of the patients had had a Yersinia enterocolitica infection, detected by stool culture and elevated serum antibody titers, preceding the diagnosis of collagenous colitis. Four patients had duodenal villous atrophy, which in two patients was refractory to a gluten-free diet. We propose that Yersinia enterocolitica infection may be a triggering factor for the development of collagenous colitis in some cases. Duodenal villous atrophy not responding to gluten withdrawal is common in association with collagenous colitis.

Adult↗
PubMed1997

MPN-PCR-quantification method for staphylococcal enterotoxin c1 gene from fresh cheese.

PCR detection methods have been extensively used in diagnostic microbiology. However, a lack of a simple and reliable method for quantification of the PCR products has partly hindered the use of PCR in routine food laboratories. The quantification of PCR products can be done by combining the principles of MPN statistics and PCR technique. We have developed a simple and sensitive MPN-PCR assay for detection and enumeration of enterotoxin C producing Staphylococcus aureus NCTC 10655 from fresh cheese. By amplifying single copy chromosomal enterotoxin C gene fragment, we could detect as little as 20 cfu/g. By Moran's test, most of the DNA dilution series appeared to fulfill the basic mathematical assumptions of ordinary MPN methods. The analysis with MPN-PCR took one day to perform compared with three days analysis time with plate counting. This MPN-PCR method can be readily applied with different primer systems without extensive development work.

Cheese↗
PubMed1997

Hepatobiliary and coexisting pancreatic duct abnormalities in patients with inflammatory bowel disease.

BACKGROUND: We performed a cross-sectional study to evaluate the prevalence of hepatobiliary disease in unselected patients with inflammatory bowel disease (IBD), to estimate the frequency of coexisting cholangiographic and pancreatographic duct abnormalities, and to correlate the findings with clinical, endoscopic, and histologic variables. METHODS: We screened 237 IBD patients for increased liver function values. Further, hepatobiliary evaluation consisted of transabdominal ultrasonography, endoscopic retrograde cholangiopancreatography (ERCP), and a liver biopsy. In addition, we evaluated the ERCP findings of patients with abnormal pancreatic screening tests (pancreatic enzymes or para-aminobenzoic acid excretion). RESULTS: Laboratory signs of hepatobiliary disease were found in 37 (16%) of our IBD patients. Abnormal liver test results were commoner in patients with Crohn's disease (CD) than in patients with ulcerative colitis (UC) (30.4% versus 11.2%, P < 0.05), and a similar trend was observed in the frequency of primary sclerosing cholangitis (PSC) in the respective groups of IBD patients. When the ERCP findings were combined with liver histology, 26 (11% of the whole study group) patients with PSC were found, with small-duct disease included. In 23 (10% of the whole study group) patients, definite cholangiographic changes consistent with PSC were found. Eleven (48%) of these showed coexisting pancreatic duct abnormalities. The prevalence of coexisting cholangiographic and pancreatographic duct changes in the whole study group was 4.6%. CONCLUSION: Hepatobiliary disease is at least equally common in patients with UC and CD. Coexisting cholangiographic and pancreatographic duct abnormalities in patients with IBD are relatively frequent and are considered extraintestinal manifestations of IBD.

Adult↗
PubMed1996

Blood leukocyte differential in Helicobacter pylori infection.

Helicobacter pylori causes a chronic infection in gastric mucosa, but its systemic effects are largely unknown. Our aim was to characterize the effect of H. pylori infection and gastric mucosal inflammation on the peripheral blood leukocyte count. An endoscopic series of 96 patients (40 men and 56 women), with a mean age of 62 years (range 49-80) was studied. Endoscopy with eight stepwise biopsies was performed and the occurrence of H. pylori was studied from sections stained with Warthin-Starry. The severity of inflammation in antral and body mucosa was estimated. The peripheral blood leukocyte count and differential count were determined by the automatic flow cytometric method. The total number of blood leukocytes and the numbers of lymphocytes and basophils were significantly increased in H. pylori-positive patients (N = 58), as compared with H. pylori-negative ones (N = 38). The total number of blood leukocytes correlated with the numbers of neutrophils, eosinophils, and mononuclear cells in the gastric mucosa. The number of basophils correlated with the number of mucosal neutrophils and mononuclear inflammatory cells. The results show that mucosal inflammation due to H. pylori infection is reflected in the amount of peripheral blood leukocytes. Basophilia suggests involvement of allergic mechanisms in H. pylori gastritis.

Aged↗
PubMed1996

Dietary calcium intake and its relation to bone mineral density in patients with inflammatory bowel disease.

OBJECTIVES: To investigate calcium intake and its association with bone mineral density (BMD) and the type and extent of the disease in patients with inflammatory bowel disease (IBD). SETTING: University hospital clinic. SUBJECTS: A total of 152 unselected IBD patients and 73 healthy controls. MEASUREMENTS: Dietary calcium intake was assessed with a food frequency questionnaire and BMD of the lumbar spina and proximal femur was measured. RESULTS: The IBD patients had lower dietary calcium intake (1034 [SD 493] mg) than the controls (1334 [514] mg, P < 0.001). The difference was significant in the males (1047 [552] mg and 1575 [586] mg, respectively, P < 0.001), but not in the females (1020 [422] mg and 1112 [303] mg). The dietary daily calcium intake was below 1000 mg in 53% of the patients and 27% of the controls (P = 0.0004) and below 400 mg in 9.2% of the patients and none of the controls (P = 0.007). The calcium intake was not associated with the severity or the type of IBD. Seventy-one (47%) patients and eight (11%) controls avoided lactose in their diet (P < 0.001). In the IBD patients, no association between the calcium intake and BMD was detected, whereas in the controls a positive correlation between the calcium intake and the BMD of the proximal femur was found. CONCLUSIONS: Calcium intakes below the recommendations are seen more often in the IBD patients than in the healthy controls, but in the IBD patients the calcium intake is not associated with BMD in a cross-sectional study. A low-lactose diet is common among IBD patients. To reduce the risk of inadequate calcium intake, unnecessary dietary restrictions concerning, e.g. milk products, should be avoided for these patients.

Adult↗
PubMed1996

Could Helicobacter pylori infection increase the risk of coronary heart disease by modifying serum lipid concentrations?

OBJECTIVE: To investigate the relation between Helicobacter pylori infection and coronary heart disease (CHD). DESIGN: A case-control study. SETTING: Northern Finland (about 650,000 inhabitants). PATIENTS: 116 patients with angiographically documented CHD and 116 controls matched for age and gender randomly recruited from the register of the Finnish Social Insurance Institute. MAIN OUTCOME MEASURES: The odds ratio (OR) estimates for the association of H pylori infection with CHD. RESULTS: 64% of the CHD patients and 53% of the controls were seropositive for H pylori; the OR adjusted for age and gender was 1.5 (95% confidence interval (CI) 0.9 to 2.5). An additional adjustment for the common risk factors of CHD, including lipid concentrations, in a logistic regression analysis produced an OR estimate of 1.1 (95% CI 0.6 to 2.1). Among the controls, those who were H pylori positive had significantly (P = 0.03) higher concentrations of serum triglycerides than those who were H pylori negative: the trend among the cases was similar, but non-significant. The concentrations of HDL cholesterol tended to be lower in those who were H pylori positive than in those who were H pylori negative, among both the cases and the controls. CONCLUSIONS: The impact of H pylori infection as an independent risk factor for CHD seems to be minor. On the other hand the results are consistent with the hypothesis that H pylori infection might modify the serum lipid concentrations in a way that could increase the risk of CHD.

Adult↗
PubMed1996

Pancreatic duct abnormalities and pancreatic function in patients with chronic inflammatory bowel disease.

BACKGROUND: We performed a cross-sectional study to estimate the prevalence of duct abnormalities and exocrine pancreatic dysfunction in an unselected group of patients with inflammatory bowel disease (IBD) and to correlated the findings with clinical, endoscopic, and histologic variables. METHODS: A total of 237 IBD patients were screened for pancreatic enzymes and with a PABA test. Seventy-one (30%) patients with values more than twice the upper normal limit in biochemical tests or with a PABA test < 40% were further evaluated. The pancreatic evaluation included endoscopic retrograde pancreatography, ultrasonography, and a secretin test. The endoscopic and histologic findings were systematically evaluated. RESULTS: The secretin test was completed in 54 patients, and in 10 (19%) it showed a decreased maximal bicarbonate concentration, corresponding to 4% of the whole study group. The pancreatograms of 59 patients were studied. In 20 (34%) patients unequivocal duct abnormalities were found. The prevalence of pancreatic duct abnormalities in IBD was 8.4%. CONCLUSION: Our results show the presence of pancreatic duct abnormalities and exocrine pancreatic insufficiency in some patients with IBD.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1995

Ten year follow up study of lymphocytic gastritis: further evidence on Helicobacter pylori as a cause of lymphocytic gastritis and corpus gastritis.

AIMS: To examine the course of lymphocytic gastritis and its relation to Helicobacter pylori (H pylori) infection in a 10 year follow up. METHODS: Ninety six patients were originally examined for dyspepsia in 1981. Gastroscopies with stepwise biopsies were performed on all the patients initially and after an interval of 10 years. RESULTS: Nine per cent of the patients (9/96) had features of lymphocytic gastritis in gastric biopsy at the first examination, and 12.5% (12/96) at the second examination; 7/9 patients (78%) had persistent lymphocytic gastritis during the follow up; in two the diagnostic features of lymphocytic gastritis had disappeared, and five had a new diagnosis of lymphocytic gastritis at the second examination. At the second examination 9/12 lymphocytic gastritis patients (75%) were H pylori positive histologically, while all had specific antibodies to H pylori. The lymphocytic gastritis patients had higher grades of gastritis (p = 0.009), neutrophilic and eosinophilic granulocytes, mononuclear inflammatory cells, and foveolar hyperplasia in the corpus mucosa, but smaller numbers of H pylori, than the H pylori positive patients without lymphocytic gastritis. The appearance of lymphocytic gastritis during the 10 year interval was associated with increases in the grades of corpus gastritis and neutrophilic granulocytes (p = 0.043 for both). During the follow up, the patients with lymphocytic gastritis, but not the H pylori positive patients without lymphocytic gastritis, appeared to have a significant increase in the grade of intestinal metaplasia in the corpus mucosa (p = 0.043). CONCLUSIONS: In some patients H pylori may cause a gastritis that predominates in the corpus and is associated with an increase in the intraepithelial lymphocyte count. This form of gastritis may cause progression of intestinal metaplasia.

Adult↗
PubMed1995

Helicobacter pylori-associated gastritis. Evolution of histologic changes over 10 years.

BACKGROUND: Helicobacter pylori seems to be the commonest cause of chronic gastritis, but the natural course of H. pylori-associated gastritis is largely obscure. METHODS: We present a histologic follow-up of 39 patients with H. pylori-positive gastritis. Gastroscopies with stepwise biopsies were performed in all the patients at an interval of 10 years. RESULTS: Of the patients 87% (34/39) had a persistent infection and showed a significant decrease in the grades of antral gastritis, eosinophilic granulocytes, corpus eosinophilic granulocytes, and foveolar hyperplasia and a significant increase in the grade of corpus neutrophilic granulocytes. The quantities of H. pylori as estimated histologically did not change significantly during the follow-up period in patients with a persistent infection. In the five other patients (13%) the H. pylori infection had apparently disappeared spontaneously, and this was accompanied by decreases in the amount of inflammatory cells in the gastric mucosa. CONCLUSIONS: H. pylori infection in the gastric mucosa is chronic and may be associated with both regressive and progressive histologic changes. Spontaneous healing of H. pylori infection is possible and is associated with partial resolution of the inflammatory changes in the gastric mucosa.

Adult↗
PubMed1995

Chronic gastritis in patients with gastric ulcer; a 10-year follow-up.

BACKGROUND: The course of gastric ulcer disease and its relations to certain indicators of inflammation and Helicobacter pylori in the gastric mucosa were examined in a 10-year follow-up. METHODS: Thirty-three patients with gastric ulcer were examined endoscopically with biopsies in 1981-82 and invited for re-examination in 1991-92. Twenty-one of them were able to comply with the invitation. A gastroscopy with biopsies was performed on each of these, and the results were compared with those of age- and sex-matched control patients with non-ulcer H. pylori-positive gastritis. RESULTS: All the patients were H. pylori-positive at the first examination and had a persistent infection at the second examination, if they had not undergone a gastric resection. Thirteen patients had a non-operated stomach at the second examination. The grades of gastritis and intestinal metaplasia in the antrum at the second examination were significantly higher in the ulcer patients than in the controls (p = 0.009 and p = 0.04, respectively). Eosinophilic granulocytes in both the antral and the corpus mucosa had decreased significantly in the controls (p = 0.002 and p = 0.04, respectively) but not in the ulcer patients. CONCLUSIONS: The results suggest that the course of ulcer-associated H. pylori-positive gastritis is different from that of non-ulcer-associated H. pylori-positive gastritis and that abnormal eosinophilic infiltration persists in patients with gastric ulcer.

Aged↗
PubMed1991

Helicobacter pylori in dyspeptic patients: quantitative association with severity of gastritis, intragastric pH, and serum gastrin concentration.

The relationship between different features of gastric mucosal inflammation, intragastric pH and serum gastrin concentration and the distribution and quantity of Helicobacter pylori was studied in a series of 107 dyspepsia patients. H. pylori was identified in 62 cases (59%), and its presence was associated with increased amounts of mononuclear inflammatory cells and neutrophilic and eosinophilic leucocytes in both the antrum and the corpus. The number of H. pylori in the antral mucosa was significantly associated with the quantity of mononuclear inflammatory cells. It was also associated with glandular atrophy in antral mucosa, so that slight and moderate glandular atrophy were significantly more common in cases with abundant H. pylori. Intragastric pH and serum gastrin concentration were inversely related to the number of H. pylori in both the antral and corpus mucosa. H. pylori positive patients were also divided into groups according to proportions of H. pylori in the antral and corpus mucosa. In 5 of these patients (8%) the bacteria were present only in the corpus, and this group had a significantly more pronounced degree of glandular atrophy in the corpus mucosa, higher intragastric pH and a higher serum gastrin concentration than the other H. pylori positive patients. The other patients with a higher corpus H. pylori than antral H. pylori score (n = 25; 34%) also had a significantly higher intragastric pH and serum gastrin concentration than those with a corpus H. pylori score lower than or equal to the antral score, while the latter had more severe inflammation in the antral mucosa and a lower intragastric pH and serum gastrin concentration. The results suggest that inflammation in the antrum forms a favourable environment for H. pylori, while atrophy of the corpus glands, being connected with increased pH, leads to a diminished amount of H. pylori. They thus support the view that proliferation of H. pylori is dependent on acid produced by the corpus mucosa.

Adult↗
PubMed1990

Helicobacter pylori induces lymphocyte activation in peripheral blood cultures.

Helicobacter pylori-induced in vitro stimulation of mononuclear cells was characterized by measuring DNA synthesis response, interferon-gamma (IFN-gamma) secretion and the number of immunoglobulin-secreting cells. The strength of these responses was measured in 51 subjects comprising 36 dyspeptic patients from the Gastroenterological Unit and 15 members of the laboratory staff. Nineteen subjects had antibodies to H. pylori and 32 did not. The responses were compared with respect to H. pylori antibody status. Positive stimulation of DNA synthesis (stimulation index greater than 2) was obtained in 96% of the subjects, and the bacterium induced IFN-gamma secretion in all of them. The induction of immunoglobulin-secreting cells revealed B cell in vitro stimulation. The antibody-positive subjects had a tendency to synthesize less DNA (P not significant) and secrete less IFN-gamma (P less than 0.05) in response to H. pylori than did the antibody-negative ones, but the differences were not marked. The results show that the whole H. pylori bacterium stimulates mononuclear cells. The nature of the stimulation is not yet characterized (non-specific versus specific).

Antibodies, Bacterial↗