Marjo Kapraali
Karolinska Institutet
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Featured researches published by Marjo Kapraali.
Scandinavian Journal of Gastroenterology | 2007
Susanna Jäghult; Jenny Larson; Regina Wredling; Marjo Kapraali
Objective. Health-related quality of life is impaired in patients with inflammatory bowel disease and improved disease-related information can improve this situation. The aims of this study were to create an education programme that could be readily applicable at the clinic and would be suitable for newly diagnosed patients with inflammatory bowel disease, and to investigate whether the programme could improve their health-related quality of life. Material and methods. Ninety-three patients with inflammatory bowel disease in remission were included and randomized to an intervention group or a control group. The intervention group attended a multiprofessional education programme while the control group received regular information. Four questionnaires were used for measuring health-related quality of life. Both groups completed the questionnaires at baseline and after 6 months. The intervention group also completed the questionnaires after 1 month. Results. No significant differences were found when comparing the two groups at 6 months. However, the multiprofessional education programme was highly appreciated by the patients. Conclusions. In the present study no improvement could be seen in health-related quality of life in patients with inflammatory bowel disease after participating in an education programme in comparison with the control group. This might be due to the fact that the questionnaires were not sensitive enough or that some patients were not in clinical remission. The patients’ enthusiasm for the multiprofessional education programme has led to its being part of the regular care at the clinic.
Case Reports | 2011
Izabella Janczewska; Qayium Nekzada; Marjo Kapraali
Bariatric surgery for the treatment of severe obesity has increased dramatically in recent years in the USA and parts of Western Europe. The most commonly used technique is the Roux-en Y gastric bypass (RYGBP). Several nutritional and gastrointestinal complications after bariatric surgery have been described during the last 10 years. The authors present two patients with diarrhoea and malnutrition; one after RYGBP and the other after jejunoileal bypass surgery. These patients were subsequently diagnosed with Crohn’s disease.
Thrombosis Research | 2014
Roza Chaireti; Rupesh Rajani; Annika Bergquist; Tor Melin; Ingalill Friis-Liby; Marjo Kapraali; Stergios Kechagias; Tomas L. Lindahl; Sven Almer
INTRODUCTION In recent years there have been increasing evidence associating liver disease with hypercoagulability, rather than bleeding. The aim of the study was to evaluate the haemostatic potential in patients with liver disease. PATIENTS AND METHODS We measured thrombin generation in the presence and absence of thrombomodulin in patients with portal vein thrombosis (PVT, n=47), Budd-Chiari syndrome (BCS, n=15) and cirrhosis (n=24) and compared the results to those obtained from healthy controls (n=21). Fifteen patients with PVT and 10 patients with BCS were treated with warfarin and were compared to an equal number of patients with atrial fibrillation matched for prothrombin time-international normalized ratio. We assessed resistance to thrombomodulin by using ratios [marker measured in the presence/absence of thrombomodulin]. RESULTS There were no differences in thrombin generation between patients on warfarin treatment and their controls. Cirrhotic patients generated more thrombin in the presence of thrombomodulin and exhibited thrombomodulin resistance compared to controls [p=0.006 for endogenous thrombin potential (ETP) and p<0.001 for peak thrombin and both ratios ETP and peak] and patients with non-cirrhotic PVT (p=0.001, p=0.006, p<0.001, p<0.001 for ETP, peak, ratio ETP, ratio peak, respectively). The patients with cirrhotic PVT exhibited higher ETP (p=0.044) and peak (p=0.02) in the presence of thrombomodulin than controls, as well as thrombomodulin resistance (ETP and peak ratios: p=0.001). CONCLUSIONS Hypercoagulability and thrombomodulin resistance in patients with cirrhosis were independent of the presence of splanchnic vein thrombosis. The hypercoagulability in patients with cirrhotic PVT could have implications for considering longer or more intensive treatment with anticoagulants in this group.
Scandinavian Journal of Gastroenterology | 2012
Izabella Janczewska; Marjo Kapraali; Fredrik Saboonchi; Q Nekzada; A Wessulv; J Khoshkar; F Marouf; J Gorsetman; D Risberg; M Lissing; G Wirström; B Sandstedt
Abstract Methods. The newly described – multigene analysis test (DiBiCol) identifying 7 inflammatory bowel disease (IBD)-specific genes in colonic mucosal biopsy differentiating between ulcerative colitis (UC) and Crohns disease (CD) with active inflammation – is a new addition to existing methods with a higher stated sensitivity and specificity. Method biopsy material from 78 patients with a complicated course diagnosed as most probably UC in 38, CD in 18 and inflammatory bowel disease unclassified (IBDU) in 22 were investigated by DiBiCol. Results. DiBiCol showed a pattern consistent with CD in 13 patients with UC and led to change of diagnosis in 3 patients and a strong suggestion of CD in 8 patients. A total of 2 patients remained as UC. DiBiCol showed a pattern of UC in 4 patients of 18 with CD leading to a changing of diagnosis to UC in 3 patients, but the fourth remained as CD. In 22 patients with IBDU DiBiCol showed a pattern consistent with UC in 7 cases and with CD in 13 cases. A new evaluation 1 year after the DiBiCol allowed the assessment of clinical diagnosis in 10 patients confirmed in 9 of 10 patients by DiBiCol. In patients with acute flare of colitis the clinical diagnosis corresponded in 10 of 12 UC and in 5 of 6 CD cases. Summary. Adopting the DiBiCol test led to a change of the primary diagnosis in a significant number of patients with the initial diagnosis of UC and CD and suggested a clinically probable diagnosis in most of the patients with IBDU and in those with an acute flare of colitis.
Gastroenterology Research | 2013
Susanna Jäghult; Fredrik Saboonchi; Jette Möller; Unn-Britt Johansson; Regina Wredling; Marjo Kapraali
Background It is important to identify factors that influence the risk of relapses in inflammatory bowel disease. Few studies have been conducted and with limited methodology. This prospective case-crossover study, aims to examine whether perceived stress has a short-term acute effect, namely whether it acts as a trigger, on the risk of relapse in inflammatory bowel disease. Methods Sixty patients with inflammatory bowel disease and in remission were included. The case-crossover design was employed, which is an epidemiological design developed to study triggers for acute events and diseases. To collect information regarding symptoms and potential trigger factors, such as perceived stress, a structured diary was constructed. The participants were instructed to fill in the diary daily during six months. Fifty patients completed the study. Results The analysis showed an effect for high level of perceived stress. Being exposed to “quite a lot” of stress, yield an increase in risk for relapse during the forthcoming day (OR = 4.8, 95% CI 1.09 - 21.10). No statistically increased risk for lower levels of perceived stress was found, although elevated effect estimates were found for “some” stress. Conclusion This study supports earlier findings regarding perceived stress as an important factor in triggering relapses in IBD. However, this is the first case-crossover study performed to explore the trigger risk of stress in this population. Further investigations with larger patient samples are needed to confirm the findings.
Regulatory Peptides | 1999
Marjo Kapraali; Olle Johansson; Andrés Uribe
BACKGROUND/AIM To investigate whether endogenous prostaglandins participate in the regulation of the gastrointestinal endocrine cell system. METHODS Sprague-Dawley rats were treated with 1 mg/kg indomethacin subcutaneously or indomethacin subcutaneously and 500 microg/kg oral prostaglandin E2 or solvents for 2 months. Endocrine cells were visualized by using immunohistochemistry and by the Sevier-Munger silver stain on specimens from the gastroduodenal mucosa, and their total volume was estimated, using standard stereological methods. Plasma and gastrointestinal tissue concentrations of regulatory peptides were analyzed by radioimmunoassay. RESULTS Fundic mucosa. The total volume of cells stained with the Sevier-Munger silver stain (enterochromaffin-like) was increased by indomethacin, but reduced by the administration of prostaglandin E2 (P < 0.05 vs. indomethacin). Indomethacin increased the total volume of somatostatin-immunoreactive. Similarly, rats given indomethacin and prostaglandin E2 had higher values than controls. Indomethacin increased the tissue concentration of somatostatin in the gastric fundus whereas prostaglandin E2 prevented such changes (P < 0.05 vs. indomethacin). Antral mucosa. The total volume of serotonin-immunoreactive cells was reduced by indomethacin, but increased by prostaglandin E2 (P < 0.05 vs. controls and indomethacin, respectively). Duodenal mucosa. The total volume of somatostatin-immunoreactive cells was reduced in the rats given indomethacin and prostaglandin E2 (P < 0.05 vs. controls and indomethacin). Indomethacin reduced and simultaneous administration of prostaglandin E2 increased the total volume of CCK-immunoreactive cells (P < 0.05 vs. controls and indomethacin). Indomethacin reduced the total volume of serotonin-immunoreactive cells whereas the simultaneous administration of PGE2 comparatively increased their total volumes (P < 0.05 vs. indomethacin), although they were still lower than the control values. The total volume of GIP-immunoreactive cells was slightly increased in the rats given both indomethacin and indomethacin + prostaglandin E2. The tissue concentration of somatostatin in the duodenum was reduced in rats given indometacin and prostaglandin E2 (P < 0.05 vs. controls and indomethacin). CONCLUSION Endogenous prostaglandins, particularly prostaglandin E2, regulate CCK-, enterochromaffin-like-, somatostatin-, GIP- and enterochromaffin cells in the gastroduodenal mucosa of the rat.
European Journal of Gastroenterology & Hepatology | 1997
Andrés Uribe; Marjo Kapraali; Mahbub Alam; Charlotte Söderman; Elvar Theodorsson
Objective: To examine the effect of long‐term administration of indomethacin on regulatory peptides and DNA synthesis. Design: Sprague‐Dawley rats were treated with 1 mg/kg indomethacin subcutaneously or indomethacin and 500&mgr;g/kg oral prostaglandin E2 or solvents for 2 months before labelling with methyl‐3H‐thymidine. Methods: The labelling index, growth fraction and the number of epithelial cells were determined on autoradiographs of the stomach small intestine and colon. Plasma and gastrointestinal tissue concentrations of regulatory peptides were analysed by radioimmunoassay. Results: Indomethacin increased the concentration of somatostatin in the gastric fundus and ileum and reduced it in the colon. Prostaglandin E2 reduced the somatostatin concentration in the duodenum and colon. Indomethacin increased the concentration of neurotensin, neurokinin A and glucagon in the distal small intestine and reduced the glucagon level in the colon. Prostaglandin E2 prevented such changes. Indomethacin increased DNA synthesis in the small intestine and produced hypoplasia of the villi. These changes were prevented by prostaglandin E2, except for the villous hypoplasia observed in the distal small intestine. Prostaglandin E2 reduced the labelling index in the antrum and colon. Conclusion: Endogenous prostaglandins selectively modulate the synthesis and/or release of regulatory peptides and regulate the outflow of cells from the epithelial surface. Indomethacin induces hypoplasia, which triggers a secondary trophic reaction in the epithelium that may, at least partially, be mediated by regulatory peptides.
Gastroenterology Research | 2010
Susanna Jäghult; Fredrik Saboonchi; Unn-Britt Johansson; Regina Wredling; Marjo Kapraali
Background Worries and concerns of patients with IBD comprise an important negative factor in their HRQOL. The Rating Form of Inflammatory Bowel Disease Patient Concerns (RFIPC) was developed to describe the nature and degree of the worries and concerns of IBD patients. In the original version, the specific issues of worries are divided into four separate factors. These factors provide useful information about HRQOL and the kind of worries and concerns which are most important to the patient. However, the Swedish version of the RFIPC is often scored using a single sum score, implying that all the specific issues of worries stem from a single general worry factor. The aim of this study was to validate the factor structure of the Swedish version of the RFIPC. Methods A sample consisting of 195 patients with IBD filled out the RFIPC. Confirmatory factor analysis was performed to examine fit of three hypothesized models of factor structure. Spearman’s correlation and Mann-Whitney analysis were used to follow up the results. Results The single-factor model displayed poor fit indices. The four-factor model marked substantive improvement, but still remains inadequate. The final four-factor model permitting correlated error terms between some items displayed the most adequate fit. Conclusions The factorial structure of the RFIPC, as suggested in the original version, was able to be replicated with a slight modification in the Swedish version. The separate factors identified in this structure provide more detailed information about the worries and concerns of IBD patients as these components of worries are different related to HRQOL and general health.
Digestion | 1997
Marjo Kapraali; Charlotte Söderman; Luis Marín; Olle Johansson; Elvar Theodorsson; Andrés Uribe
Groups of Sprague-Dawley rats were given placebo or prostaglandin E2 (PGE2) at 25 or 5,000 micrograms/kg or 15,R,15-methyl-PGE2 (MePGE2) at 5 or 50 micrograms/kg, twice daily, orally, for 1 month. Histological sections from the proximal duodenum were processed for immunohistochemistry and the volume density of immunoreactive endocrine cells was determined using point-counting grids. The surface density of the villous lining was estimated by using a cycloid test system. Thereafter, the total volumes of endocrine cells and the total surface area of the villous lining were calculated after estimating the mucosal volume. The volume density of serotonin-immunoreactive cells was increased in the duodenum of rats given 25 or 5,000 micrograms/kg PGE2 (p < 0.05). The total volume of these cells increased in the animals given 25 micrograms/kg PGE2 (p < 0.05). The total volume of gastrin/CCK-immunoreactive cells was higher in rats given 25 micrograms/kg PGE2 or 50 micrograms/kg MePGE2 than in controls (p < 0.05). The volume density of somatostatin-immunoreactive cells increased in rats given 5 micrograms/kg MePGE2, but the total volumes were not different between the groups. The area of somatostatin-immunoreactive cell profiles was enlarged in the animals given 5,000 micrograms/kg PGE2 (p < 0.05). The mucosal volume was enlarged by prostaglandins. The epithelial thickness increased in rats given the highest doses of PGE2 (p < 0.05). The concentration of motilin-like immunoreactivity increased in the duodenum of rats given 5 micrograms/kg MePGE2 (p < 0.05). We conclude that oral administration of PGE2 for 1 month increased the total volumes of serotonin- and gastrin-CCK-immunoreactive cells and the tissue concentration of motilin-like immunoreactivity, which indicates that prostaglandins modulate endocrine cells in a stable steady-state condition.
Journal of Clinical Nursing | 2011
Susanna Jäghult; Fredrik Saboonchi; Unn-Britt Johansson; Regina Wredling; Marjo Kapraali