| 1. |
- Bahmanyar, Shahram, et al.
(författare)
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Cystic fibrosis gene mutations and gastrointestinal diseases
- 2010
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Ingår i: Journal of Cystic Fibrosis. - : Elsevier BV. - 1569-1993 .- 1873-5010. ; 9:4, s. 288-291
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Tidskriftsartikel (refereegranskat)abstract
- Background: This study examined if CF mutation heterozygosity is associated with diseases of gastrointestinal epithelial barrier function. Design and methods: Swedish registers identified 865 patients with a diagnosis of CF between 1968 and 2003 and matched with 8101 individuals without CF. Gastrointestinal disease risk was examined among 1534 biological parents and 1396 siblings of CF patients, compared with 15,526 parents and 15,542 siblings of individuals without CF. Results: First-degree relatives of CF patients were not at lower risk of the gastrointestinal diseases, in contrast with a raised risk among CF patients. Conclusion: Heterozygosity for CF gene mutations does not protect against gastrointestinal diseases where impaired barrier function may be relevant. (C) 2010 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.
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| 2. |
- Bahmanyar, Shahram
(författare)
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Etiological aspects of gastroesophageal cancers : an epidemiological approach
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Aims: The aims of this thesis were to study the association of overall dietary habits, duodenal ulcer and gastric ulcer diseases, as two models of Helicobacter pylori (H. pylori) infection and the development of gastroesophageal cancers to further explore the etiology of these malignancies. Moreover, the association between parity, a proxy for high level of female hormones, and stomach cancer risk was studied to shed light on the enigma of male predominance in this cancer. Methods: In a nationwide population-based case-control study in Sweden with 165 esophageal squamous cell carcinoma, 185 esophageal adenocarcinoma and 258 cardia cancer cases and 815 randomly selected controls we estimated relative risks associated with dietary patterns. Furthermore, cohorts of 61,548 and 81,379 unoperated patients with duodenal ulcer and gastric ulcer, respectively, recorded in the Swedish Inpatient Register since 1965, were followed and standardized incidence ratios were estimated for esophageal cancer by histology, compared with the Swedish general population. We also followed cohorts of 59,550 and 79,412 unoperated patients with duodenal ulcer and gastric ulcer, respectively, plus 12,840 patients with partial gastric resection and 8,105 with vagotomy, recorded since 1970. We estimated relative risks for stomach cancer by anatomical subtype compared to the Swedish general population for unoperated cohorts, whereas relative risks were estimated among operated patients relative to unoperated ones with the same ulcer type. Finally, in a case-control study, nested within a cohort of Swedish women born in 1925 or later, with 286 cardia cancer and 2,498 non-cardia stomach cancer as well as corresponding 1,430 and 12,490 controls, we investigated the relationship between parity and risk of stomach cancer by anatomic subsite. Results: A “healthy diet” tended to moderately decrease the risk of esophageal and cardia cancers, “Western diet” increased risks of cardia cancer and esophageal adenocarcinoma, whereas a dietary pattern characterized by high beer and liquor intake significantly increased the risk of squamous-cell carcinoma of the esophagus. We observed that patients with duodenal ulcer had a significant 70% excess risk of esophageal adenocarcinoma, a non- significant small excess risk of esophageal squamous cell carcinoma, a halved risk of non-cardia cancer, and a risk of cardia cancer slightly above expectation. Gastric ulcer was unrelated to esophageal adenocarcinoma but linked to 80% increased risk of esophageal squamous cell carcinoma, and doubled risks for both anatomical types of stomach cancer. Duodenal ulcer patients who underwent gastric resection had a 60% risk elevation for noncardia cancer compared to unoperated ones. Vagotomy was associated with a greater risk in the first 10 years, but this excess disappeared with further follow-up. Resected gastric ulcer patients had a 40% risk reduction for non-cardia cancer relative to their unoperated peers. We found no association between parity and risk of non-cardia stomach cancer comparing everparous women with nulliparous, whereas a statistically significant 30% risk reduction for postmenopausal cardia cancer was noted among everparous women relative to nulliparous. Conclusions: Overall dietary habits seem to play an important role in the carcinogenesis of esophageal and cardia cancer. The well-established strong inverse association of H. pylori seropositivity and risk of esophageal adenocarcinoma does not pertain to all infections. The duodenal ulcer related protection against stomach cancer does not seem to affect cardia cancer. It seems that the pattern of stomach colonization and/or the clinical consequences in the stomach might play a pivotal role in the long term outcome of H. pylori infection. With gastric resection, risks are shifted toward normality, regardless of underlying ulcer type. Exposure to female sex hormones is not associated with protection against stomach cancer and does not seem to explain the male predominance for such cancer. However the observed moderate inverse relationship between parity and cardia cancer might be mediated by other factors than hormonal.
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| 3. |
- Bahmanyar, Shahram, et al.
(författare)
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Maternal smoking during pregnancy, other prenatal and perinatal factors, and the risk of Legg-Calvé-Perthes disease
- 2008
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Ingår i: Pediatrics. - : American Academy of Pediatrics. - 0031-4005 .- 1098-4275. ; 122:2, s. e459-e464
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The causes of Legg-Calvé-Perthes disease are largely unknown, but this pediatric disease seems to result from interruption of the blood supply to the proximal femur and is considered a vascular disease. Because maternal smoking during pregnancy influences fetal development and is associated with cardiovascular diseases in offspring, we hypothesized that this exposure is a risk for Legg-Calvé-Perthes disease and also investigated other markers of impaired fetal development and early-life exposures.MATERIALS AND METHODS: The Swedish Inpatient Register identified 852 individuals with a diagnosis of Legg-Calvé-Perthes disease from 1983 to 2005, individually matched by year of birth, age, sex, and region of residence with 4432 randomly selected control subjects. Linkage with the Swedish Medical Birth Register provided information on prenatal factors, including maternal smoking. Conditional logistic regression examined associations of maternal smoking during pregnancy and the other measures with the risk of Legg-Calvé-Perthes disease in offspring, adjusted for socioeconomic index and other potential confounding factors.RESULTS: Maternal smoking during pregnancy was associated with an increased Legg-Calvé-Perthes disease risk, and heavy smoking was associated with a risk increase of almost 100%. Very low birth weight and cesarean section were independently associated with approximately 240% and 36% increases in the risk of Legg-Calvé-Perthes disease, respectively.CONCLUSION: Maternal smoking during pregnancy and other factors indicated by impaired fetal development may be associated with an increased risk of Legg-Calvé-Perthes disease.
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| 4. |
- Bahmanyar, Shahram, et al.
(författare)
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Pharmacological treatment and demographic characteristics of pediatric patients with Attention Deficit Hyperactivity Disorder, Sweden
- 2013
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Ingår i: European Neuropsychopharmacology. - : Elsevier BV. - 0924-977X .- 1873-7862. ; 23:12, s. 1732-1738
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to describe the pediatric population with ADHD and their pharmacological treatment. Using the Swedish National Patient Register and the Prescribed Drug Register we identified individuals below 19 years of age who were diagnosed or medically treated for ADHD for the first time 2006-2007. The unique patient identifiers were used to link information from the two registers to describe demographic characteristics, hospital care and drug treatments. Logistic regression model estimated the association between age, sex, frequency of hospitalization, diagnosis or treatment for other mental disorders and risk of gap in the treatment. Totally the study included 7931 patients of whom 74% were males. The mean age at first diagnosis was 12 years. Some 84% were medically treated for ADHD and approximately 90% received methylphenidate as the first substance. Combination therapy was rare and the most common combination was methylphenidate and atomoxetine. More than 55% of the patients, which could be followed up for two years after start of treatment, had at least one treatment gap of six months. Older age at diagnosis, lower number of hospitalizations and comorbidity with other mental disorders increased risks of gaps in medication. Approximately one fifth of the patients recorded in the National Patient Register as diagnosed with ADHD did not receive pharmacological treatment. Medication adherence seems to be low, when measured as gaps in treatment.
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| 5. |
- Bergendal, Annica, et al.
(författare)
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Non-steroidal anti-inflammatory drugs and venous thromboembolism in women
- 2013
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Ingår i: Pharmacoepidemiology and Drug Safety. - : Wiley. - 1053-8569 .- 1099-1557. ; 22:6, s. 658-666
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Tidskriftsartikel (refereegranskat)abstract
- Background Non-steroidal anti-inflammatory drugs (NSAIDs) might increase the risk of venous thromboembolism (VTE), and risks might differ by type of NSAID. Compared with men, women have a higher incidence of VTE at younger age, and they more often use NSAIDs. Objectives To assess risks of VTE in young and middle-aged women in association with use of NSAIDs. Patients/Methods In a nationwide case-control study (Thrombo Embolism Hormone Study) performed in Sweden 2003-2009, we included as cases 1433 women, 18 to 64years of age with a first time VTE. Controls were 1402 randomly selected women, frequency matched by age. Information was obtained by telephone interviews and DNA analyses of blood samples. We calculated adjusted odds ratios (ORs) with 95% confidence intervals (CIs) adjusting for degree of immobilization, chronic disease, smoking, body mass index, use of hormonal contraception, hormone therapy or other NSAIDs. Results Use of NSAIDs was not associated with increased risks of VTE (OR=0.98, 95% CI 0.80-1.19). The OR was 0.88 for propionic acid derivatives (95% CI 0.72-1.10), 1.18 for acetic acid derivatives (95% CI 0.82-1.70) and 1.76 for coxibs (95% CI 0.73-4.27). For users of acetic acid derivatives and coxibs, the ORs increased by cumulative dose. Carriership of the prothrombin gene mutation or factor V Leiden had only minor effects on the results. Conclusions We found no increased risks of VTE in association with use of NSAIDs. Users of high cumulative doses of acetic acid derivatives and coxibs had the highest risks, suggesting a relationship with cyclooxygenase selectivity and dose.
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| 6. |
- Bergquist, Annika, et al.
(författare)
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Increased risk of primary sclerosing cholangitis and ulcerative colitis in first-degree relatives of patients with primary sclerosing cholangitis
- 2008
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Ingår i: Clinical Gastroenterology and Hepatology. - New York : Elsevier. - 1542-3565 .- 1542-7714. ; 6:8, s. 939-943
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: The importance of genetic factors for the development of primary sclerosing cholangitis (PSC) is incompletely understood. This study assessed the risk of PSC and inflammatory bowel disease (IBD) among first-degree relatives of patients with PSC, compared with the first-degree relatives of a cohort without PSC. Methods: Subjects from the national Swedish cohort of PSC patients (n = 678) were matched for date of birth, sex, and region to up to 10 subjects without a diagnosis of PSC (n = 6347). Linkage through general population registers identified first-degree relatives of subjects in both the PSC and comparison cohorts (n = 34,092). Diagnoses among first-degree relatives were identified by using the Inpatient Register. Results: The risk of cholangitis was statistically significantly increased in offspring, siblings, and parents of the PSC patient cohort, compared with relatives of the comparison cohort, with the hazard ratios and 95% confidence intervals, 11.5 (1.6–84.4), 11.1 (3.3–37.8), and 2.3 (0.9–6.1), respectively. The hazard ratios for ulcerative colitis (UC) among first-degree relatives of all PSC patients was 3.3 (2.3–4.9) and for Crohn's disease 1.4 (0.8–2.5). The risk of UC for relatives of PSC patients without IBD was also increased, 7.4 (2.9–18.9). Conclusions: First-degree relatives of patients with PSC run an increased risk of PSC, indicating the importance of genetic factors in the etiology of PSC. First-degree relatives of PSC patients without IBD are also at an increased risk of UC, which might indicate shared genetic susceptibility factors for PSC and UC.
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| 7. |
- Burkill, Sarah M., et al.
(författare)
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Pain and Painkiller Use Among Multiple Sclerosis Patients in Sweden
- 2017
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Ingår i: Pharmacoepidemiology and Drug Safety. - : John Wiley & Sons. - 1053-8569 .- 1099-1557. ; 26:Suppl. 2, s. 634-634
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: Multiple sclerosis is an autoimmune disease which leads to demyelination and subsequent damage of axons and neurons. Pain is known to commonly affect MS patients, however the clinical characteristics of this pain are not fully described. Prescribed pain medication identifies more severe and chronic pain and different drug types can be used to identify other pain characteristics.Objectives: To assess whether MS patients in Sweden are at increased risk of receiving medication for pain relative to non-MS comparators. We aim to study overall pain, neuropathic pain, musculoskeletal pain and migraine.Methods: This cohort study using data on 5,555 MS patients in Sweden individually matched to 5,555 non-MS Swedish residents on sex, year of birth and place of residence at the time of MS diagnosis. We used Cox PH models using date of entry or 1stJuly 2006 as the beginning of follow up, whichever occurred later, and end of study was date of death, date of prescription of a painkiller or December 31st 2014, whichever occurred first. Painkillers were identified through relevant ATC codes. For neuropathic pain, pregabalin, gabapentin, amitriptyline, capsaicin or nortriptyline were used for identification, and for migraine prescriptions of anti-migraine preparations were included in the outcome. Musculoskeletal pain was identified primarily through topical products for joint and muscular pain.Results: Cox PH models showed MS patients to be at a 2.43 (CI 2.31–2.55) times increased risk of being prescribed any painkiller. The risk increased to 5.63 (CI 5.03–6.31) for neuropathic painkillers, however there was no significant difference for musculoskeletal painkillers (RR = 0.92 (CI 0.79–1.07)). MS patients were at a 1.28 (CI 1.10-1.50) times increased risk of being prescribed anti-migraine preparations. Restricting the data to MS patients showed that exposure to neuropathic painkillers was present in 32.8% of MS patients, and is associated with lower educational attainment and female sex. Conclusions: MS patients are at significantly increased risk of pain overall, with a particularly elevated risk for neuropathic pain. It seems that lower educational attainment and female sex are risk factors of neuropathic pain. However, the reason for this is not fully understood.*We would like to acknowledge the funding from the Science for Life - Astra Zeneca collaborative grant that supported this research
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| 8. |
- Burkill, Sarah, et al.
(författare)
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Mortality trends for multiple sclerosis patients in Sweden from 1968 to 2012
- 2017
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Ingår i: Neurology. - : Lippincott Williams & Wilkins. - 0028-3878 .- 1526-632X. ; 89:6, s. 555-562
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To assess trends in mortality and causes of death for patients with multiple sclerosis (MS) relative to those without MS in Sweden.Methods: Patients with an MS diagnosis in Sweden between 1964 and 2012 were identified with the Patient Register and the Multiple Sclerosis Register. For this cohort study, each patient with MS (n = 29,617) was matched with 10 individuals without MS (n = 296,164) on sex, year of birth, vital status, and region of residence at the time of MS diagnosis with the Total Population Register. The Causes of Death Register was used to identify causes of death. Cox proportional hazard models were constructed to assess whether risk of mortality was increased for patients with MS.Results: The hazard ratio (HR) for patients with MS was 2.92 (95% confidence interval [CI] 2.86-2.99) for all-cause mortality over the entire study period. The largest differences between the cohorts were death resulting from respiratory (HR 5.07, 95% CI 4.87-5.26) and infectious (HR 4.07, 95% CI 3.70-4.47) diseases. Overall and for each specific cause, there have been improvements for the MS group and a subsequent reduction in the HR. The HR decreased from 6.52 (95% CI 5.79-7.34) for the period of 1968 to 1980 to 2.08 (95% CI 1.95-2.22) for the time period of 2001 to 2012. An interaction between time period and MS exposure showed that the decrease in mortality over time was statistically significant, with a larger decrease for patients with MS than their matched comparators.Conclusions: There has been a substantial improvement in mortality overall and for each specified cause of death for patients with MS compared with individuals without MS; however, large differences still remain.
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| 9. |
- Burkill, Sarah, et al.
(författare)
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Pharmacological Treatments Preceding Diagnosis Of Progressive Multifocal Leukencephalopathy
- 2016
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Ingår i: Pharmacoepidemiology and Drug Safety. - : Wiley-Blackwell. - 1053-8569 .- 1099-1557. ; 25:Suppl. 3, s. 496-497
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: Progressive multifocal leukencephalopathy (PML) is a rare, often fatal viral disease, which affects the white matter of the brain. It is caused by John Cunningham (JC) polyomavirus, which is present in most people and is usually harm-less. For immunocompromised persons, such as those who are taking immunosuppressive treatments, the risk of JC virus causing PML is increased, although still rare. As PML diagnosis is not always accurate, epidemiology of PML, including the true incidence and patient characteristics, is incompletely described.Objectives: To identify pharmacological treatments preceding diagnosis of definitive, probable and possible PML, after excluding incorrect PML diagnoses by medical record review.Methods: Patients with a PML diagnosis in Sweden between 1988 and 2013 were identified through the Patient register using ICD 9 code 046D and ICD 10code A81.2 (n = 281). Medical records were reviewed and information on clinical characteristics and pharmacological treatments were collected. Each of the diagnoses was determined as definite PML, possible PML, probable PML or non-PML based on the consensus statement for the AAN neuroinfectious disease section published in 2013. (PMCID: 3662270).Results: Medical records for 251 patients (89%) were available and examined. In total, 84 (33%) of the 251 PML diagnoses were confirmed. For those with a record of being exposed to immunosuppressant drugs, 60 (65%) of the 92 records were confirmed as being definite PML. Among 12 patients exposed to rituximab 11 (92%) had definite and 1 (8%) had probable PML. For the 9 natalizumab users, 8 (89%) had definite PML and 1 (11%) was diagnosed incorrectly.Conclusions: A substantial proportion of PML diagnoses recorded in Sweden are incorrect, however amongst those exposed to immunosuppressants such as rituximab and natalizumab the majority of diagnoses are correct. Assessing immunosuppressive drug history could be an important part of the diagnostic processes for PML.
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| 10. |
- Burkill, Sarah, et al.
(författare)
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The association between exposure to interferon-beta during pregnancy and birth measurements in offspring of women with multiple sclerosis
- 2019
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Ingår i: PLOS ONE. - : PLOS. - 1932-6203. ; 28:Suppl. 2, s. 371-372
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Interferon-beta (IFN-beta) is a commonly used treatment for multiple sclerosis (MS). Current guidelines recommend cessation of treatment during pregnancy, however the results of past studies on the safety of prenatal exposure to IFN-beta have been conflicting. A large scale study of a population of MS women is therefore warranted.OBJECTIVES: To assess whether, among those born to women with MS, infants prenatally exposed to IFN-beta show evidence of smaller size at birth relative to infants which were not prenatally exposed to any MS disease modifying drugs.METHODS: Swedish and Finnish register data was used. Births to women with MS in Sweden and Finland between 2005-2014 for which a birth measurement for weight, height, and head circumference was available were included. The exposure window was from 6 months prior to LMP to the end of pregnancy.RESULTS: In Sweden, 411 pregnancies were identified as exposed to IFN-beta during the exposure window, and 835 pregnancies were counted as unexposed to any MS DMD. The corresponding numbers for Finland were 232 and 331 respectively. Infants prenatally exposed to interferon-beta were on average 28 grams heavier (p = 0.17), 0.01 cm longer (p = 0.95), and had head circumferences 0.14 cm larger (p = 0.13) in Sweden. In Finland, infants were 50 grams lighter (p = 0.27), 0.02 cm shorter (p = 0.92) and had head circumferences 0.22 cm smaller (p = 0.15) relative to those unexposed.CONCLUSIONS: This study provides evidence that exposure to IFN-beta during pregnancy does not influence birth weight, length, or head circumference.
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