BACKGROUND: Drug therapy for Crohn's disease and ulcerative colitis is based on anti-inflammatory and immunodulating drugs, nutritional support and surgical resection. Recently, new drugs have been introduced. AIM: To report drug prescriptions, costs and adverse reactions among inflammatory bowel disease patients in Sweden between 1988 and 1997. METHODS: Drug use was calculated from the national Diagnosis and therapy survey and drug costs from prescriptions and drug sales. Adverse drug reactions were obtained from the Medical Products Agency's National Pharmacovigilance system. RESULTS: The annual drug exposure for Crohn's disease was 0.55 million daily doses per million population, mainly supplementation and aminosalicylic acids. Mesalazine and olsalazine had 61% within this group. For ulcerative colitis patients, drug exposure was 0.61 million daily doses per million per year and aminosalicylic acids fell from 70% to 65%. For inflammatory bowel disease patients, corticosteroids and nutritional supplementation were common. The annual average cost for inflammatory bowel disease drugs was 7.0 million US dollars. Annually, 32 adverse drug reactions were reported, mainly haematological reactions such as agranulocytosis and pancytopenia (60%), followed by skin reactions. Only two deaths were reported. Aminosalicylic acids were the most commonly reported compounds. CONCLUSIONS: Drug use for inflammatory bowel disease in the pre-biologic agent era rested on aminosalicylic acid drugs and corticosteroids with stable levels, proportions and costs. The level of adverse drug reactions was low but haematological reactions support the monitoring of inflammatory bowel disease patients.
OBJECTIVE: Several studies have suggested that patients with acromegaly have an increased risk of benign and malignant neoplasms, especially of the colon. To further investigate this relationship we evaluated cancer risk in population-based cohorts of acromegaly patients in Sweden and Denmark. METHODS: Nationwide registry-based cohorts of patients hospitalized for acromegaly (Denmark 1977-1993; Sweden 1965-1993) were linked to tumor registry data for up to 15-28 years of follow-up, respectively. Standardized incidence ratios (SIR) and 95% confidence intervals (CI) were calculated to estimate cancer risk among 1634 patients with acromegaly. RESULTS: The patterns of cancer risk in Sweden and Denmark were similar. After excluding the first year of follow-up, 177 patients with acromegaly had a diagnosis of cancer compared with an expected number of 116.5 (SIR = 1.5. 95% CI = 1.3-1.8). Increased risks were found for digestive system cancers (SIR = 2.1, 95% CI = 1.62.7), notably of the small intestine (SIR = 6.0, 95% CI = 1.2-17.4), colon (SIR = 2.6, 95% CI = 1.6-3.8), and rectum (SIR = 2.5, 95% CI= 1.3-4.2). Risks were also elevated for cancers of the brain (SIR = 2.7, 95% CI= 1.2-5.0). thyroid (SIR = 3.7, 95% CI = 1.8-10.9), kidney (SIR = 3.2, 95% CI = 1.6-5.5), and bone (SIR= 13.8, 95% CI= 1.7-50.0). CONCLUSIONS: The increased risk for several cancer sites among acromegaly patients may be due to the elevated proliferative and anti-apoptotic activity associated with increased circulating levels of insulin-like growth factor-1 (IGF-1). Pituitary irradiation given to some patients may have contributed to the excess risks of brain tumors and thyroid cancer. Our findings indicate the need for close medical surveillance of patients with acromegaly, and further studies of the IGF-I system in the etiology of various cancers.
BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.
A population-based cohort study of 36 856 women diagnosed with alcoholism in Sweden between 1965 and 1995 found that alcoholic women had only a small 15% increase in breast-cancer incidence compared to the general female population. It is therefore apparent, contrary to expectation, that alcoholism does not increase breast-cancer risk in proportion to presumed ethanol intake.
The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965-83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.3-1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3-1.6) and among women (SIR = 1.5, CI = 1.1-2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9-5.7), esophagus (SIR = 6.8, CI = 4.5-9.9), larynx (SIR = 3.3, CI = 1.7-6.0), and lung (SIR = 2.1, CI = 1.7-2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9-2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6-1.4), large bowel (SIR = 1.1, CI = 0.8-1.5), prostate (SIR = 1.0, CI = 0.8-1.3), urinary bladder (SIR = 1.0, CI = 0.6-1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3-1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6-2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5-9.1).(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to determine the risk of developing primary liver cancer in patients with a diagnosis of alcoholism, liver cirrhosis, or both. Three population-based, mutually exclusive cohorts were defined on the basis of hospital discharge diagnosis between 1965 and 1983. Complete follow-up through 1984--excluding the first year of follow-up--showed that among 8,517 patients with a diagnosis of alcoholism, 13 cancers occurred, vs. 4.2 expected (standardized incidence ratio (SIR) = 3.1; 95% confidence interval (CI) = 1.6 to 5.3); among 3,589 patients with liver cirrhosis, 59 cancers occurred, vs. 1.7 expected (SIR = 35.1; 95% CI = 26.7 to 45.3), and among 836 patients with both diagnoses, 11 cancers occurred, vs. 0.3 expected (SIR = 34.3; 95% CI = 17.1 to 61.3). Thus, alcoholism alone entailed a moderately increased risk and alcoholism with liver cirrhosis did not increase the high relative risk for liver cancer more than cirrhosis alone. We conclude that alcohol intake may be a liver carcinogen only by being causally involved in the development of cirrhosis; and further, that the risk of developing liver cancer following cirrhosis in this population is similar to or higher than that after chronic hepatitis-B-virus infection in other Western countries.
BACKGROUND: Conflicting results have provided support for two distinct and contradictory hypotheses: (i) allergy has a protective effect against cancer by enhanced immune surveillance, and (ii) allergy is associated with an increased risk of cancer by chronic immune stimulation. We therefore aimed us to perform a large epidemiological study with a defined allergic disease cohort. METHODS: During the years 1988-2000, 70 136 patients tested for total serum immunoglobulin E (IgE) and 57 815 tested with Phadiatop for diagnosing allergic disease at Karolinska University Hospital, Stockholm, Sweden, were linked with the Swedish Cancer Registry for a virtually complete follow up with regard to cancer. FINDINGS: The total number of observed cancers was normal in the total serum IgE-cohort; standardized incidence ratio (SIR) = 0.98 (95% CI: 0.92-1.04) and in the Phadiatop-cohort: SIR = 0.99 (0.92-1.06) independent of the level of IgE and positive or negative Phadiatop. Specific analysis was done for cancer of the lung, cervix, pancreas, lymphoma, and nonmelanoma skin cancer. None of these forms of cancer had increased risks. INTERPRETATION: The study does not support the hypothesis that allergy has a protective effect against cancer, nor does it support an increased risk.
TNF inhibitors (TNFi) have been shown to reduce the need for surgery in Crohn's disease, but few studies have examined their effect beyond the first year of treatment.
To conduct a register-based observational cohort study in Sweden 2006-2014 to investigate the risk of bowel resection in bowel surgery naïve TNFi-treated Crohn's disease patients and whether patients on TNFi =12 months are less likely to undergo bowel resection than patients discontinuing treatment before 12 months.
We identified all individuals in Sweden with Crohn's disease through the Swedish National Patient Register 1987-2014 and evaluated the incidence of bowel resection after first ever dispensation of adalimumab or infliximab from 2006 and up to 7 years follow-up.
We identified 1856 Crohn's disease patients who had received TNFi. Among these patients, 90% treatment retention was observed at 6 months after start of TNFi and 65% remained on the drug after 12 months. The cumulative rates of surgery in Crohn's disease patients exposed to TNFi years 1-7 were 7%, 13%, 17%, 20%, 23%, 25% and 28%. Rates of bowel resection were similar between patients with TNFi survival
We analyzed all appendectomies in Sweden 1989-1993 (n = 60,306) recorded in the national Inpatient Registry. Our focus was on diagnostic accuracy, incidence rate of appendicitis, perforative appendicitis, and length of stay by day of admission and hospital category. The incidence rate of appendectomy decreased by 9.8% in women compared to 4.1% in men. Since the number of patients with an end diagnosis of appendicitis remained almost constant, diagnostic accuracy increased each year. This was more pronounced in women than men, seen in all hospital categories, and was higher for those admitted during periods of low capacity (weekends/ holidays). Perforated appendicitis did not increase. Duration of hospital stay decreased continuously, especially among the oldest. We found no indications of an increased frequency of complications, such as increases in the incidence rate of perforations or in the length of stay.
In adults, impaired fasting glycemia (IFG) increases the risk for type 2 diabetes mellitus (T2DM). This study aimed to investigate to which extent children with obesity develop T2DM during early adulthood, and to determine whether IFG and elevated hemoglobin A1c (HbA1c) in obese children are risk markers for early development of T2DM.
In this prospective cohort study, 1620 subjects from the Swedish Childhood Obesity Treatment Registry - BORIS who were ?18 years at follow-up and 8046 individuals in a population-based comparison group, matched on gender age and living area, were included. IFG was defined according to both ADA (cut-off 5.6 mmol?l(-1)) and WHO (6.1 mmol?l(-1)). Elevated HbA1c was defined according to ADA (cut-off 39 mmol?l(-1)). Main outcome was T2DM medication, as a proxy for T2DM. Data on medications were retrieved from a national registry.
The childhood obesity cohort were 24 times more likely to receive T2DM medications in early adulthood compared with the comparison group (95% confidence interval (CI): 12.52-46). WHO-defined IFG predicted future use of T2DM medication with an adjusted hazard ratio (HR) of 3.73 (95% CI: 1.87-7.45) compared with those who had fasting glucose levels
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Cites: Int J Obes (Lond). 2014 Jan;38(1):40-523828099