Caroline Nordenvall

Cancer risk among patients with condylomata acuminata

Condylomata acuminata have been shown to increase the risk of anogenital cancers. However, previous studies have been of limited sample size and/or short follow‐up duration, which prevent precise estimates of long‐term excess risk, especially for specific cancer sites. We estimated the risk of specific cancers in a large cohort of hospitalized patients with condylomata acuminata, as recorded in the Swedish Inpatient Register between 1965 and 1999. Altogether, 10,971 patients (1,685 men and 9,286 women) were followed through 1999 for a median of 13 years. The standardized incidence ratio (SIR)—the ratio of the observed number of cancers to the number expected on the basis of the incidence in the Swedish population at large—was used as a measure of relative risk. After excluding the first‐year of follow‐up, we observed 43 cases of anogenital cancer in women, and 7 cases in men. Risks were elevated for cancers of the vulva (N = 13, SIR = 10.2, 95% confidence interval (CI) = 5.4–17.4), vagina (N = 4, SIR = 12.0, 95% CI = 3.3–30.7) and penis (N = 5, SIR = 21.9, 95% CI = 7.1–51.2). There was a moderate excess risk of cervical cancer in situ (N = 259, SIR = 1.9, 95% CI = 1.7–2.1), but not invasive cervical cancer. Excess risks of esophageal, buccal cavity, nonmelanoma skin, lung and bladder cancers, and Hodgkin and non‐Hodgkin lymphoma, were also observed in both men and women. In conclusion, condylomata acuminata are strongly associated with increased risk of cancers of the vulva, vagina, penis and anus, as well as some nonanogenital malignancies, but not invasive cervical cancer.

A prospective study of gout and cancer

Gout patients might be at an increased risk of cancer because of obesity and heavy alcohol drinking, but uric acid has antioxidant properties, which may protect against carcinogenesis. We compared the incidence of cancer among 16 857 gout patients admitted to hospitals in Sweden during 1965–1995 with that of the national population. A total of 1425 malignant neoplasms were diagnosed in gout patients (standardized incidence ratio 1.25, 95% confidence limits 1.18, 1.31). The incidence of cancers of the oral cavity and pharynx, colon, liver and biliary tract, pancreas, lung, skin (melanoma and nonmelanoma), endometrium and kidney, as well as of malignant melanoma was increased among gout patients. With the exception of lung cancer, the risk remained elevated during the entire follow-up. This study provides no evidence of a protective effect of uric acid. Hyperuricemia may be an early manifestation of the carcinogenic process.

The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease

Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N‐nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register‐based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record‐linkages allowed complete follow‐up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3–38 of follow‐up, we observed a 20% excess risk (95% confidence interval [CI] 10–40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10–110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4–3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.

Smoking, snus use and risk of right- and left-sided colon, rectal and anal cancer: a 37-year follow-up study.

Although some authorities consider smoking to be an established risk factor for colorectal cancer, the international literature is not entirely consistent. Further, only 1 study has addressed the association with smokeless tobacco and none with Scandinavian moist snuff (snus). This retrospective cohort study included 336,381 male Swedish construction workers with detailed information on tobacco use at cohort entry in 1971–1992. Complete follow‐up through 2007 was accomplished by means of linkage to population and health registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) derived from Cox proportional hazards regression models estimated relative risks, adjusted for age and body mass index. Subjects who were never‐users of any tobacco served as reference. After up to 37 years of follow‐up, pure smoking was associated with a marginally increased risk of colon cancer (HR 1.08, 95% CI 0.99–1.19), a modestly elevated risk of rectal cancer (HR 1.16, 95% CI 1.04–1.30) and a substantial excess risk of anal cancer (HR 2.41, 95% CI 1.06–5.48). Snus use was not significantly associated with an increased risk of colorectal or anal cancer, although the point estimate for colon cancer was similar to that observed among smokers. Swedish data provide meager support for the association between tobacco use and colorectal cancer. A general tendency among Swedish men to quit smoking in recent decades might have attenuated true associations. A link between smoking and anal cancer was confirmed.

Interpreting trends of pancreatic cancer incidence and mortality: a nation-wide study in Sweden (1960-2003)

ObjectiveWe investigated temporal trends of pancreatic cancer in Sweden measured with suboptimal sensitivity and specificity both by incidence and by mortality rates.Methods46,257 incident cases of pancreatic cancer from the Swedish Cancer Register and 53,686 mortality cases from the Causes of Death Register during 1960–2003 were used to calculate age-standardized incidence or mortality rates. We further assessed the impact of changes in diagnostic practice on the observed trends, and investigated the effect of calendar period and birth cohort by age-period-cohort modeling.ResultsOverall, the pattern of trends in age-adjusted rates of pancreatic cancer was similar irrespective of whether incidence or mortality was used. The age-adjusted rates of pancreatic cancer increased during the first decade and then peaked for both sexes (the male peak occurred in the early 1970s and the female peak in the1980s) followed by a steady decline in both groups. An age-period model provided the best fit to the observed trends among patients diagnosed at ages 35–74 in both sexes.ConclusionThe close agreement between the incidence and mortality and the gender disparity suggest a true decline in pancreatic cancer incidence in recent years in Sweden, and gender-specific trends in exposure to environmental risk factors.

Tobacco use and cancer survival: A cohort study of 40,230 Swedish male construction workers with incident cancer

On theoretical grounds, nicotine has been implicated as a modifier of cancer progression. We investigated possible associations of smoking or use of Scandinavian moist snuff (snus) with survival after cancer among Swedish male construction workers. Snus use is associated with substantial exposure to nicotine but not to the combustion products in smoke. Among 336,381 workers with detailed information on tobacco use in 1971–1992, we observed 40,230 incident cancers. Complete follow‐up through 2007 was accomplished through linkage to population and health registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) for death from any cause, cancer‐specific death and death from other causes were derived from Cox proportional hazards regression models adjusted for age at diagnosis, body mass index at study entry and period of diagnosis. Never users of any tobacco served as reference. Increased risks of cancer‐specific death were observed both among exclusive smokers (HRall cancer 1.15, 95% CI: 1.10–1.21) and never‐smoking snus users (1.15, 95% CI: 1.05–1.26). As regards deaths due to other causes, exclusive smokers had higher relative risks than exclusive snus users (p = 0.03). A history of tobacco use, even exclusive use of the seemingly benign snus, is associated with moderately increased cancer‐specific mortality. Although nicotine might play a role, the mechanisms warrant further investigation.

Elevated anal squamous cell carcinoma risk associated with benign inflammatory anal lesions

Background: The association between benign anal lesions and anal cancer is still unclear. Few data from large cohort studies are available. Methods: We conducted a register based retrospective cohort study including 45 186 patients hospitalised for inflammatory anal lesions (anal fissures, fistulas, and perianal abscesses) as well as 79 808 haemorrhoid patients, from 1965 to 2002. Multiple record linkages identified all incident anal (squamous cell carcinoma only) and colorectal cancers through to 2002. Relative risk was estimated by standardised incidence ratio (SIR), the ratio of observed number of cases divided by that expected in the age, sex, and calendar year-matched general Swedish population. Results: There was a distinct incidence peak in the first three years of follow up among patients with inflammatory lesions. SIR then levelled off at around 3 and remained at this level throughout follow up (SIR during years 3–37 of follow up was 3.3 (95% confidence interval 1.8–5.7)). A similar initial incidence peak was observed among haemorrhoid patients but was confined to the first year; SIR was 2.8 in the second year, and then it decreased further and was close to unity in the following years (SIR during years 3–37 was 1.3 (95% confidence interval 0.7–2.1)). Among inflammatory lesion and haemorrhoid patients, a significantly increased risk of colorectal cancer was observed only in the first year after hospitalisation. Conclusions: Inflammatory benign anal lesions are associated with a significantly increased long term risk of anal cancer. In contrast, haemorrhoids appear not to be a risk factor for this malignancy.

Mortality after total colectomy in 3084 patients with inflammatory bowel disease: a population-based cohort study

A high post‐operative mortality has been reported following colectomy in patients with inflammatory bowel disease (IBD), especially in some patient groups.

Probability, rate and timing of reconstructive surgery following colectomy for inflammatory bowel disease in Sweden: a population-based cohort study

Many patients with inflammatory bowel disease (IBD) need colectomy, but the rate of reconstructive surgery with restoration of intestinal continuity is unknown. The aim of this study was to investigate the probability, rate and timing of reconstructive surgery after colectomy in patients with IBD in a population‐based setting.

Smoking, use of moist snuff and risk of celiac disease: a prospective study

BackgroundSmoking status has been linked to several chronic inflammatory conditions but earlier research on smoking and celiac disease (CD) is contradictive. There are little data on moist snuff use and CD. The purpose of this study was to investigate the association between smoking, moist snuff use and later CD.MethodsWe identified individuals with biopsy-verified CD (villous atrophy, histopathology stage Marsh III) through biopsy-reports from Sweden’s 28 pathology departments. Data on smoking and moist snuff were collected from the Swedish construction worker database “Bygghälsan” that includes preventive health care check-up data. Through poisson regression we calculated relative risks (RRs) for later CD according to smoking status (n = 305,722), and moist snuff status (n = 199,200) adjusting for age, sex and decade.ResultsDuring follow-up 488 individuals with smoking data, and 310 with moist snuff data had a diagnosis of CD. The risk of CD was independent of smoking status with all RRs being statistically insignificant and ranging between 0.9 and 1.0. Compared to non-smokers, neither current smokers (RR = 0.93; 95% CI = 0.76-1.14) nor ex-smokers (RR = 0.98; 95% CI = 0.75-1.28) were at increased or decreased risk of CD. Risk estimates were similar in moderate smokers (RR = 0.92; 0.72-1.16) and heavy smokers (RR = 0.95; 0.74-1.24), and did not change when we examined the risk more than ten years after health examination (RR-moderate: 0.90; and RR-heavy: 0.95; both p > 0.05). Moist snuff use was not associated with later CD (RR = 1.00; 0.78-1.28), or with CD after more than ten years of follow-up (RR = 1.05; 0.80-1.38).ConclusionsWe found no association between smoking, moist snuff use and future CD.