Can you die from crohn’s

Can Crohn’s disease be fatal?

Below are some severe complications of Crohn’s disease:

Colorectal cancer

People with IBD have an increased risk of developing dysplasia. This occurs when abnormal cells form in the lining of the colon or rectum. Over time, these cells can become cancerous.

When Crohn’s disease affects the colon, a person may have an increased risk of colorectal cancer, compared to the general population.

This risk is higher for people who have had Crohn’s for 8–10 years or more.

To help a doctor detect dysplasia early and possibly prevent colorectal cancer:

  • have a routine colonoscopy every 1–2 years
  • see a gastroenterologist every year
  • notify a doctor of any new symptoms or concerns
  • manage inflammation with prescription medication
  • tell the doctor if a family member develops colorectal cancer
  • exercise regularly and eat a healthful diet

Symptoms

Despite the increased risk, the vast majority of people with Crohn’s disease never develop colorectal cancer.

Nonetheless, people should be familiar with the symptoms of this type of cancer and report any to a doctor. The disease is highly treatable in the early stages.

Symptoms of colorectal cancer include:

  • diarrhea or constipation lasting more than a few days
  • a constant feeling of needing to make a bowel movement
  • bleeding from the rectum
  • stools that are dark or contain fresh blood
  • abdominal pain or cramping
  • weakness and fatigue
  • unintended weight loss

Fistulas

Inflammation from Crohn’s disease can spread through the intestinal wall, creating an abscess.

As the abscess grows, it forms a small hole in the wall, and this hole can develop into a fistula. A fistula is an abnormal passageway that connects one organ to another.

Around 1 in 4 people with Crohn’s develop fistulas. In most cases, fistulas originate in the bowel. They may connect to other parts of the bowel or other internal organs.

Sometimes, a fistula forms a tunnel from the intestine to the outer surface of the skin. The medical term for this is an enterocutaneous fistula (ECF).

Most people with ECFs experience at least one complication, such as malnutrition or sepsis. Sepsis is a whole-body inflammatory response to infection. Without treatment, malnutrition and sepsis can result in death.

Fistulas usually contain intestinal bacteria and other infectious material, so doctors will use antibiotics to treat them.

Large, numerous, or persistent fistulas usually require surgery.

Symptoms

The symptoms of a fistula differ, depending on the location. However, some common symptoms include:

  • frequent urinary tract infections
  • nausea and vomiting
  • diarrhea
  • abdominal pain
  • vaginal symptoms, such as leaking urine from the vagina, or leaking gas or feces into the vagina

Fistulas that do not respond to medications increase the risk of sepsis and may require emergency surgery.

Sepsis constitutes a medical emergency, and it can be fatal.

Symptoms of sepsis include:

  • signs of infection, including fever, fatigue, and pain
  • confusion
  • tiredness and fatigue
  • severe pain or discomfort

Intestinal obstruction

Share on PinterestSymptoms of intestinal obstruction can include nausea and vomiting.

An intestinal obstruction is the most common complication of Crohn’s disease.

An obstruction usually results when a buildup of scar tissue narrows a section of the colon, making it difficult for the stool to pass. Doctors call these narrowed passages “strictures.”

The medical community generally does not consider strictures to be life-threatening. However, the narrowing of the passage can lead to a tear, or perforation, in the colon.

A perforated colon can be life-threatening, so strictures and other forms of intestinal obstruction usually require immediate surgery.

Symptoms

Symptoms of an intestinal stricture include:

  • severe abdominal pain and cramping
  • nausea and vomiting
  • constipation
  • a bloated and distended abdomen
  • loud noises emanating from the gut

Perforated colon

Chronic inflammation, abscesses, fistulas, and strictures can weaken points in the intestinal wall.

Over time, the wall can tear, or perforate, allowing bacteria and other infectious substances to leak from the intestine into the abdomen. The medical term for this is peritonitis.

Peritonitis can cause more severe complications, such as blood poisoning and sepsis.

Symptoms

A perforated colon is a medical emergency. A person needs surgery to repair the hole in the intestine.

Symptoms of a perforated colon include:

  • severe abdominal pain
  • nausea
  • vomiting
  • chills
  • fever

Toxic megacolon

Toxic megacolon is a rare but life-threatening complication of IBD. Although it is more common among people with ulcerative colitis, it can also occur in people with Crohn’s disease.

Toxic megacolon occurs when inflammation causes the colon to expand to such an extent that it cannot contract. The result is a buildup of gas.

The buildup can cause the colon to burst, leaking harmful bacteria and toxins into the bloodstream.

This can lead to a range of life-threatening complications, including:

  • internal bleeding
  • sepsis
  • shock

Symptoms

Recognizing indications of toxic megacolon and receiving prompt treatment can reduce the risk of life-threatening complications.

Symptoms of toxic megacolon include:

  • swelling and pain in the abdomen
  • frequent or bloody diarrhea
  • dehydration
  • a rapid heart rate
  • fever

A Life Cut Short By Crohn’s

This article is part of a series of personal essays that explore death and disease from an outsider’s perspective. Some names have been changed to protect the privacy of the individuals involved.

I met Eddie during what my wife and I affectionately call my first senior year of college. Before we got married, she and I spent a year studying abroad in Asia. Because I’m a master of planning and foresight, I was completely unaware that the University of Virginia would accept precisely zero transfer credits from my school in Thailand, so it would take a fifth year for me to finish my degree.

I hadn’t made any living arrangements for my fifth year, so the university randomly assigned me three total strangers as roommates in an on-campus apartment. One was the progeny of Austrian Olympic athletes. Another was a metrosexual trailblazer.

Then there was sweet, sweet Eddie, who was mightily afflicted with Crohn’s disease.

He and I were to share a bathroom, and on day one, moments after introductory handshakes, Eddie made it known that his bathroom usage was frequent and time consumptive because his bowels were chronically inflamed.

I’d never even heard of Crohn’s, so I’ll admit that the prospect of sharing a toilet with him was unsettling, but the only alternative was to try and split the second bathroom with the Olympic spawn – who was partial to morning sex with his girlfriend in the shower – and a guy who had more hair products than we had counter space. So Eddie and I were stuck with one another.

The thing about Eddie, though, was that he was the sweetest guy imaginable, and sharing anything with him, bathroom or otherwise, was a privilege. He was so easy-going, so fun, so generous. If you needed a ride, he was your man. Whenever I was heartsick for my beloved, who was finishing school across the country, he was always there to make me laugh. Like that one time he came home from the mall with a framed pencil portrait of Mike Tyson and hung it up in our living room for all to enjoy. Or the times he would perform impromptu renditions of obscene hip-hop songs for our delight.

And he was loyal to a fault.

One weekend, a childhood friend of Eddie’s slept over. In the morning, I discovered the guy had inexplicably used my toothbrush. When I notified Eddie, he stalked out of the room to find his friend at the dining hall. He came back an hour later, bloody and beaten, with his similarly abused friend and a brand-new toothbrush in tow. Eddie was just that kind of a guy. He’d fight tooth and nail for your dental hygiene.

Crohn’s seemed to spell doom for his love life.

Eddie was a tenderhearted soul and fell passionately in love with a different girl every month. She’d usually let him take her out a couple of times, but once the unfortunate nature of his illness became apparent, she’d excuse herself from any further romance.

He never held it against them.

Eddie’s dating game was like an endless Merry-Go-Round of emotions. His tenacity was admirable, but the size of his heart was simply amazing.

After that year, I moved out of the apartment to live with my then-girlfriend, now-wife. Eddie helped me pack up and we swore to one another that we’d stay in touch. We promised to call and email and comment on one another’s Twitter posts. But as often happens, out of sight, out of mind.

Even though we lost touch, I thought of him often. I’d tell most everyone about the roommate who’d once gotten into fisticuffs over my toothbrush. We’d laugh, but it never occurred to me to investigate Eddie’s whereabouts any further until I realized one day that I hadn’t seen him post anything online in quite some time.

A quick Google search brought up an “In Memoriam” Facebook page.

Eddie had passed away from surgical complications while doctors tried to resection his small bowel. He’d suffered from malnutrition all his life, and the surgery was common and generally very safe.

He was just too frail.

There were a lot of posts on that Facebook page about how kind and generous he was, how he was the life of every party. Stories just like mine that seemed to run from his first moments alive to his last. It’s obvious he left a large hole in this world. I only hope someone thought to bring that Mike Tyson drawing to his funeral. Eddie would have loved that.

Crohn’s Disease

What is Crohn’s disease?

A hundred years ago, before Crohn’s disease had a name, doctors dismissed it as an untreatable illness or possibly a tumor. Doctors didn’t know that patients’ immune systems, the weapons for battling disease, were attacking their own digestive tracts.

In people with Crohn’s disease, tissues deep within the lining of the digestive system become inflamed. The inflammation usually starts in the colon or the lower part of the small intestine, but it can occur anywhere along the digestive tract, including the anus, stomach, esophagus, and even the mouth.

Crohn’s disease is very similar to another condition called ulcerative colitis — so similar that it’s not always possible to tell them apart. Both Crohn’s disease and ulcerative colitis are often called inflammatory bowel disease (IBD).

Although the cure for Crohn’s disease is still a mystery, the treatment isn’t. Today, with the right arsenal of defenses, patients with the disease are not only surviving, they’re thriving.

What are the symptoms of Crohn’s disease?

In the early stages, the most common symptoms of Crohn’s disease are frequent diarrhea, crampy abdominal pain, fever, and loss of appetite. Because the disease can cause internal bleeding, the stools may be black or tinged with blood. Children with Crohn’s disease may not have any gastrointestinal trouble at all. Instead, their main symptoms may be inflamed joints, fever, anemia, or slow growth.

Crohn’s disease tends to be an on-again, off-again malady. After a bout of symptoms, you may go for weeks, months, or even years without any more trouble. Unfortunately, there’s no way to predict when the symptoms will return.

What causes Crohn’s disease?

Nobody knows for sure, but Crohn’s disease seems to be caused by an overactive immune system. When viruses or bacteria invade the digestive tract, the body unleashes powerful antibodies to repel the attack. In people with Crohn’s disease, these antibodies may be missing the target and attacking the digestive system instead.

This theory received a major boost around the millenneum, when researchers announced the discovery of a faulty gene that may contribute to the disease. Normal versions of the gene help the intestines fight bacterial infections. A damaged version, however, can significantly raise the risk of Crohn’s disease. Since that discovery, even more genes have been identified as being associated with Crohn’s disease, bringing the number to more than thirty.

Contrary to common belief, emotional stress won’t cause Crohn’s disease (or, for that matter, ulcerative colitis). However, many patients say their symptoms tend to flare up during rough times in their lives.

Several other factors can help bring on attacks or worsen the symptoms of Crohn’s disease, including upper respiratory infections, use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), and cigarettes. Some patients find that alcohol, dairy products, spicy foods, and raw vegetables can also cause trouble.

Who is at risk for Crohn’s disease?

Crohn’s disease can strike people of any age, from toddlers to the elderly, but it most often arises in people in their 20s. It’s equally common in men and women. As you would expect from a disease linked to faulty genes, Crohn’s disease often runs in families. In fact, if one of your siblings has the disease, your risk increases more than 35-fold.

What are the possible complications?

Crohn’s disease is rarely fatal, but it can lead to complications that turn it into a serious health threat. For one thing, inflamed intestines can’t absorb water and nutrients as well as they should. If you aren’t careful, you can easily become severely dehydrated or shortchanged in proteins, potassium, calcium, and other vital nutrients. A shortage of nutrients can set off a cascade of other problems; for instance, a lack of calcium can make you especially vulnerable to osteoporosis.

If left untreated, the disease can inflict serious damage to your intestines and other organs. Often, the intestines become blocked by scar tissue, causing severe cramps and vomiting. The inflamed lining can become infected, causing pus-filled sores called abscesses. You may also develop sores that break through the intestinal wall and burrow into adjacent parts of the intestine or other tissues. This results in abnormal tunnels or “fistulas.” Some fistulas run all the way to the surface of the skin, especially around the anus.

If Crohn’s disease affects your colon, you have a greater-than-normal risk for colon cancer. The longer you’ve had Crohn’s disease, the greater the danger. Your doctor will want to perform regular colonoscopies or other exams to check for early signs of cancer.

Some people with Crohn’s disease also have other conditions related to an overactive immune system. When your gastrointestinal symptoms flare up, you may develop arthritis in your joints, inflammation in the whites of your eyes, mouth sores, and blue-red, pus-filled sores on the skin. Painful inflammation associated with Crohn’s disease can develop in other parts of your body, including your spine (ankylosing spondylitis), pelvic joints (sacroiliitis), eye (uveitis), or bile ducts (primary sclerosing cholangitis).

How is Crohn’s disease diagnosed?

If your doctor suspects Crohn’s disease, he or she may run blood tests to check for anemia (a possible sign of internal bleeding) or elevated white blood cells (a sign of inflammation). In order to confirm the diagnosis, your doctor will have to take a close look at your digestive system with either a barium x-ray or an endoscope. Barium tests are especially useful for tracking Crohn’s disease in the small intestine and upper digestive tract. If the condition seems to be affecting your colon, your doctor will probably want to conduct a colonoscopy (a medical procedure in which a tube with a light and a tiny camera is inserted into a patient’s colon to view the intestinal tract.)

How is Crohn’s disease treated?

It takes a team effort to control Crohn’s disease. Your doctor can prescribe medications to slow the disease and ease your symptoms, but you can do your part to stay healthy as well.

Treatment usually starts with with oral medications that control inflammation. If you have a mild to moderate case, sulfasalazine (Azulfidine) is a good first choice. If you’re allergic to sulfa drugs or experience side effects like headache and nausea, mesalamine (Pentasa) can be an effective substitute. The antibiotic metronidazole (Flagyl) is another option, especially if the disease affects your colon. Some patients have suffered side effects, including weakness or pain in their muscles, when they took metronidazole for more than a few weeks; let your doctor know if you experience these side effects.

If these drugs aren’t enough to control the disease, you may need powerful corticosteroids, such as prednisone. These drugs will make you feel better, but large doses can eventually cause joint damage, acne, mood swings, and other serious side effects. If your doctor prescribes a corticosteroid, he or she will probably start steadily lowering the dose as soon as your symptoms improve. The FDA has approved a steroid therapy, budesonide (Entocort EC) to ease the symptoms of mild to moderate cases of Crohn’s disease, though it, too, can produce side effects such as headache, respiratory infection and nausea.

The Food and Drug Administration has approved a class of drugs called biologics in the treatment of moderate to severe Crohn’s disease. Biologic drugs work by blocking a compound that causes inflammation. Infliximab (Remicade), manufactured by Centacor, is one of these drugs — and studies show that a single injection can improve symptoms in up to 82 percent of patients. However, Centacor, along with the FDA, has warned health professionals that some patients treated with Remicade have come down with tuberculosis and other serious opportunistic infections, including pneumocystosis.

According to the health warning, patients should be evaluated for tuberculosis with a skin test prior to Remicade treatment. Centocor, which has added a boxed warning to the product label, has also advised that Remicade should not be used by people with congestive heart failure. Remicade may also increase the risk for potentially fatal blood or nervous system disorders. If you’re taking Remicade and have any questions about the warnings, contact your health care provider, call the FDA consumer inquiry line (1-888-463-6332), or call Centocor (1-800-457-6399). You may want to ask your doctor to switch to a treatment with fewer serious side effects.

The FDA has also approved the drug certolizumab pegol (Cimzia) to treat adults with moderate to severe Crohn’s disease who haven’t responded to other therapies. Cimzia is given in an injection, and, like Remicade, may have potentially serious side effects, so will be monitored closely by your doctor.

Natalizumab (Tysabri), which is usually prescribed to treat advanced cases of multiple sclerosis, may now be used to treat Crohn’s in certain patients. If your doctor prescribes this drug for you, you must be enrolled in a risk minimization program to help prevent side effects.

In addition, adalimumab (Humira) is approved for the treatment of moderate to severe Crohn’s disease in adults whose condition hasn’t improved with standard therapies.

The most severe cases of Crohn’s disease can send a person to the hospital. If heavy diarrhea has left you malnourished and dehydrated, you may need intravenous fluids. If the medications no longer work, you may even need to have a section of your intestines or your rectum surgically removed, especially if you are losing large amounts of blood, if sores have broken through the intestinal wall, or if there’s a blockage. Unfortunately, surgery won’t cure Crohn’s disease. Over time, the inflammation usually comes back.

Are there therapies with fewer side effects?

Recently researchers have begun looking at using ginger nanoparticles to treat Crohn’s disease and ulcerative colitis. They created the nanoparticles from raw ginger bought at a local farmer’s market, mixed in a blender, and then put in a high-speed centrifuge. In mouse experiments, the ginger nanoparticles repaired the lining of the colon by helping the cells lining it to survive and proliferate, according to a study published in Biomaterials. This treatment is not on the market yet, but keep an eye out for it: Not only was it effective in mice, but it was non-toxic.

What can I do about Crohn’s disease?

Getting the right medical treatment is only part of the battle. You should also talk to your doctor about diet and other lifestyle changes that can speed your recovery. Many patients find their symptoms improve when they drink plenty of fluids, switch to a lower-fiber diet (this means taking the skin off fruit and vegetables and limiting your consumption of such foods as beans and wheat bran), avoid spicy food, and go easy on alcohol. With your doctor’s guidance, you may also need to take supplements of iron, vitamin B12, folic acid, or other vitamins and minerals to replace those lost to diarrhea. (Your doctor may have additional recommendations as well.)

Finally, you should take care of yourself. Be sure to eat nutritious meals, get plenty of rest, cut back on stress, and avoid cigarettes. This will not only help with Crohn’s disease, but improve your overall health as well.

Further Resources

Crohn’s & Colitis Foundation of America Inc.
386 Park Avenue South, 17th Floor
New York, NY 10016-8804
212-685-3440 or 800-932-2423
Fax: 212-779-4098
E-mail: [email protected]

This Web site is useful for families and patients with Crohn’s disease looking for information on medications, research, or clinical trials. It also features a director of doctors who treat the disease.

Ginger Nanoparticles May Help Treat Inflammatory Bowel Disease. Medical News Today, August 19, 2016. http://www.medicalnewstoday.com/articles/312440.php

Hanauer SB et al. Management of Crohn’s disease in adults. The American Journal of Gastroenterology. Vol. 96(3): 635-642.

National Digestive Diseases Information Clearinghouse. Crohn’s disease.

Merck Manual of Diagnosis and Therapy. Inflammatory Bowel Disease (IBD).

Food and Drug Administration. Facts about Crohn’s Disease. Consumer Health Information.

NIH News. Scientists Define 21 New Genes Associated with Crohn’s Disease.

Mayo Clinic. Crohn’s Disease.

Mortality in ulcerative colitis and Crohn’s disease. A population-based study in Finland

2.2 Statistical analysis

Mortality figures are updated annually and are based on the death certificates. Frequencies and medians (with ranges) were used to describe the patients and their follow-up time. Person years at risk were calculated at 5-year age and calendar intervals using the R environment (version 2.10.1, R Foundation for Statistical Computing, Vienna, Austria). Expected numbers of deaths were calculated using age, gender and calendar-year-specific mortality in the Finnish population, separately for CD and UC. Standardised mortality ratios (SMR) were calculated by dividing observed numbers of deaths by expected numbers. SMRs were accompanied by 95% confidence intervals assuming that the observed number of cases followed a Poisson distribution. They were calculated using CIA (Confidence Interval Analysis, version 2.1.2, University of Southampton, UK).

3 Results

3.1 Overall mortality

We observed 223 deaths among 1915 patients with IBD during the follow-up time: 151 with UC, 52 with CD and 20 with IBDU. The overall mortality in CD was increased (SMR 1.14, 95% CI (0.84–1.49)) while the overall mortality in UC was decreased (SMR 0.90, 95% CI.77–1.06) ( Table 2 .). The number of deaths among patients with IBDU was too small for meaningful statistical analysis.

3.2 Cause-specific mortality

Nine had died of colorectal cancer, 7 with UC and 2 with CD (SMR 1.8 and 1.88, respectively); the total number of colorectal cancer patients was 22. Nine patients had died of malignancies of the trachea or lung and four of malignancies of the liver or biliary tract (one cholangiocarcinoma).

In analysis of disorders of the digestive system (ICD-codes K00–K93, n = 20), the death rate was significantly increased in CD (SMR 5.8; primary cause of death in 4), and not significantly in ulcerative colitis (SMR 2.1; 2). Of the remaining 14 patients ( Table 2 ) six had alcoholic liver disease, three had died of acute vascular disorder of the intestine, one of gastric ulcer, one of ulcer in the oesophagus, one of Mallory–Weiss syndrome, one of volvulus and one of unspecified pancreatitis.

Compared to the background population, there were significantly fewer deaths due to disorders classified as mental and behavioural disorders due to use of alcohol (ICD-code F10) ( Table 2 ).

4 Discussion

Compared to the population in general, we found in Crohn’s disease an increased and in UC a decreased mortality rate, though the results did not reach statistical significance. Comparable results have been obtained in several other studies, 1 – 6 but also contrary results have been reported: Probert et al. reported that in Europeans the overall mortality was not increased. 17 In cause-specific mortality, an increased SMR for diseases of the digestive system was observed in our patients with CD. However, deaths due to colorectal cancer were not significantly increased in UC or CD. As a whole, the SMR for IBD in general and colorectal cancer in particular were both close to 1. Close follow-up and effective surveillance may explain this favourable result. In accordance, Solberg et al. 18 stated that the prognosis for CD seems better than previously reported, although they did not give any risk ratios for mortality.

A recent Finnish study reported that coronary heart disease was more common in IBD patients than in controls. 19 In the present series, the SMR for circulatory diseases did not differ significantly between patients with UC and CD; although those with UC are typically non-smokers, the SMR was marginally below 1 only in men with UC. The number of cases was probably too small to show any possible differences here.

An interesting finding was the significantly decreased mortality in disorders classified as mental and behavioural disorders due to use of alcohol, as we observed no such cases in our series. This category embraces acute drunkenness in alcoholism, harmful effects of alcohol and withdrawal state with delirium. We consider that this finding is valid, since same trend was seen in both UC and CD ( Table 2 ), and when combining both disorders, the 95% confidence intervals for SMR become 0–0.36. The majority of our patients had been under regular surveillance, which may explain the good social behaviour. However, since our follow-up mortality rates also comprised the few cases lost to follow-up, the selection bias in surveillance does not explain this finding. High alcohol intake has been associated with an increased risk of relapse. 20 , 21 This might be the case especially in countries where drinking habits involve high amounts of alcohol once in a while 22 as is the case in Finland. 23 , 24 The alcohol-related mortality in Finland is higher than in e.g. France, Sweden, United Kingdom, but lower than in Russia. 25 , 26 Patients with IBD possibly avoid heavy drinking if they have noticed an activation of the disease in such circumstances. Whether the alcohol consumption is lower in IBD than in the population in general is a subject for further studies, but on the other hand, our cases were not free of deaths due to alcohol liver disease.

Our data were based on a local register designed to catch all IBD patients in the area. We made meticulous efforts to enrol cases fulfilling the diagnostic criteria for IBD. The participating hospitals and health centres were contacted regularly to ensure registration of new patients. Diagnostic facilities including open access endoscopy were easily available throughout the study.

The IBD prevalence up to 1986 may be an underestimate as it was based on retrospectively scrutinised hospital records. Nevertheless, even prior to 1986, almost all symptomatic patients with IBD were treated in the same centres which participated in the prospective survey. For these reasons, it is evident that the series represented IBD in general, not only cases managed in tertiary centres. Even in the retrospective series, the date of diagnosis and possible death was as accurate as in the prospective series. Some patients with mild proctitis or distal IBD may have remained unregistered as having been treated exclusively in private care. The smaller endoscopy units in this study were in fact primary centres for detecting IBD. Thus, probably only a few cases could not be traced, which does not make any significant selection bias. In other words, we consider that this is population-based incident cohort.

Statistics Finland covers all the mortality causes in our country. The case records were scrutinised to ensure that there is no discrepancy between the records and death certificates. In some cases, the disease history before the death was not available. This may obviously make some bias, but it is also the case in the controls, that is in the general population.

To conclude, the overall mortality in IBD was not different from that in the population. In cause-specific mortality diseases of the digestive system were significantly increased in CD, though the number of cases remained relatively low. Deaths related to mental and behavioural disorders due to alcohol use were significantly less common in IBD than in the population. The risk of colorectal cancer was only non-significantly increased. As to the surveillance policy in IBD, we consider that patients with CD have a minor increased risk of mortality, especially in diseases of the digestive system, while patients with CU are not at increased risk of mortality when they are subject to regular follow-up.

Conflict of interests

The authors have no conflict of interests to declare. The authors alone are responsible for the content and writing of the manuscript.

Acknowledgements

All authors have made significant contributions to the research described in this manuscript. ALK founded and maintained IBD-register. PM carried out the study, collected and analysed the data and drafted the manuscript. HH carried out the statistical analysis. PC and ALK took part in the planning and designing of the study and revised the draft of the manuscript. MR, MS, LM and IP carried out the enrolment of patients and the collection of data. All authors read and approved the final manuscript. We acknowledge Robert McGilleon M.A., for revising the English language to the manuscript.

This study was financially supported by the Competitive Research Funding of the Pirkanmaa Hospital District, Finland (9M005 and 9H166). The sponsor did not have any involvement in study design, collection, analysis, interpretation, writing or submitting the manuscript.

1 Hoie O. Schouten L.J. Wolters F.L. Solberg I.C. Riis L. Mouzas I.A. et al. Ulcerative colitis: no rise in mortality in a European-wide population based cohort 10 years after diagnosis Gut 56 2007 497 – 503 2 Jess T. Gamborg M. Munkholm P. Sorensen T.I. Overall and cause-specific mortality in ulcerative colitis: meta-analysis of population-based inception cohort studies Am J Gastroenterol 102 2007 609 – 617 3 Jess T. Loftus E.V. Jr. Harmsen W.S. Zinsmeister A.R. Tremaine W.J. Melton L.J. III et al. Survival and cause-specific mortality in patients with inflammatory bowel disease: a long term outcome study in Olmsted County, Minnesota, 1940–2004 Gut 55 2006 1248 – 1254 4 Masala G. Bagnoli S. Ceroti M. Saieva C. Trallori G. Zanna I. et al. Divergent patterns of total and cancer mortality in ulcerative colitis and Crohn’s disease patients: the Florence IBD study 1978–2001 Gut 53 2004 1309 – 1313 5 Palli D. Trallori G. Saieva C. Tarantino O. Edili E. D’Albasio G. et al. General and cancer specific mortality of a population based cohort of patients with inflammatory bowel disease: the Florence Study Gut 42 1998 175 – 179 6 Viscido A. Bagnardi V. Sturniolo G.C. Annese V. Frieri G. D’Arienzo A. et al. Survival and causes of death in Italian patients with ulcerative colitis. A GISC nationwide study Dig Liver Dis 33 2001 686 – 692 7 Card T. Hubbard R. Logan R.F. Mortality in inflammatory bowel disease: a population-based cohort study Gastroenterology 125 2003 1583 – 1590 8 Duricova D. Pedersen N. Elkjaer M. Gamborg M. Munkholm P. Jess T. Overall and cause-specific mortality in Crohn’s disease: a meta-analysis of population-based studies Inflamm Bowel Dis 16 2010 347 – 353 9 Jess T. Winther K.V. Munkholm P. Langholz E. Binder V. Mortality and causes of death in Crohn’s disease: follow-up of a population-based cohort in Copenhagen County, Denmark Gastroenterology 122 2002 1808 – 1814 10 Persson P.G. Bernell O. Leijonmarck C.E. Farahmand B.Y. Hellers G. Ahlbom A. Survival and cause-specific mortality in inflammatory bowel disease: a population-based cohort study Gastroenterology 110 1996 1339 – 1345 11 Wolters F.L. Russel M.G. Sijbrandij J. Schouten L.J. Odes S. Riis L. et al. Crohn’s disease: increased mortality 10 years after diagnosis in a Europe-wide population based cohort Gut 55 2006 510 – 518 12 Manninen P. Karvonen A.L. Huhtala H. Rasmussen M. Collin P. The epidemiology of inflammatory bowel diseases in Finland Scand J Gastroenterol 45 2010 1063 – 1067 13 Lennard-Jones J.E. Classification of inflammatory bowel disease Scand J Gastroenterol Suppl 170 1989 2 – 6 14 Stange E.F. Travis S.P. Vermeire S. Reinisch W. Geboes K. Barakauskiene A. et al. European evidence-based consensus on the diagnosis and management of ulcerative colitis: definitions and diagnosis J Crohns Colitis 2 2008 1 – 23 15 Stange E.F. Travis S.P. Vermeire S. Beglinger C. Kupcinkas L. Geboes K. et al. European evidence based consensus on the diagnosis and management of Crohn’s disease: definitions and diagnosis Gut 55 Suppl. 1 2006 1 – 15 16 Geboes K. Van Eyken P. Inflammatory bowel disease unclassified and indeterminate colitis: the role of the pathologist J Clin Pathol 62 2009 201 – 205 17 Probert C.S. Jayanthi V. Wicks A.C. Mayberry J.F. Mortality from Crohn’s disease in Leicestershire, 1972–1989: an epidemiological community based study Gut 33 1992 1226 – 1228 18 Solberg I.C. Vatn M.H. Hoie O. Stray N. Sauar J. Jahnsen J. et al. Clinical course in Crohn’s disese: results of a Norwegian population-based ten-year follow-up study Clin Gastroenterol Hepatol 5 2007 1430 – 1438 19 Haapamaki J. Roine R.P. Turunen U. Farkkila M.A. Arkkila P.E. Increased risk for coronary heart disease, asthma and connective tissue diseases in inflammatory bowel diseases J Crohns Colitis 5 2011 41 – 47 20 Hey H. Schmedes A. Nielsen A.A. Winding P. Gronbaek H. Effects of five different alcoholic drinks on patients with Crohn’s disease Scand J Gastroenterol 42 2007 968 – 972 21 Jowett S.L. Seal C.J. Pearce M.S. Phillips E. Gregory W. Barton J.R. et al. Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study Gut 53 2004 1479 – 1484 22 Bjarnason I. Alcohol: a friend or foe of IBD Scand J Gastroenterol 42 2007 899 – 901 23 Helasoja V. Lahelma E. Prattala R. Petkeviciene J. Pudule I. Tekkel M. The sociodemographic patterning of drinking and binge drinking in Estonia, Latvia, Lithuania and Finland, 1994–2002 BMC Public Health 7 2007 241 24 Parna K. Rahu K. Helakorpi S. Tekkel M. Alcohol consumption in Estonia and Finland: Finbalt survey 1994–2006 BMC Public Health 10 2010 261 25 Herttua K. Makela P. Martikainen P. Changes in alcohol-related mortality and its sosio-economic differences after a large reduction in alcohol prices: a natural experiment based on register data Am J Epidemiol 168 2008 1110 – 1118 26 Rehm J. Sulkowska U. Manczuk M. Boffetta P. Powles J. Popova S. et al. Alcohol accounts for a high proportion of premature mortality in central and eastern Europe Int J Epidemiol 36 2007 458 – 467

Tables

Table 1

Characteristics of patients with inflammatory bowel disease.

Table 1

Characteristics of patients with inflammatory bowel disease.

Table 2 a

Cases with inflammatory bowel disease unclassified n = 20, 10 deaths of diseases of the circulatory system, 4 of diseases of the digestive system, 2 malignant neoplasms, 1 neurological disorder and 1 accidental death.

Table 2 a

Cases with inflammatory bowel disease unclassified n = 20, 10 deaths of diseases of the circulatory system, 4 of diseases of the digestive system, 2 malignant neoplasms, 1 neurological disorder and 1 accidental death.

Author notes

☆ Preliminary results from this study were presented as poster at XLI Nordic meeting of gastroenterology 2010 in Copenhagen (abstract published in Scand J Gastro 2010; 45, Suppl 247: 48–49). © 2011 European Crohn’s and Colitis Organisation

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