What Is Lymphocytic Colitis?
Lymphocytic colitis is a microscopic inflammation of the large intestinal mucosa with infiltration of lymphocytes (IELs) that is characterized by secretory diarrhea.
Secretory diarrhea describes bowel movements that consist of a large volume of liquid stool.
Q: What are IELs?
A: IELs is an abbreviation for intraepithelial lymphocytes, which are white blood cells that infiltrate within epithelial cells or between them. Epithelial cells form the surface mucosa of the large intestine also called the colon.
The histopathological criteria (biopsy) for lymphocytic colitis are a density of at least 20 IELs per 100 surface epithelial cells; chronic inflammatory infiltrate of mononuclear cells in the lamina propria; epithelial damage; and a subepithelial collagen layer of less than 10 µm. The increased collagen band consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin.1That is, the mucosa is reacting to some irritative substance.
Up to 10% of adults undergoing colonoscopy for investigation of chronic diarrhea and having visibily normal appearing mucosa may have lymphocytic colitis.2
Bile acid malabsorption has been shown to coexist in 60% of patients with lymphocytic colitis.3
What Is Lymphocytic Colitis In Celiac Disease and/or Gluten Sensitivity?
IMG_1010a sigmoid normalRelationship between lymphocytic colitis and celiac disease. Lymphocytic colitis is a complication of celiac disease.
Relationship between lymphocytic colitis and lactose intolerance. Intolerance to lactose is a common condition in lymphocytic colitis. It has been found to affect 54% of adult patients with lymphocytic colitis4 and 80% of children.5
Lactose is a double molecule sugar composed of the two simple sugars galactose and glucose that must be digested by lactase. Lactase is the specific enzyme normally produced in the tips of small intestinal villi that digest lactose which otherwise cannot be digested. Damage to the villi caused by gluten destroys the cells that produce lactase, and this in turn ruins the body’s ability to digest milk sugar, causing the condition known as lactose intolerance.
Relationship between lactose and celiac disease. Lactose itself causes leaky gut which adds to the altering effect of gluten on the small intestinal barrier.
How Prevalent Is Lymphocytic Colitis In Celiac Disease and/or Gluten Sensitivity?
Celiac disease is common in lymphocytic colitis, occurring in 14.8% of patients with lymphocytic colitis.6
What Are The Symptoms Of Lymphocytic Colitis?
Lymphocytic colitis is marked by non-bloody diarrhea, with or without cramping, bloating, weight loss, and lactose intolerance.7
How Does Lymphocytic Colitis Develop In Celiac Disease and/or Gluten Sensitivity?
Lymphocytic colitis results from an unclear mechanism.8
Omega-3 fatty acid and vitamin A deficiencies may exacerbate lymphocytic colitis.9
Does Lymphocytic Colitis Respond To Gluten-Free Diet?
Yes. Celiac disease-related diarrhea in lymphocytic colitis improves on gluten free diet along with the avoidance of dairy products such as cow’s milk and cheese and/or the use of lactase enzyme, which breaks down the naturally ocurring lactose sugar in milk associated with lymphocytic colitis.
6 Steps To Improve Lymphocytic Colitis In Celiac Disease and/or Gluten Sensitivity:
1Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:
Treatment. This condition responds to the complete elimination of gluten, which is the required treatment that improves both lymphocytic colitis and gut health.
Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.
Correct Your Individual Nutritional Needs.
Eat foods that can replenish missing nutrients. Find them under NUTRIENT DEFICIENCIES.
Take nutritional supplements as needed. Find them under NUTRIENT DEFICIENCIES.
Recovery. You should begin to feel better within a week and notice more energy as inflammation subsides and the absorbing cells that make up the surface lining of your small intestine are better able to function.
Intestinal lining cells are replaced every 5 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.
Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.10
The intestinal lining may take up to a year to heal.
2 Reduce Inflammation. Foods to Eat and Foods Not to Eat:
Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).
Here Are Major Inflammatory Food Types That Reduce Healing:
Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.11
Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.12
Fats. Limit deep fried foods, trans-fats, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.13.
Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.14
Refined Sugars. Includes white sugar, corn fructose and high fructose corn syrup.
Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.15
Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.16
Here Are Important Anti-Inflammatory Food Types to Promote Health:
Fruits. Contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.
Non-Starchy Vegetables. Support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals. Includes green leafy vegetables such as lettuce and kale, also onion, broccoli, garlic, and others.
High Quality Complex Carbohydrates. Provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. Includes whole grains, legumes, and root vegetables such as carrots, parsnips, sweet potatoes, turnips, red beets, and others.
Antioxidants. Protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.
Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
Probiotics. Supply normal microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.
Prebiotics/ High Fiber Foods. Food with fiber keeps our population of colonic microbes healthy.
Protective Herbs and Spices. See below #6 below for examples.
3 Information Sheet You Can Take to Your Doctor or Other Health Professional:
Click here.
4 Manage Your Medications Safely:
Certain medications deplete vitamin A that may exacerbate lymphocytic colitis. Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.
This is not a complete listing.
WEIGHT LOSS DRUGS THAT BIND FAT also interfere with absorption of some nutrients.
Zenicol (Orlistat®) depletes Vitamin A.
ANTACIDS / ULCER MEDICATIONS
Pepcid®, Tagamet®, Zantac® deplete Vitamin A.
Magnesium and Aluminum Antacid preparations (Gaviscon®, Maalox®, Mylanta®) deplete Vitamin A.
CHOLESTEROL DRUGS
Colestid® and Questran® deplete Vitamin A.
5Nutritional Supplements To Help Correct Deficiencies:
The type and quantity of nutritional supplements that may be needed depend on which nutrients are deficient.
Multivitamin/mineral combination once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.
Vitamin A as retinyl palmitate as prescribed following blood test for vitamin A status. Please be sure the supplement is NOT retinyl acetate which should be avoided because it is can be synthetically derived from toxic benzene.17
Storage Note: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet – not in the bathroom or on the kitchen table.
6Manage Natural Remedies:
Hydration:
Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water — from all beverages and foods each day for women and 3.7 liters (125 ounces daily) of total water for men.
If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.
Carminitives. The following anti-inflammatory plant sources called carminitives help heal the digestive tract. They also tone the digestive muscles which improves peristalsis, thus aiding in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort.
Carminitive Food Remedies:
Raspberry.
Carrot is also a cleansing digestive tonic.
Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
Redbeets also stimulate and improve digestion and are easily digested.
Cabbage also stimulates and improves digestion and is also a liver decongestant.
Lettuce also stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.
Carminitive Herb Remedies:
Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa. Drink as tea or use in cooking.
Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.
Parsley also relieves indigestion.
Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion.
Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.
Carminitive Spice Remedies:
Cloves are also antispasmodic.
Nutmeg is also useful for indigestion.
Ginger.
Exercise Helps: Exercise improves circulation and rids the body of toxins.
Walking is aerobic exercise that reconditions the whole body to improve stamina. Read more about Exercise and Fitness.
Weight training builds muscle. Read more about Exercise and Fitness.
Stretching improves flexibilty. Read more about Exercise and Fitness.
Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal.
What Do Medical Research Studies Tell About Lymphocytic Colitis In Celiac Disease and/or Gluten Sensitivity?
“Association of lymphocytic colitis and lactase deficiency in pediatric population.“ This study investigating the occurrence of lymphocytic colitis in children found that a large of portion of the patients had associated lactase deficiency and improved on Lactaid supplement alone or avoidance of dairy products.
Ten cases each of lymphocytic colitis and of colonic lymphocytosis of other diagnosis, all with duodenal disaccharidases [double sugar molecule] analysis data, were collected from the files of the researchers’ institution. The electronic medical records were reviewed and multiple variables were analyzed. The ten patients with lymphocytic colitis presented with diarrhea. Of these, three had abdominal pain. The age range was 2-18 years. Nearly all patients were Caucasian (90%) and 70% were female. Endoscopically, most had normal appearing colonic mucosa.
Significant past medical history, family medical history and associated comorbidities included celiac disease, Down syndrome, juvenile arthritis and other autoimmune diseases. Interestingly, the most revealing observation was that the majority of cases (80%) were associated with lactase deficiency and, for the most part, gastrointestinal symptoms improved simply by treatment with Lactaid or avoidance of dairy products. This association is statistically significant.18
“Clinical characteristics of collagenous and lymphocytic colitis.” This study investigating the clinical features of collagenous colitis and lymphocytic colitis demonstrated collagenous colitis and lymphocytic colitis are largely similar but the differences in the occurrence of autoimmune conditions and bronchial asthma in collagenous colitis suggest that they differ in immunopathogenesis. Hypolactasia (lactose intolerance) is common, affecting 54% of patients with lymphocytic colitis.19
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. ↩
Abdo AA, Urbanski SJ, Beck PL. Lymphotcytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. Canadian Journal of Gastroenterology. Jul 2003;17(7):425-32. ↩
Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. ↩
Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. ↩
Sun J, Lin J, Parashette K, Zhang J, Fan R. Association of lymphocytic colitis and lactase deficiency in pediatric population. Pathol Res Pract. 2014 Nov 25. pii: S0344-0338(14)00340-9. doi: 10.1016/j.prp.2014.11.009. ↩
Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. ↩
Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. ↩
Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. ↩
Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition & Diet Therapy, 10th Edition. Philadelphia, PA. USA: W.B. Saunders Company, 2000. ↩
Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease. Clinical Science. Apr 2001;100(4):379-86. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. ↩
http://www.bt.cdc.gov/agent/benzene/basics/facts.asp ↩
Sun J, Lin J, Parashette K, Zhang J, Fan R. Association of lymphocytic colitis and lactase deficiency in pediatric population. Pathol Res Pract. 2014 Nov 25. pii: S0344-0338(14)00340-9. doi: 10.1016/j.prp.2014.11.009. ↩
Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. ↩
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Tex, what do you think of this article?
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Tex, what do you think of this article?
MC diagnosed 2007
Could you post a link to the article? That's such a disorganized list of questions and comments that it takes way too much time to try to read it and make any sense out of it. It looks more like a random assortment of search items than an article.
IOW, my initial impression is not good.
Tex
IOW, my initial impression is not good.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Sorry about that. I don't know if the link will work because I have a paid subscription, but here it is.
http://glutenfreeworks.com/health/lymphocytic-colitis/
http://glutenfreeworks.com/health/lymphocytic-colitis/
MC diagnosed 2007
My impression is that it's written by someone with a medical background who doesn't really understand the disease but they collected random bits and pieces from various references and then tried to organize them into an article of sorts. Of course that's how many "studies" that reexamine medical research articles are written. While the descriptions and terminology used are not really technically incorrect, many of them are not exactly appropriate, either. For example the statement about diagnostic criteria refers to "surface epithelial cells". True, they are epithelial cells, but they are more correctly referred to as enterocytes. Enterocytes are special, vertically elongated cells bordered by the tight junctions that determine intestinal permeability.
The second sentence says, "Secretory diarrhea describes bowel movements that consist of a large volume of liquid stool." Well that's certainly true, but it doesn't medically describe secretory diarrhea. Secretory diarrhea is the result of the infusion of large volumes of water and electrolytes into the colon — exactly the opposite of the normal function of the colon (normally the colon removes water and electrolytes from the fecal stream). If the author is going to use such a simplified (non-medical) description of the primary mechanism that causes the main symptom that identifies LC (watery diarrhea), why use all the medical/technical terms everywhere else?
This sentence, "The increased collagen band consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin.", suggests that the author is confusing CC with LC, because there is no increase in collagen band thickness with LC. And specifically listing collagen types is of no value to the average reader, or to anyone else for that matter, except possibly a few pathologists, but I doubt that any pathologists will ever read that article.
Which brings me back to my first impression — the author doesn't actually understand the disease, but was assigned to write an article, or felt obligated to write an article.
That said, the chances are good that most people, including many GI specialists, probably would never notice the issues that I pointed out, so most people would probably view it as an OK article. Much better current information is available free of charge. For example:
http://www.drfalkpharma.com/uploads/tx_ ... SK183e.pdf
Tex
The second sentence says, "Secretory diarrhea describes bowel movements that consist of a large volume of liquid stool." Well that's certainly true, but it doesn't medically describe secretory diarrhea. Secretory diarrhea is the result of the infusion of large volumes of water and electrolytes into the colon — exactly the opposite of the normal function of the colon (normally the colon removes water and electrolytes from the fecal stream). If the author is going to use such a simplified (non-medical) description of the primary mechanism that causes the main symptom that identifies LC (watery diarrhea), why use all the medical/technical terms everywhere else?
This sentence, "The increased collagen band consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin.", suggests that the author is confusing CC with LC, because there is no increase in collagen band thickness with LC. And specifically listing collagen types is of no value to the average reader, or to anyone else for that matter, except possibly a few pathologists, but I doubt that any pathologists will ever read that article.
Which brings me back to my first impression — the author doesn't actually understand the disease, but was assigned to write an article, or felt obligated to write an article.
That said, the chances are good that most people, including many GI specialists, probably would never notice the issues that I pointed out, so most people would probably view it as an OK article. Much better current information is available free of charge. For example:
http://www.drfalkpharma.com/uploads/tx_ ... SK183e.pdf
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Glutenfreeworks response to my concern
From: Cleo Libonati [mailto:cleo.libonati@glutenfreeworks.com]
Sent: Wednesday, August 17, 2016 4:49 PM
To: customerservice@glutenfreeworks.com
Subject:
I looked over the material and find it accurate. You should send her the paper below for her sake.
Therap Adv Gastroenterol. 2015 Jan; 8(1): 37–47.
doi: 10.1177/1756283X14550134
PMCID: PMC4265085
New insights and challenges in microscopic colitis
Bodil Ohlssoncorresponding author
Author information ► Copyright and License information ►
Go to:
Introduction
Chronic diarrhea is reported in 4–5% of individuals and makes up a considerable proportion of the consultations in gastroenterology [Thomas et al. 2003]. Diarrhea has for a long time been considered as functional after exclusion of celiac disease, inflammatory bowel disease (IBD), malignancy and so on [Drossman et al. 2006]. Over recent decades, microscopic colitis (MC) has emerged as a common cause of diarrhea, especially in middle-aged or older women, and the disease is regarded as a subgroup within IBD [Münch et al. 2012]. The disease is characterized by chronic, watery diarrhea and normal or close to normal findings by endoscopic examination. Intestinal, mucosal biopsies show characteristic histopathological changes [Robert, 2004; Thijs et al. 2005; Temmerman and Baert, 2009]. Although as many as 63% of patients only have a single attack of the disease [Olesen et al. 2004a], the patients who have received the diagnosis are considered to be suffering from a chronic disease. MC can be considered a primary lymphocytic disorder of the gut, whereas many other disorders may be associated with lymphocytic infiltration or collagenous deposition, in which cases MC could be considered a secondary disorder [Carmack et al. 2009].
Histopathology
In 1976, Lindström described microscopic inflammatory changes in colon with a remarkable subepithelial collagen band and called the condition collagenous colitis (CC) [Lindström, 1976]. Read and colleagues introduced the term microscopic colitis [Read et al. 1980]. In 1989, Lanzeby and colleagues showed that an increased number of colonic intraepithelial lymphocytes (IELs) was the most characteristic feature of MC and suggested the term lymphocytic colitis (LC) [Lazenby et al. 1989]. The diagnosis of MC is based on histopathological examination of mucosal biopsies from the colon, obtained through endoscopy [Robert, 2004; Thijs et al. 2005; Temmerman and Baert, 2009], in combination with nonbloody diarrhea [Olesen et al. 2004a; Pardi and Kelly, 2011]. The histopathological criteria for CC are a thickened subepithelial collagen layer of at least 10 µm (reference value: 2–7 µm); inflammation in the lamina propria with increased numbers of lymphocytes and plasma cells; epithelial damage; and increased numbers of IELs may be present. The histopathological criteria for LC are a density of at least 20 IELs per 100 surface epithelial cells; chronic inflammatory infiltrate of mononuclear cells in the lamina propria; epithelial damage; and a subepithelial collagen layer of less than 10 µm. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in MC consists basically of collagen type I and III [Flejou et al. 1984], which are the subtypes produced by repair functions, indicating a reactive origin [Braskén, 1991]. The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region [Jessurun et al. 1987; Wang et al. 1988; Carpenter et al. 1992; Fernandez-Banares et al. 1999].
Recently, Carmack and colleagues have introduced the terms primary and secondary lymphocytic disorders of the gastrointestinal tract [Carmack et al. 2009]. Infiltration of lymphocytes in the lamina propria is unspecific and can be observed in all segments of the gastrointestinal tract. A common cause of lymphocyte infiltration in the stomach is infection by Helicobacter pylori, whereas celiac disease may cause MC throughout the gastrointestinal tract [Carmack et al. 2009]. Autoimmune diseases, bacterial and viral enteritis, and drugs are other etiologies of secondary LC [Carmack et al. 2009]. Seasonal fluctuations in the histopathology have been identified and suggest an allergic origin of MC in some circumstances [LaSala et al. 2005]. Surgical traction per se may lead to invasion of lymphocytes into the tissue [Lee et al. 2009].
CC-like findings have been reported in patients suffering from colon cancer, carcinoid lesions, adenomas and hyperplastic polyps, bacterial infections, lactose intolerance, and constipation [Flejou et al. 1984; Teglbjaerget al. 1984; Nussinson et al. 1988; Wang et al. 1988; Gubbins et al. 1991; Leigh et al. 1993]. Both CC and LC are described in ulcerative colitis and Crohn’s disease, together with the characteristics of these diseases [Goldblum and Wang, 2000]. MC in this context should be considered as a part of the original IBD disease, and not as a separate entity [Jegadeesan et al. 2013]. Furthermore, these changes can also be found in persons without any signs of gastrointestinal symptoms or diseases [Wang et al. 1988; Thörn et al. 2013]. Altogether, there is no histopathological hallmark that differentiates primary, idiopathic MC from a MC evolved secondary to another syndrome or its treatment, or that differentiate MC in healthy subjects from patients with symptoms.
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Epidemiology
Population studies have shown an increasing incidence of MC over recent decades, with a mean incidence rate of 1.1–7.0/100,000 inhabitants for CC and an incidence rate of 3.1–5.5/100,000 inhabitants for LC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Pardi et al. 2007; Vigren et al. 2012; Thörn et al. 2013]. The increased incidence has stabilized over the past years, and the incidence is associated with female gender and increasing age [Gentile et al. 2014]. Reports indicate that MC is more frequent in colder, northern countries than in southern countries [Pardi et al. 2007; Fernandez-Banares et al. 2011; Gentile et al. 2014]. This north–south gradient has led to speculations that vitamin D is involved in the pathogenesis, but this has not been confirmed [Sjöberg et al. 2013]. The female-to-male ratio ranges from 2.8:1 to 7.5:1 for CC and from 2.1:1 to 2.7:1 for LC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Vigren et al. 2012], whereas in a later review, the ratio was 3.0–9.0:1 for CC and 6.0:1 to no difference in LC [Pardi and Kelly, 2011]. The average age at diagnosis is approximately 65 years [Münch et al. 2012].
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Etiology and pathophysiology in MC
The etiology is in most cases unknown, and is probably multifactorial, also when only primary MC is included, as the terminology constitutes a morphological, descriptive term, representing many different entities, presenting with an inflammation in the mucosa.
Genetic predisposition
Only a limited number of familial MC cases have been reported [Abdo et al. 2001; Järnerot et al. 2001], but as many as 12% of patients with MC have a family history of IBD [Olesen et al. 2004a]. There is an association between the expression of MC and HLA-DQ, and patients with MC have a high prevalence of tumor necrosis factor α and metalloproteinase-9 gene polymorphisms [Fernandez-Banares et al. 2005;Koskela et al. 2008; Madisch et al. 2011].
Hormonal factors
Endocrine factors have been discussed since most studies report a female predominance of MC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Vigren et al. 2012]. The intestinal epithelium provides a protective barrier for the internal milieu against luminal factors, which is dependent on intercellular, epithelial tight junctions [Turner, 2006]. Increased paracellular permeability has been implicated in the pathogenesis of chronic, mucosal inflammation [Meddings, 1997; Teshima et al. 2012]. Estrogens and progesterone have been shown to exhibit anti-inflammatory and epithelial barrier-enhancing properties in experimentally induced colitis in rats [Günal et al. 2003; Karatepe et al. 2012; Moussa et al. 2012], and the fall in hormone levels at menopause could theoretically explain the peak age of debut of MC in middle-aged women [Pardi and Kelly, 2011]. However, no differences in reproductive factors between CC and LC, or between patients with MC or healthy controls, could be identified [Roth et al. 2013c].
Autoimmunity and comorbidity
The association of MC with various autoimmune diseases such as celiac disease, thyroid disease, rheumatoid arthritis, and diabetes mellitus has given rise to the hypothesis that MC is an autoimmune disease [Pardi et al. 2002; Olesen et al. 2004a]. The predominance of middle-aged female patients further strengthens the autoimmune hypothesis, although no specific autoantibody has been identified [Pardi and Kelly, 2011]. Several small studies have proposed an increased prevalence of antinuclear antibody, antigliadin IgA, and anti-Saccharomyces cerevisiae antibodies in serum in patients with MC [Holstein et al. 2006]. Scrutinizing a greater cohort of patients with MC with 11 different autoantibodies did not show any increased prevalence of autoantibodies in patients with MC compared with healthy controls [Roth and Ohlsson, 2013; Roth et al. 2013b; Gustafsson et al. 2013]. Recent research suggests an increased morbidity in a wide range of chronic diseases in patients with MC, irrespective of autoimmunity, including ischemic cardiovascular diseases, hypertension, asthma, and allergy [Roth et al. 2013d].
Smoking and alcohol habits
Smoking has been confirmed to be associated with MC [Yen et al. 2012; Vigren et al. 2011], and smokers contract MC 10 years earlier than nonsmokers [Vigren et al. 2011]. Accordingly, lung cancer is associated with MC [Chan et al. 1999]. Current MC and MC in combination with abdominal pain were associated with smoking, whereas transient MC was associated with past smoking, and pure MC without abdominal pain was not associated with smoking [Roth et al. 2013a, 2014].
In one study, alcohol consumption was higher in patients with MC compared with healthy controls [Yen et al. 2012]. Nevertheless, wine drinking did not tend to increase the risk of developing MC. Rather, wine drinking seemed to provide protection against the development of MC in smokers [Roth et al. 2014].
Luminal factors
The histological changes in MC are resolved by diverting the fecal stream by ileostomy, supporting the hypothesis of the role of luminal factors [Jarnerot et al. 1995], but the effect of food has been only rudimentarily studied.
Several drugs have been associated with the development of MC as causative or triggering agents [Olesen et al. 2004a]; the most common being nonsteroidal anti-inflammatory drugs (NSAIDs), proton-pump inhibitors (PPIs), and antidepressant or antipsychotic drugs [Chassany et al. 2000; Beaugerie and Pardi, 2005;Fernandez-Banarnes et al. 2007]. The pathophysiology can be explained by altered intestinal flora, a direct pharmacological effect on the colon, or an idiosyncratic hypersensitivity reaction [Münch et al. 2012]. A chronological connection must be established between the introduction of the drug and the histopathological changes in combination with symptoms, and improvement or disappearance of the diarrhea and restored histological picture when the treatment is ceased [Beaugerie and Pardi, 2005].
There is growing evidence for involvement of gut microbiota in the development of IBD [Wagner, 2008;Shim, 2013], but its effect on the development of MC has not been adequately studied. Bacterial and viral gastroenteritis may induce MC [Makinen et al. 1998; Perk et al. 1999; Erim et al. 2003]. Bile acid malabsorption has been shown to coexist in 60% of patients with LC and in 44% of patients with CC [Ung et al. 2000; Fernandez-Banares et al. 2001]. It remains to be determined whether bile acid malabsorption is causative or secondary.
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Clinical presentation
The clinical features of MC are described and defined as chronic, relapsing, nonbloody, watery diarrhea [Olesen et al. 2004a; Pardi and Kelly, 2011]. The diarrhea may be mild, but severe, frequent diarrhea with urgency is common [Bohr et al.1996]. Nevertheless, some patients with histopathological features of MC are asymptomatic [Wang et al. 1988; Gubbins et al. 1991; Thörn et al. 2013]. About 50% of patients with diagnosed MC fulfill the criteria for irritable bowel syndrome (IBS) [Roth and Ohlsson, 2013]. These patients have abdominal pain, and some patients also have constipation. In fact, all gastrointestinal symptoms are accentuated in patients with MC compared with healthy controls [Roth and Ohlsson, 2013]. The clinical aspects of CC and LC are indistinguishable [Rasmussen and Munck, 2012; Roth and Ohlsson, 2013]. The onset is often insidious, but 25–40% of the patients have a sudden onset [Bohr et al. 1996; Olesen et al. 2004a]. The majority of patients have only a single attack of the disease with spontaneous remission in about 10% [Gubbins et al. 1991; Olesen et al. 2004a; Roth et al. 2013a; Thörn et al. 2013], and the patients are in symptomatic remission after 3–4 years [Bonner et al. 2000]. Thirty percent of patients with MC have a chronic intermittent disease, and only 7% have a chronic, continuous course which may be refractory to treatment [Järnerot et al. 1995; Olesen et al. 2004a].
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Diagnosis and treatment
First, it is mandatory to exclude inflammation secondary to another gastrointestinal disease, drug treatment or infection [Carmack et al. 2009]. When secondary MC is the case, the MC must be regarded as a part of the original disease, and the original disease or condition must be treated. Withdrawal of toxic agents and drugs is mandatory when MC was evolved after such administration [Fernandez-Banares et al. 2007]. As many of these patients are past or current smokers, and older, intestinal ischemia must be considered [Roth et al. 2014]. Smoking abstinence should be encouraged, as past smoking is associated with transient, and not persistent, MC [Roth et al. 2014]. After exclusion of secondary MC, the diagnosis of true, primary MC can be set [Pardi and Kelly, 2011].
The primary aim in the treatment of MC is to achieve clinical remission and improve the patient’s quality of life [Hjortswang et al. 2009]. The secondary aim is maintenance of clinical remission [Ianiro et al. 2012].
As most patients complain of diarrhea, traditional antidiarrheal agents such as loperamide are frequently used as first-line therapy [Pardi et al. 2002; Olesen et al. 2004a]. Budesonide is the only drug which has been proved to be efficient by randomized, placebo-controlled trials, and it is to date the standard treatment for moderate to severe MC [Münch et al. 2012; Storr, 2013]. Budesonide therapy resulted in a significant improvement in both clinical symptoms and histological inflammatory changes, but the relapse frequency is about 61–80% [Baert et al. 2002; Bonderup et al. 2003; Bonderup et al. 2009; Mielke et al. 2005; Miehlke et al. 2009]. The relapse frequency is reduced by sustained treatment at low dosage [Stewart et al. 2011]. Budesonide has the advantage over corticosteroids due to the high, hepatic first-pass elimination, thus avoiding the side effects of steroids [Stewart et al. 2011], and the efficacy of budesonide is superior to prednisolone, although no comparative studies are available [Munck et al. 2003].
Treatment with bile acid bindings is efficient to diminish the symptoms, but has no effect on the histopathological changes [Ung et al. 2001]. Bismuth subsalicylate was effective in MC in a small, randomized, placebo-controlled trial [Fine and Lee, 1998]. Aminosalicylates have, in uncontrolled or retrospective studies, had a moderate to good effect in MC [Pardi et al. 2002; Chande et al. 2008]. The experience of other immunosuppressive therapies are gathered in some systematic reviews, based on retrospective studies and case reports [Riddell et al. 2007; Münch et al. 2012]. In severe, refractory cases, these therapies or surgical intervention may be appropriate to test [Järnerot et al. 1995].
Treatment strategy of MC
Cessation of possible offending irritants or medications.
Antidiarrheal drugs.
Budesonide.
Cholestyramine, immunomodulating drugs, or ileostomy and colectomy.
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Discussion
Over the past century, the population, especially women, have changed their life habits and lifestyle substantially. A microscopic inflammation in the colonic mucosa may hypothetically be the reaction to all the irritants the colon is exposed to in daily life. The barrier function of the gut epithelium may be diminished in the course of a lifetime, due to fall in estrogen levels around the menopause and changes in microbiota diversity [Günal et al. 2003; Karatepe et al. 2012; Moussa et al. 2012; Patten and Collett, 2013; Kamada et al. 2013], facilitating the penetration of irritants into the mucosa. The greater prevalence of MC findings in the ascending than descending colon suggests an important role for luminal factors [Jessurun et al. 1987;Carpenter et al. 1992]. Thus, the increased incidence of MC with increasing age could represent a normal ageing process [Gentile et al. 2014].
Surgical traction of the tissue is enough for lymphocyte invasion [Lee et al. 2009]. During colonoscopy, the bowel is cleaned by laxatives and biopsies are taken at the end of the examination, after traction of the bowel. Biopsy-taking at the start of the examination should perhaps be more appropriate and reduce the incidence of LC. The nature of the collagen layer in CC has only been studied sparsely, but the few studies performed suggest the collagen layer is a secondary reaction to prior damage, and thus not causal [Braskén, 1991].
Younger people with abdominal pain and altered bowel habits are often diagnosed as having IBS and colonoscopy is avoided not to aggravate the condition further [Drossman et al. 2006]. Older people with gastrointestinal complaints are often prescribed a colonoscopy to rule out malignancy. Thus, younger people are less frequently examined by colonoscopy than older patients, which may affect the age at incidence peak of MC. During the past two decades, colonoscopy has almost completely replaced X-ray examination of the colon, an examination which could never yield the diagnosis MC. Awareness by pathologists may also increase the incidence figures. CC was observed in the biopsies only at re-examination, not initially [Wang et al. 1988; Olesen et al. 2004b]. All these scenarios influence the diagnosis setting, the peak age at diagnosis, and whether the diagnosis IBS or MC is set. Thus, the true incidence figures over time and peak age at diagnosis setting must be recognized in the light of these aspects. A recent population-based study shows a stability in incidence figures, which may reflect the truth when all factors stated above have been settled [Gentile et al. 2014].
Smoking has been described as a risk factor for developing postinfectious, functional gastrointestinal disorders (FGIDs) [Parry et al. 2005], for overlapping syndromes of reflux diseases and FGID [Fujiwara et al. 2011], and for functional dyspepsia, but not for IBS [Boekema et al. 2001]. Another study has shown that both visceral and peripheral pain are increased by smoking [Pisinger et al. 2011]. Smoking was associated with patients fulfilling both the criteria for IBS-like symptoms and MC, and not with pure MC [Roth et al. 2013a, 2014]. It remains to be determined whether smoking causes IBS, with the ensuing need of a colonoscopy whereby microscopic inflammation can occasionally be found, or whether smoking induces true MC. Another hypothesis is that smokers with MC also experience abdominal pain. Furthermore, the atherosclerosis evolved in smokers may cause intestinal ischemia with signs of lymphocyte infiltration [O’Neill and Yalamarthi, 2012]. Associations between MC and smoking may reflect confounders and do not prove any causality. Further studies should attempt to elucidate whether there is a protective effect against the consequences of smoking when combined with alcohol, in analogy with the protective effect of alcohol against the induction of rheumatoid arthritis [Maxwell et al. 2010].
The reported connection between MC and autoimmune diseases [Pardi et al. 2002; Olesen et al. 2004a] may be explained by the fact that a patient already in hospital care due to another chronic disease is more often referred to a specialist in gastroenterology and for a colonoscopy when presenting with gastrointestinal complaints than a healthy person in primary care. Thus, many cohorts presented in the literature, also epidemiological studies, constitute selected cases of the disease [Fernandez-Banares et al. 1999; Olesen et al. 2004a, 2004b; Pardi et al. 2007]. Diabetes mellitus and MC is one of the connections reported [Pardi et al. 2002; Olesen et al. 2004a]. When analyzed further, this connection was seen between MC and diabetes mellitus type 2, and not type 1 [Roth et al. 2013d]. Thus, the connection may rather reflect mechanisms other than autoimmunity, for example, cardiovascular changes and metabolic dysfunction. A microscopic inflammation is sometimes seen throughout the gastrointestinal mucosa in celiac disease, and therefore, the connection between celiac disease and MC may in some cases represent one entity instead of two different entities [Carmack et al. 2009]. As the villi are absent in the colon, the only possible reaction to gluten in the colon is infiltration of lymphocytes and other inflammatory cells into the lamina propria. This is further underlined by healing of the MC after introduction of a gluten-free diet [Olesen et al. 2004a]. Both the MC and the villus atrophy are sometimes resistant to diet [Olesen et al. 2004a; Carmack et al. 2009]. All patients with both MC and any type of thyroid disorder were found to be under treatment with levothyroxine, and in most cases, the drug was introduced prior to the debut of MC [Gustafsson et al. 2013]. Furthermore, patients with MC had a lower prevalence of antithyroid peroxidase antibodies than healthy controls [Gustafsson et al. 2013]. It is not surprising that a disease like MC, which is prevalent among middle-aged or older people, is associated with other chronic diseases. It is of great importance to examine patients from a whole region, and not only from tertiary centers, and to use appropriate control groups to estimate true associations [Gustafssonet al. 2013; Roth et al. 2013d].
All drugs used in the treatment of autoimmune diseases have been suspected to induce MC [Pardi et al. 2002;Beaugerie and Pardi, 2005; Fernandez-Banares et al. 2007; Carmack et al. 2009; Münch et al. 2012]. Thus, the finding of MC in patients with autoimmune diseases may reflect the treatment with NSAIDs, PPIs, and other drugs. If not taking into consideration secondary forms of MC, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide. Some scientists are more prone to exclude secondary forms of MC than others [Gentile et al. 2014]. In recent decades, the treatment of cardiovascular diseases and diabetes mellitus has been more aggressive, and patients live longer under treatment with several different vasoactive drugs, of which some are associated with MC [Fernandez-Banares et al. 2007; O’Neill S and Yalamarthi, 2012]. Vascular changes in the bowel are a frequently underestimated condition, and the characteristics for ischemic colitis are similar to those described for the MC population [Bohr et al. 1996; Olesen et al. 2004a; Pardi and Kelly, 2011; O’Neil and Yalamarthi, 2012]. Corticosteroids are used in the treatment of MC, with a better response than other anti-inflammatory drugs [Münch et al. 2012]. However, corticosteroids and budesonide have a broad, nonspecific, anti-inflammatory effect and can also be useful in the treatment of ischemic, radiatic, and toxic colitis [Kochhar et al. 1991; Onishi et al. 2008; O’Neil and Yalamarthi, 2012]. The reduced effect by other anti-inflammatory drugs [Riddell et al. 2007; Münch et al. 2012] may reflect a noninflammatory etiology of MC. The concomitant existence of many, severe diseases and the intake of several drugs may have a synergistic, harmful effect on the colonic mucosa [Roth et al. 2013d]. It is not reasonable to believe that patients in the age range of 80–90 years, with cardiovascular damage, several diseases, and drug treatments have an additional autoimmune disease as the explanation for their lymphocyte infiltration in the lamina propria.
The growing, worldwide opinion is that at least two attacks of gastrointestinal inflammation and symptoms are necessary before the diagnosis of IBD is set [Henriksen et al. 2006], as a single attack of diarrhea is impossible to differentiate from an infectious gastroenteritis. When scrutinizing all medical records in several districts of Sweden, it was found that the majority of patients had had only a single attack of MC [Olesen et al. 2004a; Roth et al. 2013a; Thörn et al. 2013]. The same rule as for IBD should be introduced with respect to MC. Accordingly, one single attack of lymphocyte infiltration may not be judged as a lifelong disease. Furthermore, we must have a new classification to differentiate primary from secondary MC, and a pure histopathological description from a clinical syndrome. This would be more useful than the classification of CC and LC, which are indistinguishable from each other in daily practice [Rasmussen and Munck, 2012;Roth and Ohlsson, 2013]. In secondary MC, treatment should focus on the original disease, and cessation of drugs must be considered before the diagnosis MC is set. The risk of overdiagnosing the disease is to stigmatize harmless conditions and weaken the person’s eligibility for health insurance. An overprescription of budesonide to older women, already sick from, or at risk of developing osteoporosis, must be avoided.
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Summary
Since 1976 when the first case of MC was reported, many studies have been conducted and new knowledge has been confirmed. MC is a nonspecific, histopathological picture which may be the result of a variety of different etiologic and pathologic processes, as well as being a normal variant in healthy subjects. The incidence of MC is associated with increased age, suggesting that MC may be a normal ageing process along with a diminished epithelial barrier, possibly due to ischemia and reduced estrogen levels, while at the same time the mucosa is exposed to many drugs.
A new classification is necessary to get more homogenous cohorts, before further research in this field can be performed to try to identify possible etiologies of primary, idiopathic MC. The importance of classification and division of MC into CC and LC must be called into question, at least in the clinical setting and in the handling of the diseases. A description of the normal ageing of the gastrointestinal mucosa should be performed, especially regarding the natural expression of inflammatory cells and thickness of the collagenous layer, related to different age groups.
A new terminology is suggested in this field.
The term MC should be reserved for a description solely of the histopathology.
A primary, idiopathic, histopathological finding, in combination with gastrointestinal symptoms, should be called primary MC. Examinations of at least two colonic biopsies at an interval of some months should be performed, and the clinical gastrointestinal symptoms, not only restricted to diarrhea, should be of a chronic, relapsing or continuous nature.
Secondary causes of the histopathological findings should be referred to as secondary MC.
One single attack of histopathological findings and gastrointestinal symptoms should be considered a transient MC and not classified under the same terminology as relapsing or chronic symptoms.
Sent: Wednesday, August 17, 2016 4:49 PM
To: customerservice@glutenfreeworks.com
Subject:
I looked over the material and find it accurate. You should send her the paper below for her sake.
Therap Adv Gastroenterol. 2015 Jan; 8(1): 37–47.
doi: 10.1177/1756283X14550134
PMCID: PMC4265085
New insights and challenges in microscopic colitis
Bodil Ohlssoncorresponding author
Author information ► Copyright and License information ►
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Introduction
Chronic diarrhea is reported in 4–5% of individuals and makes up a considerable proportion of the consultations in gastroenterology [Thomas et al. 2003]. Diarrhea has for a long time been considered as functional after exclusion of celiac disease, inflammatory bowel disease (IBD), malignancy and so on [Drossman et al. 2006]. Over recent decades, microscopic colitis (MC) has emerged as a common cause of diarrhea, especially in middle-aged or older women, and the disease is regarded as a subgroup within IBD [Münch et al. 2012]. The disease is characterized by chronic, watery diarrhea and normal or close to normal findings by endoscopic examination. Intestinal, mucosal biopsies show characteristic histopathological changes [Robert, 2004; Thijs et al. 2005; Temmerman and Baert, 2009]. Although as many as 63% of patients only have a single attack of the disease [Olesen et al. 2004a], the patients who have received the diagnosis are considered to be suffering from a chronic disease. MC can be considered a primary lymphocytic disorder of the gut, whereas many other disorders may be associated with lymphocytic infiltration or collagenous deposition, in which cases MC could be considered a secondary disorder [Carmack et al. 2009].
Histopathology
In 1976, Lindström described microscopic inflammatory changes in colon with a remarkable subepithelial collagen band and called the condition collagenous colitis (CC) [Lindström, 1976]. Read and colleagues introduced the term microscopic colitis [Read et al. 1980]. In 1989, Lanzeby and colleagues showed that an increased number of colonic intraepithelial lymphocytes (IELs) was the most characteristic feature of MC and suggested the term lymphocytic colitis (LC) [Lazenby et al. 1989]. The diagnosis of MC is based on histopathological examination of mucosal biopsies from the colon, obtained through endoscopy [Robert, 2004; Thijs et al. 2005; Temmerman and Baert, 2009], in combination with nonbloody diarrhea [Olesen et al. 2004a; Pardi and Kelly, 2011]. The histopathological criteria for CC are a thickened subepithelial collagen layer of at least 10 µm (reference value: 2–7 µm); inflammation in the lamina propria with increased numbers of lymphocytes and plasma cells; epithelial damage; and increased numbers of IELs may be present. The histopathological criteria for LC are a density of at least 20 IELs per 100 surface epithelial cells; chronic inflammatory infiltrate of mononuclear cells in the lamina propria; epithelial damage; and a subepithelial collagen layer of less than 10 µm. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in MC consists basically of collagen type I and III [Flejou et al. 1984], which are the subtypes produced by repair functions, indicating a reactive origin [Braskén, 1991]. The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region [Jessurun et al. 1987; Wang et al. 1988; Carpenter et al. 1992; Fernandez-Banares et al. 1999].
Recently, Carmack and colleagues have introduced the terms primary and secondary lymphocytic disorders of the gastrointestinal tract [Carmack et al. 2009]. Infiltration of lymphocytes in the lamina propria is unspecific and can be observed in all segments of the gastrointestinal tract. A common cause of lymphocyte infiltration in the stomach is infection by Helicobacter pylori, whereas celiac disease may cause MC throughout the gastrointestinal tract [Carmack et al. 2009]. Autoimmune diseases, bacterial and viral enteritis, and drugs are other etiologies of secondary LC [Carmack et al. 2009]. Seasonal fluctuations in the histopathology have been identified and suggest an allergic origin of MC in some circumstances [LaSala et al. 2005]. Surgical traction per se may lead to invasion of lymphocytes into the tissue [Lee et al. 2009].
CC-like findings have been reported in patients suffering from colon cancer, carcinoid lesions, adenomas and hyperplastic polyps, bacterial infections, lactose intolerance, and constipation [Flejou et al. 1984; Teglbjaerget al. 1984; Nussinson et al. 1988; Wang et al. 1988; Gubbins et al. 1991; Leigh et al. 1993]. Both CC and LC are described in ulcerative colitis and Crohn’s disease, together with the characteristics of these diseases [Goldblum and Wang, 2000]. MC in this context should be considered as a part of the original IBD disease, and not as a separate entity [Jegadeesan et al. 2013]. Furthermore, these changes can also be found in persons without any signs of gastrointestinal symptoms or diseases [Wang et al. 1988; Thörn et al. 2013]. Altogether, there is no histopathological hallmark that differentiates primary, idiopathic MC from a MC evolved secondary to another syndrome or its treatment, or that differentiate MC in healthy subjects from patients with symptoms.
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Epidemiology
Population studies have shown an increasing incidence of MC over recent decades, with a mean incidence rate of 1.1–7.0/100,000 inhabitants for CC and an incidence rate of 3.1–5.5/100,000 inhabitants for LC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Pardi et al. 2007; Vigren et al. 2012; Thörn et al. 2013]. The increased incidence has stabilized over the past years, and the incidence is associated with female gender and increasing age [Gentile et al. 2014]. Reports indicate that MC is more frequent in colder, northern countries than in southern countries [Pardi et al. 2007; Fernandez-Banares et al. 2011; Gentile et al. 2014]. This north–south gradient has led to speculations that vitamin D is involved in the pathogenesis, but this has not been confirmed [Sjöberg et al. 2013]. The female-to-male ratio ranges from 2.8:1 to 7.5:1 for CC and from 2.1:1 to 2.7:1 for LC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Vigren et al. 2012], whereas in a later review, the ratio was 3.0–9.0:1 for CC and 6.0:1 to no difference in LC [Pardi and Kelly, 2011]. The average age at diagnosis is approximately 65 years [Münch et al. 2012].
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Etiology and pathophysiology in MC
The etiology is in most cases unknown, and is probably multifactorial, also when only primary MC is included, as the terminology constitutes a morphological, descriptive term, representing many different entities, presenting with an inflammation in the mucosa.
Genetic predisposition
Only a limited number of familial MC cases have been reported [Abdo et al. 2001; Järnerot et al. 2001], but as many as 12% of patients with MC have a family history of IBD [Olesen et al. 2004a]. There is an association between the expression of MC and HLA-DQ, and patients with MC have a high prevalence of tumor necrosis factor α and metalloproteinase-9 gene polymorphisms [Fernandez-Banares et al. 2005;Koskela et al. 2008; Madisch et al. 2011].
Hormonal factors
Endocrine factors have been discussed since most studies report a female predominance of MC [Fernandez-Banares et al. 1999; Olesen et al. 2004b; Vigren et al. 2012]. The intestinal epithelium provides a protective barrier for the internal milieu against luminal factors, which is dependent on intercellular, epithelial tight junctions [Turner, 2006]. Increased paracellular permeability has been implicated in the pathogenesis of chronic, mucosal inflammation [Meddings, 1997; Teshima et al. 2012]. Estrogens and progesterone have been shown to exhibit anti-inflammatory and epithelial barrier-enhancing properties in experimentally induced colitis in rats [Günal et al. 2003; Karatepe et al. 2012; Moussa et al. 2012], and the fall in hormone levels at menopause could theoretically explain the peak age of debut of MC in middle-aged women [Pardi and Kelly, 2011]. However, no differences in reproductive factors between CC and LC, or between patients with MC or healthy controls, could be identified [Roth et al. 2013c].
Autoimmunity and comorbidity
The association of MC with various autoimmune diseases such as celiac disease, thyroid disease, rheumatoid arthritis, and diabetes mellitus has given rise to the hypothesis that MC is an autoimmune disease [Pardi et al. 2002; Olesen et al. 2004a]. The predominance of middle-aged female patients further strengthens the autoimmune hypothesis, although no specific autoantibody has been identified [Pardi and Kelly, 2011]. Several small studies have proposed an increased prevalence of antinuclear antibody, antigliadin IgA, and anti-Saccharomyces cerevisiae antibodies in serum in patients with MC [Holstein et al. 2006]. Scrutinizing a greater cohort of patients with MC with 11 different autoantibodies did not show any increased prevalence of autoantibodies in patients with MC compared with healthy controls [Roth and Ohlsson, 2013; Roth et al. 2013b; Gustafsson et al. 2013]. Recent research suggests an increased morbidity in a wide range of chronic diseases in patients with MC, irrespective of autoimmunity, including ischemic cardiovascular diseases, hypertension, asthma, and allergy [Roth et al. 2013d].
Smoking and alcohol habits
Smoking has been confirmed to be associated with MC [Yen et al. 2012; Vigren et al. 2011], and smokers contract MC 10 years earlier than nonsmokers [Vigren et al. 2011]. Accordingly, lung cancer is associated with MC [Chan et al. 1999]. Current MC and MC in combination with abdominal pain were associated with smoking, whereas transient MC was associated with past smoking, and pure MC without abdominal pain was not associated with smoking [Roth et al. 2013a, 2014].
In one study, alcohol consumption was higher in patients with MC compared with healthy controls [Yen et al. 2012]. Nevertheless, wine drinking did not tend to increase the risk of developing MC. Rather, wine drinking seemed to provide protection against the development of MC in smokers [Roth et al. 2014].
Luminal factors
The histological changes in MC are resolved by diverting the fecal stream by ileostomy, supporting the hypothesis of the role of luminal factors [Jarnerot et al. 1995], but the effect of food has been only rudimentarily studied.
Several drugs have been associated with the development of MC as causative or triggering agents [Olesen et al. 2004a]; the most common being nonsteroidal anti-inflammatory drugs (NSAIDs), proton-pump inhibitors (PPIs), and antidepressant or antipsychotic drugs [Chassany et al. 2000; Beaugerie and Pardi, 2005;Fernandez-Banarnes et al. 2007]. The pathophysiology can be explained by altered intestinal flora, a direct pharmacological effect on the colon, or an idiosyncratic hypersensitivity reaction [Münch et al. 2012]. A chronological connection must be established between the introduction of the drug and the histopathological changes in combination with symptoms, and improvement or disappearance of the diarrhea and restored histological picture when the treatment is ceased [Beaugerie and Pardi, 2005].
There is growing evidence for involvement of gut microbiota in the development of IBD [Wagner, 2008;Shim, 2013], but its effect on the development of MC has not been adequately studied. Bacterial and viral gastroenteritis may induce MC [Makinen et al. 1998; Perk et al. 1999; Erim et al. 2003]. Bile acid malabsorption has been shown to coexist in 60% of patients with LC and in 44% of patients with CC [Ung et al. 2000; Fernandez-Banares et al. 2001]. It remains to be determined whether bile acid malabsorption is causative or secondary.
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Clinical presentation
The clinical features of MC are described and defined as chronic, relapsing, nonbloody, watery diarrhea [Olesen et al. 2004a; Pardi and Kelly, 2011]. The diarrhea may be mild, but severe, frequent diarrhea with urgency is common [Bohr et al.1996]. Nevertheless, some patients with histopathological features of MC are asymptomatic [Wang et al. 1988; Gubbins et al. 1991; Thörn et al. 2013]. About 50% of patients with diagnosed MC fulfill the criteria for irritable bowel syndrome (IBS) [Roth and Ohlsson, 2013]. These patients have abdominal pain, and some patients also have constipation. In fact, all gastrointestinal symptoms are accentuated in patients with MC compared with healthy controls [Roth and Ohlsson, 2013]. The clinical aspects of CC and LC are indistinguishable [Rasmussen and Munck, 2012; Roth and Ohlsson, 2013]. The onset is often insidious, but 25–40% of the patients have a sudden onset [Bohr et al. 1996; Olesen et al. 2004a]. The majority of patients have only a single attack of the disease with spontaneous remission in about 10% [Gubbins et al. 1991; Olesen et al. 2004a; Roth et al. 2013a; Thörn et al. 2013], and the patients are in symptomatic remission after 3–4 years [Bonner et al. 2000]. Thirty percent of patients with MC have a chronic intermittent disease, and only 7% have a chronic, continuous course which may be refractory to treatment [Järnerot et al. 1995; Olesen et al. 2004a].
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Diagnosis and treatment
First, it is mandatory to exclude inflammation secondary to another gastrointestinal disease, drug treatment or infection [Carmack et al. 2009]. When secondary MC is the case, the MC must be regarded as a part of the original disease, and the original disease or condition must be treated. Withdrawal of toxic agents and drugs is mandatory when MC was evolved after such administration [Fernandez-Banares et al. 2007]. As many of these patients are past or current smokers, and older, intestinal ischemia must be considered [Roth et al. 2014]. Smoking abstinence should be encouraged, as past smoking is associated with transient, and not persistent, MC [Roth et al. 2014]. After exclusion of secondary MC, the diagnosis of true, primary MC can be set [Pardi and Kelly, 2011].
The primary aim in the treatment of MC is to achieve clinical remission and improve the patient’s quality of life [Hjortswang et al. 2009]. The secondary aim is maintenance of clinical remission [Ianiro et al. 2012].
As most patients complain of diarrhea, traditional antidiarrheal agents such as loperamide are frequently used as first-line therapy [Pardi et al. 2002; Olesen et al. 2004a]. Budesonide is the only drug which has been proved to be efficient by randomized, placebo-controlled trials, and it is to date the standard treatment for moderate to severe MC [Münch et al. 2012; Storr, 2013]. Budesonide therapy resulted in a significant improvement in both clinical symptoms and histological inflammatory changes, but the relapse frequency is about 61–80% [Baert et al. 2002; Bonderup et al. 2003; Bonderup et al. 2009; Mielke et al. 2005; Miehlke et al. 2009]. The relapse frequency is reduced by sustained treatment at low dosage [Stewart et al. 2011]. Budesonide has the advantage over corticosteroids due to the high, hepatic first-pass elimination, thus avoiding the side effects of steroids [Stewart et al. 2011], and the efficacy of budesonide is superior to prednisolone, although no comparative studies are available [Munck et al. 2003].
Treatment with bile acid bindings is efficient to diminish the symptoms, but has no effect on the histopathological changes [Ung et al. 2001]. Bismuth subsalicylate was effective in MC in a small, randomized, placebo-controlled trial [Fine and Lee, 1998]. Aminosalicylates have, in uncontrolled or retrospective studies, had a moderate to good effect in MC [Pardi et al. 2002; Chande et al. 2008]. The experience of other immunosuppressive therapies are gathered in some systematic reviews, based on retrospective studies and case reports [Riddell et al. 2007; Münch et al. 2012]. In severe, refractory cases, these therapies or surgical intervention may be appropriate to test [Järnerot et al. 1995].
Treatment strategy of MC
Cessation of possible offending irritants or medications.
Antidiarrheal drugs.
Budesonide.
Cholestyramine, immunomodulating drugs, or ileostomy and colectomy.
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Discussion
Over the past century, the population, especially women, have changed their life habits and lifestyle substantially. A microscopic inflammation in the colonic mucosa may hypothetically be the reaction to all the irritants the colon is exposed to in daily life. The barrier function of the gut epithelium may be diminished in the course of a lifetime, due to fall in estrogen levels around the menopause and changes in microbiota diversity [Günal et al. 2003; Karatepe et al. 2012; Moussa et al. 2012; Patten and Collett, 2013; Kamada et al. 2013], facilitating the penetration of irritants into the mucosa. The greater prevalence of MC findings in the ascending than descending colon suggests an important role for luminal factors [Jessurun et al. 1987;Carpenter et al. 1992]. Thus, the increased incidence of MC with increasing age could represent a normal ageing process [Gentile et al. 2014].
Surgical traction of the tissue is enough for lymphocyte invasion [Lee et al. 2009]. During colonoscopy, the bowel is cleaned by laxatives and biopsies are taken at the end of the examination, after traction of the bowel. Biopsy-taking at the start of the examination should perhaps be more appropriate and reduce the incidence of LC. The nature of the collagen layer in CC has only been studied sparsely, but the few studies performed suggest the collagen layer is a secondary reaction to prior damage, and thus not causal [Braskén, 1991].
Younger people with abdominal pain and altered bowel habits are often diagnosed as having IBS and colonoscopy is avoided not to aggravate the condition further [Drossman et al. 2006]. Older people with gastrointestinal complaints are often prescribed a colonoscopy to rule out malignancy. Thus, younger people are less frequently examined by colonoscopy than older patients, which may affect the age at incidence peak of MC. During the past two decades, colonoscopy has almost completely replaced X-ray examination of the colon, an examination which could never yield the diagnosis MC. Awareness by pathologists may also increase the incidence figures. CC was observed in the biopsies only at re-examination, not initially [Wang et al. 1988; Olesen et al. 2004b]. All these scenarios influence the diagnosis setting, the peak age at diagnosis, and whether the diagnosis IBS or MC is set. Thus, the true incidence figures over time and peak age at diagnosis setting must be recognized in the light of these aspects. A recent population-based study shows a stability in incidence figures, which may reflect the truth when all factors stated above have been settled [Gentile et al. 2014].
Smoking has been described as a risk factor for developing postinfectious, functional gastrointestinal disorders (FGIDs) [Parry et al. 2005], for overlapping syndromes of reflux diseases and FGID [Fujiwara et al. 2011], and for functional dyspepsia, but not for IBS [Boekema et al. 2001]. Another study has shown that both visceral and peripheral pain are increased by smoking [Pisinger et al. 2011]. Smoking was associated with patients fulfilling both the criteria for IBS-like symptoms and MC, and not with pure MC [Roth et al. 2013a, 2014]. It remains to be determined whether smoking causes IBS, with the ensuing need of a colonoscopy whereby microscopic inflammation can occasionally be found, or whether smoking induces true MC. Another hypothesis is that smokers with MC also experience abdominal pain. Furthermore, the atherosclerosis evolved in smokers may cause intestinal ischemia with signs of lymphocyte infiltration [O’Neill and Yalamarthi, 2012]. Associations between MC and smoking may reflect confounders and do not prove any causality. Further studies should attempt to elucidate whether there is a protective effect against the consequences of smoking when combined with alcohol, in analogy with the protective effect of alcohol against the induction of rheumatoid arthritis [Maxwell et al. 2010].
The reported connection between MC and autoimmune diseases [Pardi et al. 2002; Olesen et al. 2004a] may be explained by the fact that a patient already in hospital care due to another chronic disease is more often referred to a specialist in gastroenterology and for a colonoscopy when presenting with gastrointestinal complaints than a healthy person in primary care. Thus, many cohorts presented in the literature, also epidemiological studies, constitute selected cases of the disease [Fernandez-Banares et al. 1999; Olesen et al. 2004a, 2004b; Pardi et al. 2007]. Diabetes mellitus and MC is one of the connections reported [Pardi et al. 2002; Olesen et al. 2004a]. When analyzed further, this connection was seen between MC and diabetes mellitus type 2, and not type 1 [Roth et al. 2013d]. Thus, the connection may rather reflect mechanisms other than autoimmunity, for example, cardiovascular changes and metabolic dysfunction. A microscopic inflammation is sometimes seen throughout the gastrointestinal mucosa in celiac disease, and therefore, the connection between celiac disease and MC may in some cases represent one entity instead of two different entities [Carmack et al. 2009]. As the villi are absent in the colon, the only possible reaction to gluten in the colon is infiltration of lymphocytes and other inflammatory cells into the lamina propria. This is further underlined by healing of the MC after introduction of a gluten-free diet [Olesen et al. 2004a]. Both the MC and the villus atrophy are sometimes resistant to diet [Olesen et al. 2004a; Carmack et al. 2009]. All patients with both MC and any type of thyroid disorder were found to be under treatment with levothyroxine, and in most cases, the drug was introduced prior to the debut of MC [Gustafsson et al. 2013]. Furthermore, patients with MC had a lower prevalence of antithyroid peroxidase antibodies than healthy controls [Gustafsson et al. 2013]. It is not surprising that a disease like MC, which is prevalent among middle-aged or older people, is associated with other chronic diseases. It is of great importance to examine patients from a whole region, and not only from tertiary centers, and to use appropriate control groups to estimate true associations [Gustafssonet al. 2013; Roth et al. 2013d].
All drugs used in the treatment of autoimmune diseases have been suspected to induce MC [Pardi et al. 2002;Beaugerie and Pardi, 2005; Fernandez-Banares et al. 2007; Carmack et al. 2009; Münch et al. 2012]. Thus, the finding of MC in patients with autoimmune diseases may reflect the treatment with NSAIDs, PPIs, and other drugs. If not taking into consideration secondary forms of MC, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide. Some scientists are more prone to exclude secondary forms of MC than others [Gentile et al. 2014]. In recent decades, the treatment of cardiovascular diseases and diabetes mellitus has been more aggressive, and patients live longer under treatment with several different vasoactive drugs, of which some are associated with MC [Fernandez-Banares et al. 2007; O’Neill S and Yalamarthi, 2012]. Vascular changes in the bowel are a frequently underestimated condition, and the characteristics for ischemic colitis are similar to those described for the MC population [Bohr et al. 1996; Olesen et al. 2004a; Pardi and Kelly, 2011; O’Neil and Yalamarthi, 2012]. Corticosteroids are used in the treatment of MC, with a better response than other anti-inflammatory drugs [Münch et al. 2012]. However, corticosteroids and budesonide have a broad, nonspecific, anti-inflammatory effect and can also be useful in the treatment of ischemic, radiatic, and toxic colitis [Kochhar et al. 1991; Onishi et al. 2008; O’Neil and Yalamarthi, 2012]. The reduced effect by other anti-inflammatory drugs [Riddell et al. 2007; Münch et al. 2012] may reflect a noninflammatory etiology of MC. The concomitant existence of many, severe diseases and the intake of several drugs may have a synergistic, harmful effect on the colonic mucosa [Roth et al. 2013d]. It is not reasonable to believe that patients in the age range of 80–90 years, with cardiovascular damage, several diseases, and drug treatments have an additional autoimmune disease as the explanation for their lymphocyte infiltration in the lamina propria.
The growing, worldwide opinion is that at least two attacks of gastrointestinal inflammation and symptoms are necessary before the diagnosis of IBD is set [Henriksen et al. 2006], as a single attack of diarrhea is impossible to differentiate from an infectious gastroenteritis. When scrutinizing all medical records in several districts of Sweden, it was found that the majority of patients had had only a single attack of MC [Olesen et al. 2004a; Roth et al. 2013a; Thörn et al. 2013]. The same rule as for IBD should be introduced with respect to MC. Accordingly, one single attack of lymphocyte infiltration may not be judged as a lifelong disease. Furthermore, we must have a new classification to differentiate primary from secondary MC, and a pure histopathological description from a clinical syndrome. This would be more useful than the classification of CC and LC, which are indistinguishable from each other in daily practice [Rasmussen and Munck, 2012;Roth and Ohlsson, 2013]. In secondary MC, treatment should focus on the original disease, and cessation of drugs must be considered before the diagnosis MC is set. The risk of overdiagnosing the disease is to stigmatize harmless conditions and weaken the person’s eligibility for health insurance. An overprescription of budesonide to older women, already sick from, or at risk of developing osteoporosis, must be avoided.
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Summary
Since 1976 when the first case of MC was reported, many studies have been conducted and new knowledge has been confirmed. MC is a nonspecific, histopathological picture which may be the result of a variety of different etiologic and pathologic processes, as well as being a normal variant in healthy subjects. The incidence of MC is associated with increased age, suggesting that MC may be a normal ageing process along with a diminished epithelial barrier, possibly due to ischemia and reduced estrogen levels, while at the same time the mucosa is exposed to many drugs.
A new classification is necessary to get more homogenous cohorts, before further research in this field can be performed to try to identify possible etiologies of primary, idiopathic MC. The importance of classification and division of MC into CC and LC must be called into question, at least in the clinical setting and in the handling of the diseases. A description of the normal ageing of the gastrointestinal mucosa should be performed, especially regarding the natural expression of inflammatory cells and thickness of the collagenous layer, related to different age groups.
A new terminology is suggested in this field.
The term MC should be reserved for a description solely of the histopathology.
A primary, idiopathic, histopathological finding, in combination with gastrointestinal symptoms, should be called primary MC. Examinations of at least two colonic biopsies at an interval of some months should be performed, and the clinical gastrointestinal symptoms, not only restricted to diarrhea, should be of a chronic, relapsing or continuous nature.
Secondary causes of the histopathological findings should be referred to as secondary MC.
One single attack of histopathological findings and gastrointestinal symptoms should be considered a transient MC and not classified under the same terminology as relapsing or chronic symptoms.
MC diagnosed 2007
Tex, the above post is from someone at glutenfreeworks
I told them I would ask you if you would give them feedback on the article. Here's the contact info:
John Libonati
Glutenfreeworks.com
John Libonati
Glutenfreeworks.com
MC diagnosed 2007
I don't understand what you're trying to accomplish in your search for the ultimate article about MC, but I can tell you from experience that's an exercise in frustration. And I have absolutely no ambitions to be the watchdog/critic for MC articles on the Internet. I already have more than I can get done and not enough time in which to do it, so please don't volunteer me to critique articles or provide feedback for someone else's website.
And please don't post complete articles here. Virtually all website material is copyrighted these days, and if the owners should choose to pursue a lawsuit, it could get very unpleasant and might result in this website being forced to close down. Posting sections of articles as quotes is "fair use" allowed by copyright law, as long as the source is also posted, but copying entire articles requires express permission from the publisher. Besides, it's a huge waste of space in the database. Please post links or URLs, not copies of articles. For example, here is the link to that article:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265085/
That said, the main point of that article is simply an attempt to redefine the medical description of CC/LC/MC to MC, and to question/discourage medical treatment of the disease. Those are sort of moot points in view of the fact that there are no truly effective medical treatments for MC anyway, and it is very likely that CC/LC/MC (like celiac disease) is not actually a disease, but a symptom of food and/or drug sensitivities.
Tex
And please don't post complete articles here. Virtually all website material is copyrighted these days, and if the owners should choose to pursue a lawsuit, it could get very unpleasant and might result in this website being forced to close down. Posting sections of articles as quotes is "fair use" allowed by copyright law, as long as the source is also posted, but copying entire articles requires express permission from the publisher. Besides, it's a huge waste of space in the database. Please post links or URLs, not copies of articles. For example, here is the link to that article:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265085/
That said, the main point of that article is simply an attempt to redefine the medical description of CC/LC/MC to MC, and to question/discourage medical treatment of the disease. Those are sort of moot points in view of the fact that there are no truly effective medical treatments for MC anyway, and it is very likely that CC/LC/MC (like celiac disease) is not actually a disease, but a symptom of food and/or drug sensitivities.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.