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Unexplained weight gain is characterized by increased body mass due to excess fat accumulation that is not desired by the individual.
A body mass index (BMI) of 25 to 30 signifies being overweight.
Crohn’s disease is an inflammatory bowel disease characterized by patchy inflamed areas involving the full thickness of the intestinal wall that can occur anywhere in the intestinal tract, in addition to, mucosal disease.
In Crohn’s disease there is ongoing immune activation which produces inflammation and ulceration but the cause is not known and the severity varies among patients. At diagnosis of Crohn’s disease, factors predictive of subsequent 5-year aggressive disease are an age below 40 years, the presence of perianal disease, and the initial requirement for steroids.1
Dysbiosis is a factor that develops in and worsens Crohn’s disease and stress is a factor in both of these conditions. Psychological stress activates multiple physiological processes aimed at maintaining balance within the body. These physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut microbiota dysbiosis.2
While the relative abundance of many different bacterial types can be altered during stressor exposure, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.2
Q: Is there a cure for Crohn’s disease?
A: Presently, Crohn’s disease cannot be cured. This condition has a course of remissions, when symptoms subside, and flares, when symtpoms get worse. Treatment is aimed to reduce flares and promote remission.
A cute diarrhea is a small intestinal motility disorder characterized by excessively rapid movement of intestinal contents through the small intestine with excessive loss of fluid and electrolytes that leads rapidly to a life threatening hypokalemia (low potassium blood level) and acidosis.
Q: What is hypokalemia?
A: Hypokalemia is characterized by dehydration that may result in vascular collapse, muscular malfunction that may result in paralytic ileus (bowels do not move), paralysis (cannot stand), and respiratory hypoventilation (shallow breathing) or failure, metabolic acidosis resulting from diarrhea, and impaired nerve conduction.1
While diarrhea may be a common symptom of small bowel mucosal disease, the consequent malabsorption can lead to substantial malnutrition and nutrient deficiencies. The small intestine, unlike the colon, has been relatively inaccessible, and systematic evaluation is often necessary to identify and treat small intestinal mucosal diseases that lead to diarrhea. All patients with severe diarrhea or diarrhea associated with features suggestive of malabsorption may have a disease of the small intestinal mucosa that requires careful evaluation and targeted management.2
E rosions in the second part of the duodenum typically are superficial excoriations (sores) in the mucosal lining that do not penetrate into the muscle layer as does an ulcer.
Of note, most erosions develop in the first part of the duodenum rather than the second part.
Q: Are duodenal erosions serious?
A: Yes duodenal erosions are serious and can be life-threatening for the following reasons:
S mall intestinal edema is characterized by fluid accumulation within the intestinal mucosa so that the intestinal wall appears thick and swollen.
Intestinal edema hampers peristalsis that can result in pain and gas build-up. Peristalsis is the normal rhythmic muscular wave-like action that moves residue along the gastrointestinal tract.
Q: What part of the small intestinal lining is swollen?
A: Any part of the small intestine may be affected. Some causes of edema include allergic reactions, enteropathies such as celiac disease, cow milk enteropthy, yeast infection, parasite infection, inflammatory bowel disease such as Crohn’s disease, and certain medications.
For example, the anti-hypertensive drugs known as Angiotension Converting Enzyme (ACE) inhibitors can cause intestinal angioedema and therefore the patient may present with gastrointestinal complaints.1
P ostbulbar duodenal ulceration is a chronic inflammatory disorder characterized by thickening of the intestinal lining with excoriation penetrating the muscularis mucosae (muscle layer of the intestine) associated with villous atrophy.
The ulcer is well-defined. Stenosis due to thickening of the area narrows the hollow inside of the duodenum which impairs passage of foodstuffs and may lead to obstruction.
Q: Is postbulbar duodenal ulceration painful?
A: Postbulbar duodenal ulceration may not cause symptoms but usually causes gnawing pain that is relieved by eating food. After eating there develops nausea and bloating.
Complications include obstruction, bleeding, and perforation of the duodenal lining. Ulcers do not usually become malignant.
What Is Atherosclerosis?A therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.
The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.
Q: What happens when arteries become narrowed and less flexible?
A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.
When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.
It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).
What Is Intestinal Dysbiosis? Intestinal dysbiosis is an imbalance of the composition and quantity of microbe populations (called the microbiota), that naturally inhabit our human gut. Dysbiosis causes altered gut immunity, abnormal fermentation of undigested foodstuffs,…
Collagenous colitis is a disease of the large intestine (colon) that is characterized by microscopic inflammation of the surface mucosal lining and an abnormally thickened collagen band of tissue that develops wthin the lining of the colon.
The thicker than normal layer of collagen of at least 10 µm (reference value: 2–7 µm) can vary in different locations. Inflammation occurs with increased numbers of lymphocytes (white blood cells) and plasma cells and epithelial (surface cell) damage. These changes can only be seen under microscopic examination of multiple biopsied tissue samples taken during a colonoscopy procedure.
Q: What is collagen?
A: Collagen is a strong, fibrous protein found in connective tissue of the colon and many other tissues such as tendons. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in collagenous colitis consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin to some irritant or drug.1
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.1 Inflammation of the ileum (last segment of the small intestine next to colon) is common.2
Endoscopy and radiological (x-ray) examinations are usually normal.3
Autoimmune disorders are frequently seen in adult patients with collagenous colitis.4 In the study below by Koskela et al. concomittent autoimmune diseases were present in 53% of patients with collagenous colitis.5
Importantly, the finding of collagenous colitis in patients with autoimmune diseases may reflect the treatment with NSAIDs (non-steroidal anti-inflammatory drugs), such as Ibuprofin and aspirin, PPIs (proton pump inhibitors), and other drugs. However, if secondary forms of collagenous colitis are not taken into consideration, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide (a steroid).6
Treatment with budesonide steroid is efficacious irrespective of bile acid malabsorption.7
Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation.8
See below for nutritional deficiency problems caused by steroid usage and steps to be taken for correction.
Lymphocytic colitis is a microscopic inflammation of the large intestinal mucosa with infiltration of lymphocytes (IELs) that is characterized by non-bloody 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.1
Lymphocytic colitis (LC) is categorized as primary or secondary. Primary LC is a clinical and histopathological disease of unknown cause. Secondary LC may develop as the result of iritating factors acting on the colon such as smoking or many medications. In one study, the most common drug treatments as a percentage of the study group were corticosteroids (32.1%), proton pump inhibitors (26.0%), antidepressant drugs, specifically selective serotonin reuptake inhibitors (21.4%), angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists (18.3%), statins (17.6%), thyroid hormones (17.6%), and beta-blockers (16.0%).3
Secondary lymphocytic colitis is associated with several concomitant diseases including celiac disease. This is why lymphocytic changes must be interpreted with caution before considering them as a separate entity of autoimmune origin, instead of secondary reactions to ischemia and toxic stimulants. Efforts must be made to better classify and diagnose patients with real, primary lymphocytic colitis to avoid over-prescription of corticosteroids for treatment.3