Dr Veena Karanth
PG Scholar, Department of Practice of Medicine
Government Homoeopathic Medical College & Hospital.
Crohn’s disease causes inflammation that spreads deeply into the layers of bowel tissue and can lead to life – threatening complication. Crohn’s disease mainly associated with genetic defects in innate immunity and autophagy, smoking and low-residue, high-refined-sugar diet. Symptoms can range from mild to severe. If untreated or recurrent attack of crohn’s disease leads to various complications including cancer of colon .Homeopathy treatment option to patient suffering from has good treatment option for patients suffering from crohn’s disease.
Crohn’s disease is segmental, non-continuous, chronic inflammation that can affect any part of the digestive tract from the mouth to the anus, with a predilection for the distal ileum and colon. The inflammation is transmural and this can lead to internal abscesses and fistulae. As potential risk factors. The pathogenesis involves an interplay of genetic, environmental, microbial and immune factors, which in combination result in chronic intestinal inflammation the equilibrium between pro- and anti-inflammatory cytokines is significantly deranged. This deregulation of the immune reaction leads to excessive activation of pro-inflammatory cytokines result in causation of inflammatory bowel disease.
Crohn’s disease is frequently diagnosed in late adolescence or early adulthood, with a median age of diagnosis in the third decade. Women are slightly more likely to be affected with Crohn’s disease. Crohn’s diseases are worldwide disorders, although the precise incidence varies considerably in different countries. The United States, Northern Europe and Scandinavian countries have higher rates. In Asia, the disease was thought to be uncommon, but recent reports have highlighted the increasing incidence of the disease. The rapid changes in incidence and prevalence in Asia may point to environmental changes associated with the so-called ‘Westernisation’ of lifestyle (e.g. dietary changes, smoking, etc.).
The Crohn’s disease usually present with symptoms of abdominal pain, diarrhea and weight loss. The pain is often associated with diarrhea, which is usually watery and does not contain blood or mucus may be accompanied by extra intestinal manifestations Many patients present with symptoms of both small bowel and colonic
disease. A few patients present with isolated perianal disease, vomiting from jejunal strictures or severe oral ulceration.
There are many causes of Crohns disease, the most common causes are: The most firmly established risk-factor for developing inflammatory bowel disease is a positive family history. The incidence of inflammatory bowel disease among first-degree relatives of IBD patients is 30 to 100 times that of the general population. Approximately 15% of patients with inflammatory bowel disease have a first degree relative suffering from either Ulcerative colitis or Crohns disease; the risk being higher in patients with Crohn’s. Other factors suggesting genetic susceptibility are higher concordance amongst monozygotic than dizygotic twins, and ethnic differences in disease prevalence.
Genetics study identification of NOD2/CARD15 within the inflammatory bowel disease gene locus is an important breakthrough in genetic research for unraveling the etiology of Crohn’s disease. The major histocompatibility complex or HLA genes on chromosome 6 have a greater role in modifying the inflammatory bowel disease phenotype than overall disease susceptibility.
Westernization of lifestyle, such as changes in diet and variance in exposure to sunlight, pollution, and industrial chemicals, has been postulated to be responsible for the rising incidence.
It is postulated that improved hygiene alters the intestinal flora by decreasing exposure to certain bacteria. This may explain the higher frequency of both Crohn’s disease in higher socioeconomic groups.
It has been observed that smoking is protective against Ulcerative Colitis while patients with Crohn’s disease who smoke are more likely to have frequent relapses.
Drugs like oral contraceptives, nonsteroidal anti-inflammatory drugs, antibiotics and seasonal variation and mental stress factors that may have a role in pathogenesis or precipitation of relapse.
Clinical features of Crohn’s disease
Crohn’s disease presents with one of three major patterns: (1) disease in the ileum and cecum (40% of patients); (2) disease confined to the small intestine (30%); and Symptoms suggestive of inflammatory bowel disease include watery stools, blood or mucus in the stool, diarrhea persisting for more than 4 weeks .Crampy abdominal pain, nocturnal defecation and fever. (3) Disease confined to the colon (25%). Much less commonly, Crohn’s disease involves more proximal parts of the gastrointestinal tract–the mouth, the tongue, the esophagus, the stomach, and the duodenum,
Pathological and histological features include segmental trans mural inflammation with micro-erosions, fissures, ulcerations, granulomas, infiltration, and dilated lymph vessels. The disease is most common in distal ileum and colon (50% of patients),
small intestine only (25% to 30%), colon only (20% to 25%), rectum (10% to 15%) or gastro duodenal (3% to 5%). Anorectal disease like anal fistulae, anal fissures, perianal abscess can occur in 30% to 40% of patients .Weight loss is significant.
The diagnosis is made on the basis of careful medical history, close observation of the clinical picture, the evaluation of endoscopic, histological and radiological findings and, finally, the results of laboratory investigations. Laboratory abnormalities include elevated ESR and C-reactive protein, thrombocytosis, anemia, leukocytosis and hypoalbuminaemia. Computer tomography (CT) is sensitive in detecting both luminal and extra-luminal disease in patient with Crohn’s disease.
Life-threatening colonic inflammation- In the most extreme cases, the colon dilates (toxic mega colon) and bacterial toxins pass freely across the diseased mucosa into the portal and then systemic circulation.
Fistulae- These are specific to Crohn’s disease. Enter enteric fistulae can cause diarrhea and malabsorption due to blind loop syndrome. Enterovesical fistulation causes recurrent urinary infections and pneumaturia. An enterovaginal fistula causes a faeculent vaginal discharge.Fistulation from the bowel may also cause perianal or ischiorectal abscesses, fissures and fistulae.
Haemorrhage – due to erosion of a major artery is rare.
Cancer- The risk of dysplasia and cancer increases with the duration and extent of uncontrolled colonic inflammation.Thus patients who have long-standing, extensive colitis are at highest risk.
Extraintestinal Complications include
Vitamin deficiency (A, B12, C, D, E, K): Osteomalacia, muscular atrophy, night blindness, hyperkeratoses and anaemia.
Mineral deficiency (iron, calcium, magnesium, zinc): Anaemia,osteomalacia, growth retardation, oligospermia, immunedeficiency
Protein deficiency: Oedema
Hyperoxaluria, water loss: Kidney stones
Bile acid deficiency: Gallstones
Rubrics for Crohns disease, taken from Homoeopathic Medical Repertory by Robin Murphy:
Main Rubric Crohn’s disease-Aloes.,am-caust . ,ars. ,But-ac.,carc.,chin.,hoit.,merc-c,. Nit-ac phos.,prot.,reaj-s.
Aloes: Distension of abdomen, especially epigastrium, with flatus moving about ; worse after meals. Discharge of much flatulency, burning, smelling offensive, relieving pain in abdomen ; after each meal, in evening and morning, before stool.
Cutting across abdomen ; with ill humor, anthropophobia ; not disposed to got into open air, although it relieves.
Abdominal walls painful when rising, pressing to stool, when touched, and when standing erect. Feeling of weakness in abdomen as if diarrhœa would result ; but evacuation did not ensue for eight hours.
Aloes-Fullness in region of liver, pain under right ribs. Abdomen feels full, heavy, hot, bloated. Pulsating pain around navel. Weak feeling, as if diarrhśa would come on. Great accumulation of flatus, pressing downwards, causing distress in lower bowels. Sensation of plug between symphysis pubis and os coccygis, with urging to stool. Colic before and during stool. Burning, copious flatus. Uncertain whether gas or stool will come. Stool passes without effort, almost unnoticed. Lumpy, watery stool. Jelly-like stools, with soreness in rectum after stool. A lot of mucus, with pain in rectum after stool.
Ammonium causticum -Burning rawness in throat. Spasm of the glottis with suffocation; patient gasps for breath. Pain in śsophagus on breathing deeply. Scraping and burning in throat and esophagus. Uvula covered with white mucus.
Ars alb -Cannot bear the sight or smell of food. Great thirst; drinks much, but little at a time. Nausea, retching, vomiting, after eating or drinking. Anxiety in pit of stomach. Burning pain. . Heartburn; gulping up of acid and bitter substances which seem to excoriate the throat. Vomiting of blood, bile, green mucus, or brown-black mixed with blood. Stomach extremely irritable; seems raw, as if torn. Gastralgia from slightest food or drink. ; also faintness, icy coldness, great exhaustion Gnawing, burning pains like coals of fire; relieved by heat.
Butyric acid – Poor appetite. Much gas in stomach and bowels. Cramps in pit of stomach, worse at night. Stomach feels heavy and overloaded. Cramp in abdomen below umbilicus. Bowels irregular. Stool accompanied by pain and straining.
Carcinosin -It is claimed the Carcinosin acts favorably and modifies all cases in which either a history of carcinoma can be elicited, or symptoms of the disease itself exist Indigestion, accumulation of gas in stomach and bowels; rheumatism-Cancerous cachexia.
China -Tender, cold. Vomiting of undigested food. Slow digestion. Weight after eating. Ill effects of tea. Hungry without appetite. Darting pain crosswise in hypogastric region. Hungry longing for food, which lies undigested. Flatulence; belching of bitter fluid or regurgitation of food gives no relief; worse eating fruit. Hiccough. Bloatedness better by movement.Much flatulent colic; better bending double. Tympanitic abdomen. Pain in right hypochondrium. Internal coldness of stomach and abdomen. Gastro-duodenal catarrh. Undigested, frothy, yellow; painless; worse at night.
Merc cor – -Incessant, green, bilious vomiting. Epigastrium very sensitive.Bruised sensation; cecal region and transverse colon painful. Bloated; very painful to least touch Dysentery; tenesmus, not relieved by stool; incessant. Stool hot, bloody, slimy, offensive, with cutting pains and shreds of mucous membrane.
Nitric acid – Great straining, but little passes, Rectum feels torn. Bowels constipated, with fissures in rectum.Violent cutting pains after stools, lasting for hours . Hæmorrhages from bowels, profuse, bright. Prolapsus ani. Hæmorrhoids bleed easily. Diarrhœa, slimy and offensive. After stools, irritable and exhausted. Colic relieved from tightening clothes. Jaundice, aching in liver.
Phosphorus:cutting pains. A very weak, empty, gone sensation felt in whole abdominal Large, yellow spots on abdomen.Very fetid stools and flatus. Long, narrow, hard, like a dog’s. Difficult to expel. Desire for stool on lying on, left side. Painless, copious debilitating diarrhœa. Green mucus with grains like sago. Involuntary; seems as if anus remained open. Great weakness after stool. Discharge of blood from rectum, during stool.
India is projected to have one of the highest disease burden of IBD across the globe. The overall genetic risk and microbial signature in Indian IBD patients are similar to those of patients in the West as demonstrated by the similar incidence of IBD in second-generation Indian immigrants and matching perturbations in the structural and functional component of gut microbiota in Indian studies. The disease characteristics, long-term outcomes including the risk of colorectal cancer .Homoeopathy as a medical system contributed many remedies to cure crohn’s disease.
List of References:
1. Balakrishnan V. Rajesh G.: Inflammatory bowel disease. Munjal YP “API textbook of Medicine”. Vol 1, Ninth edition. Mumbai, The Association of Physicians of India; 2012.p.829-831.
2. Conwell Darwin L., Banks Peter A., Greenberger Norton J., Wu Bechien U., Diseases of pancreas. Longo D.L. “Harrison’s Principles of Internal Medicine”. Vol 2, 16th edition. New york, McGraw-Hill, Medical Pub. Division;2012. P.1776-1789.
3. Forsmark Chris E. Pancreatitis. “GOLDMAN-CECIL MEDICINE”. Vol.1, 25th edition. Philadelphia, Elsevier Saunders; 2016.p:959-963.
4. Murphy Robin ND. Diseases. “Homoeopathic Medical Repertory”. 2nd revised edition. New Delhi, B. Jain Publishers; 2006, 2008.p:430.
5. Kedia S, Ahuja V. Epidemiology of inflammatory bowel disease in India: the Great Shift East. Inflammatory Intestinal Diseases. 2017;2(2):102-15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5988149/