Celiac disease is actually a multisystem, immunological based disease caused by a protein “gluten” found in many foods (wheat, rye, barley and to some extent oat) and it is an “iceberg” disease. The majority of patients may remain undiagnosed which may leads to simple gastrointestinal problems like diarrhea, malabsorption, anaemia and further consequences may leads to dermatitis herpetiformis, Growth problems & failure to thrive in children or even increase the risk of malignancy/carcinoma of the gastrointestinal tract.
Gluten free diet (GFD) is currently the only conventional treatment for celiac disease and instead of GFD some patients suffer from persistent or recurrent signs and symptoms. Here, there is a need of such therapeutic methods that strengthen a person’s immune and defence system. Homeopathic medicines stimulate the body’s own defences, so homoeopathy may be a good therapeutic mode of treatment of celiac disease.
Keywords: Coeliac disease, celiac disease, Homoeopathy, Repertory, Homoeopathic medicines, Radar Homoeopathic software.
Wheat along with barley and rye are staple foods for the majority of the Indian people but for a long time we couldn’t believe that these foods also cause chronic diarrhoea and malabsorption both in adults and children. Chronic diarrhoea and malabsorption was traditionally recognised to be caused by tropical sprue, IBS, parasitic / bacterial infections or intestinal tuberculosis but celiac disease remained unrecognised as a cause of malabsorption syndrome.
COELIAC DISEASE (CD)
Coeliac disease (CD) is an autoimmune disorder caused by an immune response to the protein gluten found in many foods (wheat, rye, barley and to some extent oat) which results in gluten intolerance. It is a disorder of the small bowel occurring in genetically susceptible individuals. Celiac disease has had several other names, including non-tropical sprue, celiac sprue, adult celiac disease, and gluten-sensitive enteropathy.
Coeliac disease may have an ancient history dating back to the 1st and 2nd centuries AD. In 250 A.D., Aretaeus of Cappadocia referred to his patients (suffering from abdominal pain and diarrhea) as “koiliakos,” which meant “suffering in the bowels.” In 1856, Francis Adams gave sufferers the moniker “celiacs” or “coeliacs.” Samuel Gee, in 1888, suggested that dietary treatment might be of benefit. In 1952, Willem Karel Dicke established that exclusion of wheat, rye and oats from the diet led to dramatic improvement. He described the histologic damage to the intestinal mucosa as being directly related to celiac disease. A relationship with dermatitis herpetiformis was suggested by Samman in 1955.
The iceberg is a common model used to explain the epidemiology of coeliac disease. Coeliac disease occurs world-wide but is more common in northern Europe. The prevalence in the UK is approximately 1%, although 50% of these people are asymptomatic. In a study (Published in 2011), it was found that the prevalence of celiac disease in the north Indian community is 1% (1 in 96). The majority of patients may remain undiagnosed. It has been reported that for each diagnosed case of CD, an average of 5 to 10 cases remain undiagnosed screening studies in Western countries. Regional differences in CD can be explained by genetic, dietary and immunological factors.
CD is actually a multisystem disorder which is present with a variety of manifestations in its clinical expression, depending on the severity and extent of small bowel involvement. Coeliac disease is considered an “iceberg” disease. Less than 50% of adult patients currently present with classical gastrointestinal symptoms. Coeliac disease can present at any age ranging from the first year of life through the eighth decade. In infancy it occurs after weaning on to cereals. In adults peak onset is in the 3rd or 4th decade and females are affected twice as often as males.
Common symptoms of CD are:-
- Gastrointestinal symptoms: – diarrhea, steatorrhea, abdominal bloating, aphthae, weight loss, malabsorption and the consequences of nutrient depletion.
- Nutritional deficiencies: – commonly iron, folate, vitamin D, zinc, vitamin B12, B6.
- A severe skin rash called dermatitis herpetiformis.
- Musculoskeletal problems :- osteoporosis, muscle cramps, joint and bone pain.
- Growth problems and failure to thrive in children.
- Neurologic disorders :- paraesthesia, ataxia, polyneuropathy Seizures etc.
- Missed menstrual periods, Infertility.
Based on the clinical presentation, serology, and biopsy findings, celiac disease has been classified as:-
- Classical celiac disease (dominated by gastrointestinal symptoms).
- Atypical celiac disease (with prominent extra-intestinal symptoms e.g., iron or folate deficiency anemia, osteopenia, failure to thrive, growth and pubertal delay, hepatopathy, dermatitis herpetiformis (DH), IgA nephropathy, neurological symptoms, Infertility and neuropsychiatric symptoms of anxiety and depression).
- Silent celiac disease (asymptomatic individuals with abnormal small intestinal histopathology and serologies ) and
- Latent celiac disease (asymptomatic individuals with positive serology but normal biopsy).
DISEASE ASSOCIATIONS OF COELIAC DISEASE
Celiac disease is associated with other HLA-linked autoimmune disorders – diabetes mellitus type 1, dermatitis herpetiformis (DH), Splenic atrophy, Thyroid disease, Sjögren’s syndrome, IgA deficiency, Down syndrome.
Autoimmune diseases occur 3-10 times more in those with celiac disease than in the general population. In “diabetic diarrhea”, assay of anti-endomysial antibodies and/or a small-intestinal biopsy must be considered to exclude celiac disease.
The aetiology of celiac disease is not known, but environmental, immunologic, and genetic factors all appear to contribute to the disease.
- Environmental factor: – There is the clear association of the disease with gluten.
- Immunologic component: – An immunologic component in the pathogenesis of celiac disease is critical and involves both adaptive and innate immune responses. Serum antibodies—IgA anti-gliadin, IgA anti-endomysial, and IgA anti-tTG antibodies are present. Patients with these antibodies should undergo duodenal biopsy.
- Genetic factors:- The incidence of symptomatic celiac disease varies widely in different population groups (high in whites, low in blacks and Asians) and is 10% in first-degree relatives of celiac disease patients. The HLA molecules DQ2 and, to a lesser degree, DQ8, are intrinsic to the development of CD, playing a major role in the risk of disease development, as well as disease severity.
INDIVIDUALS AT RISK OF CELIAC DISEASE:-
- Genetic : First-degree relatives, Trisomy syndromes, Selective IgA deficiency
- Autoimmune disorders :- Hashimoto’s thyroiditis, Type I diabetes mellitus, Dermatitis herpetiformis, Rheumatoid arthritis, Autoimmune liver disease.
Celiac disease meets the World Health Organization (WHO) criteria for diseases that warrant mass screening. Screening for CD should be considered in unexplained anemia, unexplained gastrointestinal symptoms, Growth failure, idiopathic osteoporosis, unexplained infertility, firstdegree relatives of CD patients, and autoimmune diseases.
The precise mechanism of mucosal damage is unclear but immunological responses to gluten play a key role. After being taken up by epithelial cells, gluten peptides are deamidated by the enzyme tissue transglutaminase (tTG) in the subepithelial layer. They are then able to fit the antigen-binding motif on HLA-DQ2-positive antigen-presenting cells. Recognition by CD4+ T cells triggers a Th1 immune response with generation of pro-inflammatory cytokines. Lymphocytes infiltrate the lamina propria, and increased intraepithelial lymphocytes (IEL), crypt hyperplasia and villous atrophy ensue.
The diagnosis of CD is based on 3 key parameters: (1) case identification, (2) screening tests, and (3) definitive tests. Antibody testing is the first step in diagnosing patients with celiac disease. The diagnosis of celiac disease requires the presence of characteristic histological changes on small-intestinal biopsy together with a prompt clinical and histological response following the institution of a gluten-free diet.
- Small bowel mucosal biopsy: It is ‘gold standard’ for diagnosis. It is obtain from the duodenum orjejunum(multiple samples 4-8). The classical changes seen on biopsy include:- (A) an increase in the number of intra-epithelial lymphocytes (IELs); (B) absence or reduced height of villi (villous atrophy), (C) crypt hyperplasia,; and (D) increased lymphocytes and plasma cells in the lamina propria. A similar appearance can be seen in tropical sprue, eosinophilic enteritis, milk-protein intolerance and occasionally in lymphoma, Crohn’s disease, and gastrinoma. This characteristic histologic appearance that reverts toward normal following the initiation of a gluten-free diet establishes the diagnosis of CD. The uniform classification according to Marsh and its modification should be applied. In cases of histological features suggestive of CD, the diagnosis should be based on ESPGHAN criteria.
- Serology: Antibody testing can be used for dietary monitoring. These antibody tests constitute a valuable screening tool. They usually become negative with successful treatment. Most commercially available antibodies are (a) IgA tTG antibody (anti transglutaminase IgA antibody), (b) IgA EMA antibody (IgA anti-endomysial antibodies) and (c) IgG DGP antibody (Deamidated gliadin peptide). They have a sensitivity and specificity greater than 90%. Currently, DGP antibody testing is recommended for use in IgA-deficient patients to diagnose CD.
- HLA typing: Majority of people with coeliac have one of two types of the HLA-DQ protein. HLA-DQ2 is present in 90–95% of CD patients and HLA-DQ8 in about 8%. The absence of both alleles has a high negative predictive value for coeliac
HLA typing is useful for ruling out the disease, for
example in patients already on a gluten free diet.
- Gluten challenge: The gluten challenge remains the ‘gold standard’ for diagnosis of celiac disease in positive HLA patients on a GFD. Its diagnosis can be definitely excluded if serological and duodenal biopsy results are normal following the 6–8
weeks of the gluten challenge. However, this approach can be troublesome due to exacerbation of symptoms.
- Other investigations: (A) Haematology: Mild or moderate anaemia (50%), Folate deficiency, Iron deficiency, Howell–Jolly bodies due to splenic atrophy. (B) Biochemistry:- reduced concentrations of calcium, magnesium, total protein, albumin or vitamin D and high phosphate. (C) Radiology:- A small bowel follow-through may show dilatation of the small bowel with slow transit. Folds
become thicker. Radiology is now mainly used when a
complication, e.g. lymphoma, is suspected. (D) Bone densitometry (DXA) should be performed on all patients because of the risk of osteoporosis.
- Tropical sprue, bacterial overgrowth in the small intestine, Chronic pancreatitis, Inflammatory bowel disease, IBS, Irritable bowel syndrome, Dermatitis herpetiformis, Parasite infestation.