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 Th2 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.
The aims are to commence a life-long gluten-free diet (GFD) and to correct existing deficiencies of iron, folate and calcium. Diet requires the exclusion of wheat, rye, barley and initially oats, although oats may be reintroduced safely in most patients after 6–12 months. It shows a clinical improvement within days or weeks. Morphological improvement often takes months. Celiac disease is a lifelong inflammatory condition that affects multiple organ systems, so regular monitoring of symptoms, weight and nutrition is essential. Rarely, patients are ‘refractory’ and require treatment with corticosteroids or immunosuppressive drugs.
What’s out: Cakes, biscuits, doughnuts, Chapatis/ wheat bread, Asafoetida, Beer, Some health drinks.
What’s in: Rice and ricebased items such as dosa, idly, pongal, appam etc., Ragi, bajra and jowar, Curd, lassi, milk and cream, Fruits and vegetables, Meat.
WHAT IS GLUTEN?
Gluten is insoluble prolamine polypeptides found in wheat (gliadins and glutenins), rye (secalin), barley (hordein) and other closely related grains. Prolamins are damaging factors. These proteins are resistant to digestion and remain in the intestinal lumen triggering immune responses. Modern hexaploid wheats (e.g. Triticum aestivum) have highly antigenic glutens, more capable of inducing celiac disease.
WHAT IS A GLUTEN FREE DIET (GFD)?
In 2000, the Codex Alimentarius Commission of the World Health Organization and the Food and Agriculture Organization described gluten free foods with a gluten level not exceeding 20 ppm and consisting of, or made only from ingredients which do not contain any prolamines from wheat or any Triticum species, such as spelt, kamut or durum wheat, rye, barley, oats, or their crossbred varieties. Gluten intake varies from population to population and depends upon dietary practices. The GFD with the threshold at less than 20 ppm of gluten ensures an intake of less than 50 mg/day and provides a sufficient safety margin.
NON RESPONSIVE CELIAC DISEASE (NRCD) & REFRACTORY CELIAC DISEASE (RCD):-
A small subset of celiac disease patients fails to respond to a glutenfree diet. This condition is referred to as Non responsive celiac disease (NRCD). NRCD can be defined as persistent or recurrent symptoms, signs, or laboratory findings consistent with active celiac disease, despite at least 12 months of treatment with the GFD. A substantial proportion of patients with celiac disease develop NRCD (7%-30% in different series studies). Refractory celiac disease (RCD) can be defined as persistent or recurrent small intestinal villous atrophy with symptoms of malabsorption, despite ≥12 months of a strict GFD, in the absence of an overt lymphoma or another condition that causes villous atrophy. RCD makes up a small subset (approximately 10%) of NRCDs and occurs in 1% to 2% of patients with celiac disease.
COMPLICATIONS OF CELIAC DISEASE:-
The incidence of carcinoma of the oesophagus, enteropathy-associated T cell lymphoma (EATCL), ulcerative jejunitis and small bowel adenocarcinoma is also increased in coeliac disease. A twofold increased risk of malignancy and twofold increase in standard mortality ratio has been reported in adult celiac disease. EATCL is an important mortality risk in patients diagnosed above 50 years of age.
STATUS IN INDIA
Celiac disease is emerging in India. It is estimated that as many as 10 million people in India have undiagnosed celiac disease. While there is a large pool of patients with celiac disease in India, until now, only a fraction of them have been diagnosed. In a community based study, the prevalence of CeD in the Northern part of India to be 1.04% (1 in 96) and the prevalence of seropositivity (anti¬tTG ab) to be 1.44% (1 in 69). 90%95% of CD remains undetected. A retrospective analysis of confirmed cases of celiac disease between 1995 and 2000 in Dayanand Medical College & Hospital (Ludhiana) had shown a significant increase in incidence both males and females compounded annually. The recent upsurge is due to factors like improved awareness among pediatricians, costeffectiveness of serological tests, and increasing pediatric endoscopic facilities.
Celiac disease (CD) was recognized in northern India, primarily in children, since the 1960s. CD affecting adults is also now well recognized in northern India. Differences in CD prevalence between north and south India could be ascribed to differences in dietary patterns (rice being the staple cereal in south India) or due to differences in genetic makeup. Celiac diseses belt in india is Punjab hariyana, up, bihar, rajesthan, uttarakhand, delhi.
Problems and Challenges to Adapting to a Gluten Free Diet (GFD) by Indian Patients :
GFD is a less engaging option and highly burdensome to patient. The exact amount of gluten that people can tolerate without developing deleterious effects is difficult to assess and probably varies between individuals. A recent systematic review considered less than 10 mg of daily gluten intake to be safe and unlikely to cause significant abnormalities.
Problems and Challenges to Adaptation of Gluten Free Diet (GFD) are :
- Inadequate information and education about the disease and food habits. Gluten is present in daily use items such as beer, ice creams, sweets, soups and sauces, malted beverages and many more.
- The GFD can be restrictive in social situations, leading to poor quality of life. A typical North Indian diet, where flat bread is the usual meal, contains about 25–30 g of gluten per day.
- Small scale production of GFD food and Inadequate/no food labelling on the packaged food items. Poor product availability. GF food items are considerably more expensive than regular gluten¬ containing food.
- The contamination of food with gluten at various levels such as during harvesting, storage and packaging of grain, during milling, at the grocery store, at factories.
To maximize successful treatment, improve outcomes, and reduce healthcare costs and disease burden:
- a team based approach is required, including patient, family, physicians, and dietitian, Patient Education and Awareness, proper dietary counseling and supervision of patients,
- production of reliable and affordable gluten free food, and food labelling for gluten contents,
- Examination of infant feeding recommendations and wheat varieties cultivated in the country.
- Establishing nodal centers, common questionnaire to collect data at different centers, studies to estimate community prevalence.
GLUTEN RELATED DISORDERS:-
It includes (1) celiac disease, (2) wheat allergy and (3) non-celiac gluten sensitivity. Gluten related disorders have gradually emerged as an epidemiologically relevant phenomenon with a global prevalence that is estimated around 5%.
- Wheat allergy (WA): Adverse immunologic reaction to proteins contained in wheat and related grains. It is presented as asthma, rhinitis; food allergy (FA), affecting the skin, the gastrointestinal tract or the respiratory tract; wheat dependent exercise induced anaphylaxis (WDEIA) and contact urticaria. The diagnosis of WA is classically based on skin prick tests, in vitro specific Immunoglobulin E (sIgE) assays and functional assays. Challenge tests remain the gold standard for WA diagnosis.
- Non-celiac gluten sensitivity (NCGS):– CD like clinical presentation but there is the absence of celiac-specific antibodies and villous atrophy as well as of any allergy related processes. There is a non-autoimmune non-allergic process. You may be gluten sensitive and not have celiac disease. On the other hand, all those who have celiac disease are gluten sensitive.
IN MANAGEMENT OF CELIAC DISEASE
GFD is currently the only available treatment for celiac disease and instead of GFD some patients suffer from persistent or recurrent symptoms, signs, or laboratory findings consistent with active celiac disease. It is an immunological based disease where there is a need of such therapeutic methods that strengthen a person’s immune and defence system. So Homoeopathy is a good option for treatment of celiac disease. Homeopathic medicines stimulate the body’s own defences. Homoeopathy has shown the positive result in treatment of various auto-immune disorders.
The aim is not only to treat celiac disease symptoms but to address its underlying cause and individual susceptibility. It is the individual with his peculiar idiosyncrasies and constitutional inheritance with which we have to deal. For this, we should have a proper knowledge and understanding of different fields of medical science along with Organon of medicine, Materia Medica and Repertory. Application of this knowledge will help in selection of remedy based upon the individualization and symptoms similarity to regained health by using holistic approach.
Homoeopathic repertory has many rubrics related to celiac disease symptoms. Here are some rubrics related to causative modalities:
General agg. from bread:-
- Kent- GENERALS – FOOD, – bread – agg.
Ant-c. Bar-c. BRY. carb-an. Caust. chin. clem. coff. crot-h. crot-t. kali-c. merc. Nat-m. Nit-ac. Nux-v. olnd. ph-ac. phos. PULS. ran-s. Rhus-t. ruta Sars. sec. Sep. staph. Sulph. sul-ac. teucr. Zinc. zing.
- KNERR- Stomach, Eating, Bread, Aggravation:
BRY, NAT-M, NIT-AC , PH-AC, PULS, RAN-S, LYC , NUX-V, RHUS-T , SARS, SEP, SULPH, VERAT, ZINC, Carb-an, Kali-c, Merc, Ruta, Staph, Sul-ac, Bar-c, Caust, Chin, Cina, Clem, Coff, Hydr, Olnd, Phos, Teucr.
- [Knerr ] Stomach, Eating, Bread, causes, Weakness,: HYDR
- MURPHY- Food – BREAD, general – agg.
acet-ac. aids. Ant-c. Bar-c. BRY. carb-an. Caust. chin. cina clem. coff. crot-h. crot-t. cupr. cycl. erech. Hydr. ign. kali-c. lith-c. LYC. meny. merc. Nat-m. nat-s. Nit-ac. Nux-v. olnd. ph-ac. phos. plat. psor. PULS. ran-s. Rhus-t. ruta Sars. sec. Sep. staph. sul-ac. Sulph. teucr. Verat. Zinc. zinc-p. zing.
- Clark repertory- causation– nat-m, zing
Rye / black bread agg-
- BTPB, Agg., Food and drink: bread, black:
KALI-C, LYC, PH-AC, PULS, Ign, Nit-ac, Nux-v, Phos, Bry, Nat-m, Sulp
- BBCR – CONDITIONS OF AGGRAVATION AND AMELIORATION IN GENERAL – Food – bread – black (rye), agg.
bry. Ign. Kali-c. Lyc. nat-m. Nit-ac. Nux-v. Ph-ac. Phos. Puls. Sep. sulph.
- [Knerr ] stomach, Eating:Bread:Rye bread, bad effects:
KALI-C , LYC, PH-AC, PULS, Ign, Nit-ac, Nux-v, Phos, Bry, Nat-m, Sulph,
- MURPHY- Food – BREAD, general – agg. – rye bread, agg.
bry. lyc. nat-m. Nit-ac. ph-ac. Phos. psor.
- Kent- GENERALS – FOOD, – bread – black,agg.
bry. ign. Kali-c. Lyc. nat-m. nit-ac. nux-v. Ph-ac. phos. Puls. sulph.
- MURPHY- Food – BREAD, general – agg. – black, agg.
bry. ign. Kali-c. Lyc. nat-m. nit-ac. nux-v. Ph-ac. phos. Puls. sep. sulph. Symph.
- MURPHY- Food – BREAD, general – agg. – black, agg.
bry. ign. Kali-c. Lyc. nat-m. nit-ac. nux-v. Ph-ac. phos. Puls. sep. sulph. symph.