Dr Widodo Judarwanto SpA 

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

 
difference between pregnancy-related events in coeliac versus non-coeliac populations

• In a cohort study the proportion of births by caesarean section was almost 30% higher for women with coeliac disease than for the women in the comparison group. The study also showed miscarriages were slightly more common in women with coeliac disease (RR 1.31) and pregnancy experiences such as preeclampsia, postpartum haemorrhage, and still births to be similar between the two groups.
• Also none of the women with coeliac disease had babies with neural tube defects, despite the concerns about folate deficiency in coeliac disease.
• These results indicate that the risks of adverse pregnancy-related outcomes for women with coeliac disease are not as high as previously reported.

Dietary implications in pregnancy for coeliacs

• There are no specific guidelines for pregnant women with coeliac disease. Standard nutritional advice during pregnancy is appropriate for women with coeliac disease and general guidelines are suitable, in particular advice to take folic acid supplements should be followed.
• It is important that people with coeliac disease are followed up regularly, particularly at times of stress, i.e. pregnancy. Patients may experience deterioration in their symptoms and require additional support at this time. Depending on individual assessment and diet, supplementation with calcium, iron, and vitamin B12 may be required.
  
  References
  · Kolho KL et al. Screening for celiac disease in women with a history of recurrent miscarriage or infertility. British Journal of Obstetrics and Gynaecology 1999;106:171-173.
  · Norgard S et al. Birth outcomes of women with celiac disease; A nationwide historical cohort study. American Journal of Gastroenterology 1996;94:2435-2440.
  · Tata LJ et al. Fertility and pregnancy-related events in women with celiac disease: A population-based cohort study. Gastroenterology 2005;128:849-855.
  · Ciacci C et al. Coeliac disease and pregnancy outcome. American Journal of Gastroenterology 1996;91:718-722.
  · Sanders DS et al. A primary care cross-sectional study of undiagnosed adult coeliac disease. Eur J Gastroenterology and Hepatology 2003;4:407-413.
  · Meloni GF et al. The prevalence of coeliac disease in infertility. Hum Reprod 1999;14:2759-2761
  · Collins P et al. Infertility and coeliac disease. Gut 1996;39:382-384.
  · Molteni N et al. Obstetric and gynaecological problems with untreated sprue. Journal of Clinical Gastroenterology 1990;12:37-39.
  · Sher KS and Mayberry JF. Female fertility, obstetric and gynaecological history in coeliac disease. Digestion 1994;55:243-246.

ILUSTRASI KASUS

• Ooh, nyeri benar kepala ku, lagian ini perut ikutan aja bermasalaha. Banyak orang mengalami keluhan sakit kepala dan nyeri kepala saat mengalami sakit perut, hal ini seering dikaitkan karena lapar dan telat makan.
• Benarkah sakit kepala anda karena kelaparan? Adakah hubungan keluhan anda dengan penyakit seliak ? Apakah benar anda bukan penderita seliak ?
  

BACKGROUND

• Penyakit seliak terjadi pada 1% di antara populasi anak dan dewasa. Pada usia dewasa terdapat 2-3 kali lebih banyak perempuan dibandingkan laki-laki. Penyakit ini tidak hanya dikenal di Eropa tetapi juga di Timur Tengah, Asia, Amerika dan Afrika. Meskipun banyak manusia terkena penyakit ini dan angka kejadian semakin meningkat, tetapi masih banyak terjadi underdiagnosis, meskipun bahkan di salah satu negara di Eropa dilaporkan terjadi 1 penderita pada 77 orang.
• Di Indonesia sampai sekarang masih belum diketahui pasti angka kejadiannya, tetapi diduga angkanya tidak jauh dari 1 dibandingkan 100 orang. Penulis mengadakan penelitian pada penderita kesulitan makan pada anak yang berobat di Picky Eaters Clinic Jakarta (Klinik Khusus Kesulitan Makan Pada Anak) diduga sekitar 34% dari populasi anak sulit makan tersebut adalah penderita penyakit seliak, karena saat dilakukan penghindaran terhadap diet gluten terdapat perbaikan klinis yang bermakna.
  Penyakit seliak merupakan penyakit permanen yang bersifat jangka panjang. Beberapa faktor yang berpengaruh terhadap terjadinya penyakit, yaitu faktor genetik, lingkungan dan disebabkan oleh kepekaan terhadap gluten, yaitu protein yang terdapat dalam terigu dan gandum hitam, barley (jewawut) dan gandum. Makanan yang mengandung bahan tersebut adalah roti, biskuit, pasta, saos dan sebagainya. Proses terjadinya kelainan ini adalah adanya antibodi terhadap gluten yang dapat mengganggu permukaan usus halus. Gangguan ini menyebabkan lapisan usus yang berjonjot-jonjot menjadi rata. Permukaan yang rata ini kurang mampu mencerna dan menyerap makanan.
  

MANIFESTASI KLINIS

• Penyakit seliak bisa mengenai berbagai usia dan setiap individu berbeda manifestasi klinis yang terjadi. Beberapa orang gejala mulai tampak saat usia anak pada orang lain timbul saat usia dewasa. Pada usia anak biasanya gejalanya timbul setelah pemberian makanan tambahan baru yaitu sekitar usia 4-6 bulan. Bila makanan tersebut mengandung gluten maka keluhan yang timbul adalah sulit buang air besar, diare, perut kembung dan sering rewel.
• Pada anak yang lebih besar anak biasanya juga disertai keluhan nyeri perut. Beberapa anak mengalami sulit makan, kegagalan pertumbuhan, perut kembung yang terasa sakit, sering buang angin. Bentukan tinja biasanya banyak, berlemak, pucat dan sangat berbau busuk. Bila disiram di atas kloset terdapat bentukan benda padat yang melayang.
  Di dalam mulut terlihat luka seperti sariwan atau disebut aphthus ulcers dan terdapat perubahan warna gigi atau kehilangan enamel gigi. Penderita seliak sering mengalami gigi caries atau gigi keropos. Pada kulit terjadi bintil kemerahan yang agak nyeri dan gatal terutama di daerah bokong, dada atau tangan dan kaki bagian luar yang sering disebut dermatitis herpertiformis.
• Gangguan lain yang bisa terjadi adalah nyeri pada otot, tulang dan persendian atau kejang pada otot. Anak perempuan dengan penyakit seliak mungkin akan mengalami gangguan siklus menstruasi. Bahkan banyak laporan ilmiah menyebutkan gangguan infertilitas atau kesulitan punya anak sering terjadi pada penyakit ini.
  

MANIFESTASI KLINIS NEUROLOGI :

• MIGRAIN,
• NYERI KEPALA,
• SAKIT KEPALA,
• VERTIGO,
• TANGAN DAN KAKI LEMA DAN KESEMUTAN,
• BADAN LEMAS
  

CONCLUSION

• Improved case ascertainment has caused an apparent increase in the prevalence of coeliac disease. This has resulted in a changing pattern of presentation of coeliac disease with so-called atypical symptoms becoming more prominent. However, as coeliac disease becomes more commonly diagnosed, it is likely that some associated diseases may merely be a result of chance.
• The increased prevalence of a variety of neurological conditions in coeliac disease suggests that patients with neurological disease are a target population who might benefit from screening and treatment. However, no firm conclusions can be made regarding the nature of the association between coeliac disease and neurological disorders as the available data are limited by the heterogeneity of patients, inconsistency of pathological findings, and lack of adequate control data.73 A GFD and vitamin supplementation may be helpful in some cases. Data regarding the value of immunosuppressive treatment are anecdotal.
• It can be concluded that the majority of neurological syndromes have a chance association with coeliac disease. There may be a minority with a definite association, such as patients with certain forms of epilepsy, but further study is required to confirm this and the nature of the association. At present, it has to be conceded that a neurological disorder specifically associated with coeliac disease has not been identified. Deficiency of trace elements or vitamins might play an important part and this has considerable therapeutic implications. Thus far, this aspect of treatment has not been studied systematically. The role of altered autoimmunity, particularly in susceptible HLA subgroups, also merits further investigation.
• Finally, with increasing recognition that coeliac disease is under-diagnosed, it would be prudent to be vigilant in all clinical settings where it might be a possible diagnosis. In the context of neurological disease, those patients with unexplained neurological dysfunction such as ataxia should have serological tests to select those who should have a small bowel biopsy for coeliac disease and treatment with a GFD. In the case of newly diagnosed patients with coeliac disease, a careful search for neurological abnormalities should form part of the initial systemic review.
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Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

BACKGROUND

Celiac disease is a unique autoimmune disorder, unique because the environmental precipitant is known. The disorder was previously called celiac sprue, based on the Dutch word sprue, which was used to describe a disease similar to tropical sprue that is characterized by diarrhea, emaciation, aphthous stomatitis, and malabsorption. Celiac disease is precipitated, in genetically predisposed persons, by the ingestion of gluten, the major storage protein of wheat and similar grains. Originally considered a rare malabsorption syndrome of childhood, celiac disease is now recognized as a common condition that may be diagnosed at any age and that affects many organ systems. The therapy for the disease is a gluten-free diet; however, the response to therapy is poor in up to 30% of patients, and dietary nonadherence is the chief cause of persistent or recurrent symptoms. Small intestinal adenocarcinoma, refractory sprue, and enteropathy-associated T-cell lymphoma are complications of celiac disease that must be ruled out when alarming symptoms such as abdominal pain, diarrhea, and weight loss develop despite a strict gluten-free diet.

Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten-containing grains (including wheat, rye, and barley) in genetically susceptible individuals. CD is associated with HLA molecules DQ2 (90%-95%) and DQ8 (5%-10%), and in the continued presence of gluten the disease is self-perpetuating. CD is one of the most common lifelong disorders worldwide and is characterized by a variety of clinical presentations. These include the typical malabsorption syndrome (classic symptoms) and a spectrum of symptoms potentially affecting any organ or body system (nonclassic symptoms). Because CD often is atypical or even clinically silent, many cases go undiagnosed and are exposed to the risk of long-term complications. There is growing interest in the social aspects of CD because the burden of illness related to this condition is doubtless higher than previously thought.

Clinical manifestations of celiac disease vary greatly according to age group. Infants and young children generally present with diarrhea, abdominal distention, and failure to thrive. However, vomiting, irritability, anorexia, and even constipation are also common. Older children and adolescents often present with extraintestinal manifestations, such as short stature, neurologic symptoms, or anemia

MANIFESTATION IN CHILDREN

The symptoms of celiac disease in children typically become apparent three to five months after first consuming gluten- containing foods although for some few cases, the interval may be as short as one month. Several of the experts on infant feeding advise that solid foods should not be introduced to a baby’s diet until nearly five months old and that gluten-containing cereal should be avoided for the first six months of life.
The celiac, but otherwise normal baby, thrives until gluten is introduced into the diet and then begins to refuse feedings and fails to gain weight. The child may gradually become irritable or listless and develop a large abdomen. The stools will typically become abnormal, perhaps large, pale and offensive, or representative of a loose-like diarrhea. Stools generally float because of the high content of air and fat. The child may also vomit from time-to-time or in some cases exhibit forceful projectile vomiting with the consumption of selected gluten-containing foods. Many children lose weight or have a failure to gain weight and the buttocks become flattened. Some few children may become quite ill with acute diarrhea and dehydration. Symptoms vary and are different from one celiac child to the next with no two being alike in how the condition “acts out” for them and in their bodies.

Older children with more subtle symptoms of poor appetite, poor growth, and anemia are much more difficult to diagnose as there are many other reasons for failure to grow in childhood. Clinical symptoms often diminish or disappear during puberty [adolescence], although biochemical or morphologic abnormalities of the celiac condition may persist. More active symptoms will again reoccur in early adult life following the period when the immune system appears to “give more of its attention” to sexual develop- ment. While the teen may feel that he or she has “grown out of the disease,” the actuality is that the condition continues and should [must] be treated with the same strict gluten-free diet.

Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. Gluten is a protein component in wheat, a staple food for most populations in the world, and other cereals (rye and barley). The major CD-predisposing genes are located in the HLA region, namely the HLA-DQ2 and/or DQ8 genotypes found in at least 98% of patients. CD is one of the most common lifelong disorders in Europe and in the United States. This condition can manifest with a previously unsuspected range of clinical presentations, including the typical malabsorption syndrome (chronic diarrhea, weight loss, abdominal distention) and a spectrum of symptoms potentially affecting any organ or body system. Because CD often is atypical or even clinically silent, many patients remain undiagnosed and are exposed to the risk of long-term complications, such as osteoporosis, infertility, or cancer. The burden of illness related to CD is doubtless higher than previously thought and there is growing interest in the social dimensions of this condition. Although CD can present at any age, including the elderly, typical cases often manifest in early childhood.

In 1888,
Clinical Manifestation of CD in Pediatrics
Manifestations secondary to untreated CD
Associated diseases (or secondary to untreated CD?)
Genetic-associated diseases
CD with classic symptoms
Autoimmune diseases
Down syndrome
Abdominal distension
Type 1 diabetes
Turner syndrome
Anorexia
Thyroiditis
Williams syndrome
Chronic or recurrent diarrhea
Sjogren’s syndrome
IgA deficiency
Failure to thrive or weight loss
Neurologic and psychologic disturbances
Irritability
Ataxia
Muscle wasting
Autism
Celiac crisis (rare)
Depression
CD with nonclassic symptoms
Epilepsy with intracranial calcifications
Arthritis
IgA nephropathy
Aphthous stomatitis
Osteopenia/osteoporosis
Constipation
Dental enamel defects
Dermatitis herpetiformis
Hepatitis
Iron-deficient anemia
Pubertal delay
Recurrent abdominal pain
Short stature
Vomiting

The clinical spectrum of CD in children is wide

Histologic and Clinical Manifestations of CD in Pediatrics

Clinical form
Histologic and clinical manifestations
CD with classic symptoms
Fully expressed enteropathy
Intestinal symptoms
CD with nonclassic symptoms
Fully expressed enteropathy
Extraintestinal manifestations
Silent
Fully expressed enteropathy
Minimal complaints or symptom-free (occasionally discovered by serologic screening)
Potential
Minimal changes enteropathy or normal small intestinal mucosa
Sometimes symptomatic

CD with classic symptoms
This form is characterized by gastrointestinal manifestations starting between 6 and 24 months of age, after the introduction of gluten in the diet. Infants and young children typically present with impaired growth, chronic diarrhea, abdominal distention, muscle wasting and hypotonia, poor appetite, and unhappy behavior. Within weeks to months of starting to ingest gluten, weight gain velocity decreases and, finally, weight loss can be observed. A celiac crisis, characterized by explosive watery diarrhea, marked abdominal distension, dehydration, electrolyte imbalance, hypotension, and lethargy, was described more commonly at the beginning of this century, but it is now observed rarely. Despite a wide variability between countries, typical CD still represents a common presentation in the pediatric age group.

CD with nonclassic symptoms
Currently, there is a general trend of delayed onset of symptomatic CD involving older children (5-7 years old). These children tend to experience unusual intestinal complaints (eg, recurrent abdominal pain, nausea, vomiting, bloating, and constipation) or extraintestinal manifestations (eg, short stature, pubertal delay, iron deficiency, dental enamel defects, abnormalities in liver function tests). Dermatitis herpetiformis, a blistering skin disease, at present is regarded as a variant of CD rarely affecting the pediatric population.

Silent CD
CD is defined as silent when typical gluten-sensitive enteropathy is found in a patient who apparently is healthy. Large numbers of silent cases of CD have been reported in at-risk groups (such as patients with insulin-dependent diabetes and first-degree relatives) and in general population samples enrolled in screening programs. An in-depth clinical examination shows that many of these silent cases are indeed affected with a low-grade illness often associated with decreased psychophysical well being.

Potential CD
A potential form of CD is diagnosed in patients who have anti-endomysium antibodies (AEA) and/or anti-human tissue transglutaminase antibodies, the typical HLA-predisposing genotype (DQ2 or DQ8), but a normal or minimally abnormal mucosal architecture (increased intraepithelial count) at the intestinal biopsy examination. These patients are at risk for developing a typical CD enteropathy later in life.

Untreated CD is associated with a list of diseases and complications
Associated conditions
An increasing number of studies have shown that many CD-associated problems, which originally were described mostly in adults, can indeed be observed in children or adolescents . Osteoporosis is one of the well-known complications of untreated CD. Persistent villous atrophy is associated with low bone mineral density. Several clinical and epidemiologic studies have been published on the association between CD and osteoporosis. However, no conclusive data on the pathogenesis of bone involvement in CD are available yet. Bone alterations once were thought to derive from calcium and vitamin D deficiency secondary to simple intestinal malabsorption. Recently, other causes of bone metabolism impairment have been claimed, including the interaction between cytokines and local/systemic factors influencing bone formation and re-absorption. Further, there is now substantial evidence supporting the concept that a lifelong gluten-free diet (GFD) is the only effective measure to restore bone metabolism to an apparent normality. In the pediatric population, a prompt introduction of a GFD can even lead to a satisfactory recovery of the bone mass. In a group of 14 adolescents with CD. Bone mineral content, bone area, and bone mineral density were significantly lower in CD patients than in controls. Contrary to pediatric patients, adults affected by osteoporosis secondary to CD do not experience spontaneous recovery, and there are no conclusive data on the efficacy of standard therapies for osteoporosis in decreasing the fracture risk. This evidence stresses the need for early diagnosis to prevent CD complications. Supplementation of the GFD with vitamin D should be considered because a lifelong GFD may not contain adequate vitamin D for optimal bone health throughout adult life secondary to elimination of foods fortified in vitamin D.
The existence of a syndrome characterized by epilepsy, occipital calcifications, and CD is accepted widely. The selective involvement of the occipital region also is suggested increased prevalence of associated CD in children with partial epilepsy (no brain calcifications) with occipital but not centrotemporal spikes.

Autism is one of the best-studied associations between CD and behavioral disorders in pediatrics. Pavone et al evaluated 20 healthy controls and 120 patients with CD to identify behavioral problems and autistic features. The investigators also screened 11 patients with infantile autism and 11 age- and sex-matched controls. No celiac cases were detected among the group of autistic patients and, although 2 of them had slightly increased levels of AGA immunoglobulin (Ig)G and AEA, subsequent antibody determinations and jejunal biopsy specimens were normal.Moreover, none of the celiac patients had a positive Diagnostic and Statistical Manual of Mental Disorders III-R test for infantile autism. These results, together with a growing body of literature, seem to dispute a strong association between CD and autism. Systematic, well-designed studies are needed to establish whether gluten per se has a role in causing autistic behavior outside the context of CD.

One of the most controversial issues concerning the clinical presentation of CD in pediatrics is the association between the disease and other autoimmune disorders. Currently, 2 main theories have been proposed to explain this association. The first theory postulates that this association is secondary to a linkage disequilibrium of genes predisposing for both CD and the associated autoimmune disease. The alternative theory suggests that CD leads to the onset of other autoimmune disorders in genetically susceptible individuals. This second hypothesis is supported by the evidence that tissue transglutaminase seems to be only one of the autoantigens involved in gluten-dependent autoimmune reactions. Other autoantigens, normally cryptic to the immune system, can be unmasked and cause a self-aggressive immunologic response after the gliadin-initiated inflammatory process. In fact, persistent stimulation by some proinflammatory cytokines such as interferon-γ and tumor necrosis factor-α can cause further processing of autoantigens and their presentation to T lymphocytes by macrophage-type immunocompetent cells (the so-called antigen-presenting cells). The phenomenon of antigen spreading has been described in well-defined natural models such as type 1 diabetes, whose clinical manifestations appear after the patient has produced an autoimmune response to various autoantigens (ie, anti-insulin, anti-β cell, and so forth), and also might be present in CD. This would explain the high incidence of autoimmune diseases and the presence of a large number of organ-specific autoantibodies in some celiac patients on a gluten-containing diet. The question of the possible role of an early treatment of CD on the development of autoimmune complications still is open to debate. Ventura et al reported that children with untreated CD have a higher than expected prevalence of organ-specific autoantibodies (apparently gluten-dependent) that tend to disappear after starting the GFD. This study provided laboratory data supporting the hypothesis that a GFD started early in life may prevent the other autoimmune diseases. A recent increased prevalence of autoimmune disorders also is increased in first-degree relatives of CD patients. Increase of autoimmune diseases among relatives, a risk that increased with age. A subgroup of these relatives was diagnosed with silent CD and their prevalence of autoimmune disorders as compared with first-degree relatives not affected by CD was significantly higher with an odds ratio of 6.3.The investigators concluded that first-degree relatives of CD patients have an increased risk for autoimmune disease, most likely related to unrecognized CD. On the other hand, duration of gluten exposure in adult celiac patients does not correlate with the risk for autoimmune disorders.
The strong association with autoimmune thyroid disease is confirmed by the study found a 7.8% prevalence of associated CD in children with either autoimmune thyroiditis or Graves disease. The average prevalence of CD among children with type 1 diabetes mellitus in 26 reports is 4.5% (.97-“16.4%). To quote some European data, recent studies found a disease association in 6.3% of diabetic patients in Germany (205 children),6.2% in Italy (273 children),10.4% in Denmark (106 children), 3.0% in Austria (403 children), and 3.9% in Spain (177 children). The prevalence of the association of CD and type 1 diabetes reported in children living in North America is similar to that reported in Europe Wisconsin British Columbia and in the multicenter United States study.7

Genetic associated diseases
Several genetic disorders have been associated with CD . Among others, the association between Down syndrome and CD is one of the best studiedThe situation is not different in the United States, where the reported prevalence ranges between 3.2% and 10.3%. In Down syndrome children, CD is not detectable on the basis of clinical findings alone and therefore is underdetected. Even when symptoms are present, they may be considered clinically insignificant or possibly attributed to Down syndrome itself. Nevertheless, the reported resolution or improvement of gastrointestinal complaints on a GFD for all symptomatic patients suggests that identification and treatment can improve the quality of life for these children.

END POINTS
CD is a common disorder in children as well as in adults. The spectrum of clinical presentations is wide, and currently extraintestinal manifestations (eg, anemia or short stature) are more common than the classic malabsorption symptoms. A high degree of awareness among health care professionals and a liberal use of serologic CD tests can help to identify many of the nonclassic cases. Therefore, the primary care pediatrician has a central role in this process of case finding. Many key questions about this unique condition remain unanswered . The answer to some of these questions may provide a better understanding of the pathophysiologic mechanisms involved in the pathogenesis of CD, and possibly of other autoimmune diseases, paving the way to innovative treatment strategies.

Table Unresolved Issues in Pediatric CD
Is CD in children and adults the same disease?
What dictates the age of onset of the disease and the type of symptoms? Age of gluten introduction? Amount of gluten?
What are the mechanisms for failure of gluten tolerance? Early gluten introduction? Gastrointestinal infections? Abnormal increase in intestinal permeability?
Role of breast feeding: delay onset of symptoms vs disease prevention
Whom to screen? How to screen? When to screen?
Should asymptomatic children always be treated?
Association with other autoimmune diseases: gene segregation or cause and effect?

References

· Catassi C, Fabiani E, Ratsch IM, Coppa GV, Giorgi PL, Pierdomenico R. The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects. Acta Paediatr Suppl 1996;412:29-35.
· Hill I, Fasano A, Schwartz R, Counts D, Glock M, Horvath K. The prevalence of celiac disease in at risk groups of children in United States. Pediatr Res 2000;136:86-90.
· Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas JE, Erlich H, Bugawan TT, Sokol RJ, Taki I, Norris JM,
· Catassi C, Fasano A. New developments in childhood celiac disease. Curr Gastroenterol Rep 2002;4:238-243.
· Barera G, Mora S, Brambilla P, Ricotti A, Menni L, Beccio S, Bianchi C. Body composition in children with celiac disease and the effects of a gluten-free diet: a prospective case-control study. Am J Clin Nutr 2000;72:71-75.
· Labate A, Gambardella A, Messina D, Tammaro S, Le Piane E, Pirritano D. Silent celiac disease in patients with childhood localization-related epilepsies. Epilepsia 2001;42:1153-1155.
· D’Amico MA, Holmes J, Stavropoulos SN, et al. Presentation of pediatric celiac disease in the United States: prominent effect of breastfeeding. Clin Pediatr (Phila) 2005;44:249-258.
· Green PHR, Stavropoulos SN, Panagi SG, et al. Characteristics of adult celiac disease in the USA: results of a national survey. Am J Gastroenterol 2001;96:126-131.
· Rampertab SD, Pooran N, Brar P, Singh P, Green PH. Trends in the presentation of celiac disease. Am J Med 2006;119(4):355.e9-355.e14. Pavone L, Fiumara A, Bottaro G, Mazzone D, Coleman M. Autism and celiac disease: failure to validate the hypothesis that a link
· Fasano A, Catassi C. Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology 2001;120:636-651.
· Ventura A, Magazzu G, Greco L, SIGEP Study Group for Autoimmune Disorders in Celiac Disease. Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. Gastroenterology 1999;117:297-303.
· Larizza D, Calcaterra V, De Giacomo C, De Silvestri A, Asti M, Badulli C, Autelli M, Coslovich E, Martinetti M. Celiac disease in children with autoimmune thyroid disease. J Pediatr 2001;139:738-740.
· Catassi C, Fasano A. New developments in childhood celiac disease. Curr Gastroenterol Rep 2002;4:238-243.
· Hoffenberg EJ, Emery LM, Barriga KJ, Bao F, Taylor J, Eisenbarth GS, Haas JE, Sokol RJ, Taki I, Norris JM, Rewers M. Clinical
· National Institutes of Health Consensus Conference on Celiac Disease. Available: www.consensus.nih.gov/cons/118/118cdc_intro.htm.
· Hill ID, Dirks MH, Liptak GS, Colletti RB, Fasano A, Guandalini S, Hoffenberg EJ, Horvath K, Murray JA, Pivor M, Seidman EG. Guideline for the diagnosis and treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr 2005;40:1-19.

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CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

Celiac disease is a hereditary intolerance to gluten, a protein found in wheats and, to a lesser extent in barley, rye, and oats. While gluten intolerance is permanent, symptoms can be alleviated by avoiding all gluten from one’s diet. Inflammation occurs when gliadin, a peptide derivative of gluten, found in gluten-containing foods is ingested and presented to T cells. Inflammation causes damage to mucosal tissue of the small intestine, especially the villi that absorb nutrients, which results in malabsoption of food. Celiac disease affects as many as 1 in 300 people in Italy and southwestern Ireland, but is extremely rare in Africa, Japan, and China.

According to a multicenter study in 2003, there is a 1 in 133 chance that people with no risk factors or family history in the U.S. have celiac disease. Additionally, a persons risk increases to a 1 in 22 chance if they have a first-degree relative with celiac disease and a 1 in 39 chance if they have a second-degree relative Around 60,000 Americans are diagnosed with celiac disease annually and a total of over 2 million have the disease, making it perhaps the most common genetic disorder in the United States. Celiac disease can occur at any age, and females are more commonly affected than males. Of females presenting during their fertile years, the male to female ratio is almost 3 to 1

Genetic Risk Factors
Celiac disease is strongly associated with the human leukocyte antigen (HLA) DQ2 and DQ8 haplotypes. HLA genes are part of the major histocompatibility complex (MHC). The function of MHC molecules is to bind peptide fragments derived from pathogens and display them on the cell surface for recognition by T cells. Many proteins involved in antigen processing and presentation are encoded by genes within the MHC

The HLA-DQ2 allele is identified in 90 to 95% of patients with celiac disease, and HLA-DQ8 is identified in most of the remaining patients. Because these alleles occur in 30 to 40% of the general population (with HLA-DQ2 more common than HLA-DQ8), the absence of these alleles is important for its high negative predictive value. Thus, the presence or absence of HLA-DQ2 and HLA-DQ8 is important for determining which family members should be screened with serologic testing and is useful for ruling out the disease in patients already on a gluten-free diet or for patients in whom the diagnosis is unclear.

Symptoms of celiac disease are caused by a glutamine and proline rich 33-mer peptide found in gluten that initiates the inflammatory response when bound to these HLA haplotypes (Shan, Lu et al, 2002). The primary HLA association in most patients with celiac disease is with DQ2 (DQA*05/DQB1*02) and in a minority of patients with DQ8 (DQA1*03/DQB1*0302).

Approximately 97% of individuals with celiac disease have the HLA-D2Q or HLA-DQ8, compared to 40% of the general population (NIH, 2006). The x-ray crystal structure of the soluble domain of HLA-DQ2 was observed bound to the deaminated gluten epitope alpha-I-gliadin. The HLA association in celiac disease can be explained by a superior ability of DQ2 to bind the repertoire of proline-rich gluten peptides that have survived gastrointestinal digestion and that have been deaminated by tissue transglutaminase

Celiac disease is diagnosed in about 10% of first degree relatives of an individual with celiac disease. Although hereditary factors play a significant role, genetic factors alone do not explain the development of the disease because the disease is concordant in only 60% to 70% of identical twins. All people with HLA DQ2 and DQ8 do not develop into disease, and others without those alleles can develop celiac disease, so more genes may be involved. Additional factors such as hormones and infectious agents may also be involved in linking the ingestion of gluten with a chronic inflammatory reaction in the intestine in genetically predisposed individuals

REFERENCE

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

THE GREAT IMMITATOR
Many medical institutions provide lists of symptoms and health problems associated with Celiac Disease and gluten sensitivity. The list I present here is a compilation of several such lists. I have found these lists lacking in explanations of how gluten is related to each symptoms or condition. Furthermore, these lists lack descriptions of the conditions for the non-medical person (“What the heck is ‘aphthous stomatitis’, anyway?”). I am developing this list not only for the reader’s interest, but also for my own easy reference.

The very length of the lists made me dubious at first – how could one thing cause so much? Even more so, how could one thing cause or contribute to opposite problems like skinniness and obesity, diarrhea and constipation, insanity and genius? The very idea was hard to swallow, as it were. Once I could no longer deny that gluten does indeed cause and contribute to many problems as I found them in my body, I decided to teach myself how wheat gluten can do it all.

Let me point out now that having none of the following conditions is no proof that you are free from sensitivity to gluten. Neither is having any of these symptoms proof that you are sensitive. But all of these symptoms (and more not listed) should cause suspicion of gluten intolerance – some should cause a LOT of suspicion. Celiacs who have chronic symptoms are expected to develop even more chronic symptoms if they don’t stop eating gluten.[1] (Maybe a new one every two to six years, give or take?) All research papers cited in the following annotations conclude that ALL people with the listed conditions should be tested.

This annotated list is intended to be informative rather than diagnostic – I want to raise curiosity and suspicion. Readers are most strongly encouraged to further study any listed symptoms they recognize in themselves, their blood relatives, and their friends. Your doctor can only work with you 15 minutes at a time – You are with yourself at least most of the time. Caveat: Even though some very serious factors other than gluten sensitivity (such as tumors) can be involved with many of these problems, gluten sensitivity is common if not pandemic in its association with the listed symptoms and conditions.

Because a number of common factors of gliadin sensitivity lie under many different symptoms and diseases, I have prepared a short essay titled The Basics Factors of Gluten Sensitivity and Celiac Disease. The following descriptions make many references to the factors discussed in that essay.

Celiac Symptoms from Celiac Sprue Association/USA, Inc.
· Muscle Twitch
· Irritability.
· Diarrhea.
· Underweight
· Gas
· Delayed growth.
· Problems with memory and concentration.
· Anemia.
· Fatigue
· Bone problems. If you are interested in a specific condition for which you know the name, look in The Long List. Otherwise, please check out The Short List, which is organized by general subjects of high interest. The initial sources for the conditions I list here came from many lists on medical sites – if you are interested, please see the Symptom Lists From Established Medical Sites a ways down this page.

The Short List:
(Developer’s Note: This annotation is an ongoing project. I have 3+ years of research collected, but little time now to put it on line. Subjects that friends or family ask about have priority. Underlined entries are hypertext links to annotation pages that are at least partially developed.)
Diabetes
Headaches/Migraines
Rashes/Skin Problems
Arthritis
Brain/Nerve Damage
Seizures
Thyroid Disease
Developmental Disorders
Heart Disease
Sexual Issues
Depression/Mood Problems
Digestive Problems
Eye Problems
Hair Loss/White Hair
Food Cravings
Birth Defects
Alcoholism/Drugs
Skinniness/Obesity
Fatigue
Infertility, Miscarriage and other Reproductive Problems
Mouth/Dental
Lungs/Colds
Malabsorption
Weak Bones
Dizziness/Clumsiness
Eccentricity/Genius
Muscle Pain
Social Problems
Vitamin Deficiencies
Bad Teeth
Shortness/Delayed Growth
Pancreas/Gall Bladder
Cancer/Leukemia
Frequent Colds/Lung Infections

The Long List:
Some conditions appear more than once in this list where I may include both a technical name and multiple common names for a single condition.
Abdominal Distention
Abdominal Pain, Recurrent
Acid Reflux
Acne
ADD/ADHD
AIDS
ALS
Alzheimer’s AI
Addison’s disease (loss of adrenal glands) AI
Alopecia Areata (hair loss)
Anemia
Anxiety and depression
Aphthous stomatitis, Recurrent AI Mal
Arthralgia or arthropathy
Arthritis
Asperger’s Syndrome
Asthma
Ataxia
Autism
Bad Teeth:
Bi-Polar Disorder
Bird-fancier’s lung
Birth Defects
Blindness
Bloating
Bone problems
Bruising, Vitamin K deficiency
Cancer, Lymphoma, Enteropathy-associated T cell
Candidiasis
Carcinoma of the oropharynx, esophagus, and small bowel
Carpal Tunnel/Cubital Tunnel
Cistitis, intersitial
Celiac Disease
Chronic Fatigue
Clumsiness
Cluster Headaches
Colds, Frequent
Colitis, Microscopic and collagenous
Collagenous sprue
Concentration Problems
Constipation
Crohn’s Disease
Cystic Fibrosis
Delayed growth
Delayed puberty
Dementia
Depression
Dermatitis Herpetiformis
Diabetes Type 1 Mellitus
Diabetes Type 2
Diabetes, brittleness of control
Diarrhea
Diarrhea, Osmotic
Diarrhea, Secretory
Diverticulosis / Diverticulitis
Divorce
Dizziness
Down Syndrome
Drug Use
Dry Skin
Duodenal Obstruction
Dyspepsia
Ear Infections / Ear Itching & Drainage
Epilepsy (with or w/o cerebral/ occipital calcification)
Eczema
Failure to thrive
Fatigue
Female Reproductive system problems.
Fibromyalgia
Fibrosing alveolitis
Folate-deficiency anemia
Follicular keratosis
Food Cravings
Frequent respiratory infections
Gas
Gastroparesis (Slow Stomach)
Grave’s Disease
Hair Loss
Hay Fever
Headaches
Heart Disease
Heel Fissures
Hepatitis, Autoimmune (liver problem)
Huntington’s Disease
Hyperactivity
Hypertension
Hypertransaminasemia (liver problem)
Hypoglycemia
Hypoplasia (Bad Teeth)
Hypotonia
Idiopathic pulmonary hemosiderosis
IgA deficiency
IgA nephropathy, mesangial
Infertility
Inflammatory bowel disease
Iron deficiency
Irritability
Irritable Bowel Syndrome (IBS)
Jejunoileitis, Ulcerative
Joint Pain, Chronic
Lactose Intolerance
Leaky Gut
Leukemia
Lung Cavities/Lung Infections
Lupus, Systemic lupus erythematosus
Marriage Problems
Memory Problems
Migraine Headaches
Miscarriages, Abortions
Muscle Twitch
Myasthenia gravis
Myocarditis (heart)
Neuropathy
Night Blindness
Obesity
Occult (hidden) blood in stool
Osteomalcia
Osteoporosis/Osteopenia
Pancreatitis, Recurrent
Pericarditis, Recurrent (heart)
Polymyositis
Polyneuropathy
Potbelly
Primary biliary cirrhosis
Psoriasis
Psychiatric disorders
Pulmonary hemosiderosis
Recurrent abortions
Refractory sprue
Rheumatoid arthritis
Sarcoidosis
Scaly Skin
Schizophrenia
Seizures
Self-Medication
Sexual Problems
Short stature
Sinusitis
Sjögren’s Syndrome
Skin Rashes
Skin Sensitivity and Pain
Skinniness (hollow leg)
Slow Stomach (Gastroparesis)
Snow White Hair
Spinocerebellar syndrome
Social Difficulties
Split Heels
Steatorrhea
Stress/Tension
Stroke (basal)
Tendon Pain Chronic
Tetany
Thrombocytosis (hyposplenism)
Thyroid Problems
Transaminase, elevated concentration = liver problem
Vasculitis
Vomiting
Weight Loss

Some Related Symptom Lists From Established Medical Sites:
(sources for much of the above list) A good, if short list from the University of Chicago Celiac Disease Program.
Main Presentations of Extraintestinal (or ‘Atypical’) Celiac Disease
· Dermatitis herpetiformis
· Permanent enamel hypoplasia
· Iron deficiency anemia that is resistant to oral iron therapy
· Short stature, delayed puberty
· Chronic hepatitis with hypertransaminasemia
· Primary biliary cirrhosis
· Arthritis
· Osteopenia/Osteoporosis
· Epilepsy with occipital calcifications
· Primary ataxia
· Psychiatric disorders
· Infertility

Celiac Features and Associated Conditions from The New England Journal of Medicine
COMMON FEATURES ASSOCIATED CONDITIONS
Adults Definite associations
Iron-deficiency anemia Dermatitis herpetiformis
Diarrhea IgA deficiency
LESS COMMON FEATURES Type 1 diabetes
Children Autoimmune thyroid disease
Diarrhea Sjögren’s syndrome
Failure to thrive Microscopic colitis
Abdominal distention Rheumatoid arthritis
General features Down’s syndrome
Short stature IgA nephropathy
Delayed puberty Possible associations
Gastrointestinal features Congenital heart disease
Recurrent aphthous stomatitis Recurrent pericarditis
Recurrent abdominal pain Sarcoidosis
Steatorrhea Cystic fibrosis
Extraintestinal features Fibrosing alveolitis
Folate-deficiency anemia Lung cavities
Osteopenia or osteoporosis Pulmonary hemosiderosis
Dental-enamel hypoplasia Inflammatory bowel disease
Vitamin K deficiency Autoimmune hepatitis
Hypertransaminasemia Primary biliary cirrhosis
Thrombocytosis (hyposplenism) Addison’s disease
Arthralgia or arthropathy Systemic lupus erythematosus
Polyneuropathy Vasculitis
Ataxia Polymyositis
Epilepsy (with or w/o cerebral calcification) Myasthenia gravis
Infertility Schizophrenia
Recurrent abortions COMPLICATIONS
Anxiety and depression Refractory sprue
Follicular keratosis Enteropathy-associated T-cell lymphoma
Alopecia Carcinoma of the oropharynx, esophagus, and small bowel
Ulcerative jejunoileitis
Collagenous sprue

Celiac Symptoms from Web MD:
· Diarrhea.
· Underweight
· Gas
· Delayed onset of puberty.
· Delayed growth.
· Problems with memory and concentration.
· Depression.
· Frequent respiratory infections.
· Anemia.
· Fatigue
· Bone problems.
· Female Reproductive system problems.

American Journal of Clinical Nutrition. The widening spectrum of celiac disease
Presentations of gluten-sensitive enteropathy
Gastrointestinal symptoms Nongastrointestinal symptoms
——————————————————————————–
Steatorrhea Dermatitis herpetiformis
Duodenal obstruction Infertility or fetal loss
Osmotic diarrhea Anemia
Elevated transaminase concentrations Dementia
Secretory diarrhea Folate or iron deficiency
Recurrent pancreatitis Spinocerebellar syndrome
Weight loss Neuropathy
Occult blood Tetany
Constipation Osteoporosis
Enteropathy-associated T cell lymphoma Arthralgia
Bloating Abdominal pain Developmentally synchronous dental enamel defects
Failure to thrive Fatigue
Vomiting Osteomalcia
Dyspepsia Seizures
Depression
Brittleness of diabetes control

Crohn’s Disease Symptoms from Web MD
● abdominal pain
● diarrhea
● Rectal bleeding
● weight loss
● Fever
● delayed development, stunted growth
● High white blood cell

Inflammatory Bowel Disease Symptoms from Web MD (Ulcerative colitis and Crohn’s disease)
● abdominal pain
● Diarrhea
● Constipation
● Loss of appetite.
● Fever
● Weight loss
● anemia
● Ulcers in the mouth.
● Nutritional deficiencies
● Bowel obstruction
● Bowel ulcers
● Small tears (fissures) in the anus.

Complications of Inflammatory Bowel Disease outside the digestive tract
● Joint pain
● eye problems
● Eye symptoms such as cataracts, ulcers on the cornea, inflammation of the iris and blood vessels (uveitis), and inflammation of the white part of the eyes (sclera). Eye problems occur in less than 10% of people who have IBD.
● skin rash
● Liver
● Urinary tract complications
● Delayed childhood Development
● Blood Clots
● Osteoporosis.

● Hypothyroidism
● fatigue
● weight gain
● constipation
● dry skin
● dry hair
● hair loss
● high cholesterol
● drastically reduced sex drive
● brain fog
● full-feeling neck
● swollen hands and feet
● muscle pain
● carpal tunnel syndrome
● tendonitis

Sjögren’s Syndrome
● Dry, gritty, sandy, or itchy feeling in your eyes
● A “filmy” sensation in your eyes that interferes with vision
● Thick, ropelike strands of dried mucus in your eyes when you wake up in the morning
● Redness and decreased tearing
● Bright lights may bother your eyes
● Inflamed eyelids (blepharitis)
● Eye fatigue
● Decreased amount of saliva
● Difficulty swallowing food without also drinking a liquid
● Abnormal sense of taste
● Sores (fissures) on the tongue and lips
● Numerous cavities and gum (periodontal) disease caused by rapid tooth decay
● Decreased sense of taste and smell
● Mouth may feel full of cotton
● Enlarged saliva glands under the chin (submandibular glands) and in front of the ears (parotid glands) that can be sore and tender.
● Exceptionally dry skin with decreased sweat production
● Skin rashes, bumps, and bruises that can be sensitive to light.
● Vaginal dryness, causing discomfort, itching, and painful intercourse.
● Increased fatigue
● A yeast infection in the mouth (thrush).
● Burning sensation (heartburn) in the chest or throat caused by abnormal backflow of acid and other digestive juices.
● Dry nose and throat, which can lead to sinus infections, bronchitis, and pneumonia
● Allergic reactions to medications, particularly to penicillin and sulfur compounds
● Joint and muscle pain
● Thyroid problems such as hypothyroidism or hyperthyroidism
● Nervous system problems, such as numbness or tingling in extremities, or peripheral neuropathies
● Cold, numb, painful fingers and hands (Raynaud’s phenomenon).
● Pain and difficulty with dentures, which may lead to dental restorations

Symptoms of Mania – the “highs” of bipolar disorder From WebMD
● Increased physical and mental activity and energy
● Heightened mood, exaggerated optimism and self-confidence
● Excessive irritability, aggressive behavior
● Decreased need for sleep without experiencing fatigue
● Grandiose delusions, inflated sense of self-importance
● Racing speech, racing thoughts, flight of ideas
● Impulsiveness, poor judgment, distractibility
● Reckless behavior
● In the most severe cases, delusions and hallucinations

Symptoms of depression – the “lows” of bipolar disorder From WebMD
● Prolonged sadness or unexplained crying spells
● Significant changes in appetite and sleep patterns
● Irritability, anger, worry, agitation, anxiety
● Pessimism, indifference
● Loss of energy, persistent lethargy
● Feelings of guilt, worthlessness
● Inability to concentrate, indecisiveness
● Inability to take pleasure in former interests, social withdrawal
● Unexplained aches and pains
● Recurring thoughts of death or suicide

“Be careful reading medical books. You might die of a mis-print.” — Mark Twain REFERENCE

• Catassi C, Fabiani E, Ratsch IM, Coppa GV, Giorgi PL, Pierdomenico R. The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects. Acta Paediatr Suppl 1996;412:29-35.
• Hill I, Fasano A, Schwartz R, Counts D, Glock M, Horvath K. The prevalence of celiac disease in at risk groups of children in United States. Pediatr Res 2000;136:86-90.
• Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas JE, Erlich H, Bugawan TT, Sokol RJ, Taki I, Norris JM,
• Catassi C, Fasano A. New developments in childhood celiac disease. Curr Gastroenterol Rep 2002;4:238-243.
• Barera G, Mora S, Brambilla P, Ricotti A, Menni L, Beccio S, Bianchi C. Body composition in children with celiac disease and the effects of a gluten-free diet: a prospective case-control study. Am J Clin Nutr 2000;72:71-75.
• Labate A, Gambardella A, Messina D, Tammaro S, Le Piane E, Pirritano D. Silent celiac disease in patients with childhood localization-related epilepsies. Epilepsia 2001;42:1153-1155.
• D’Amico MA, Holmes J, Stavropoulos SN, et al. Presentation of pediatric celiac disease in the United States: prominent effect of breastfeeding. Clin Pediatr (Phila) 2005;44:249-258.
• Green PHR, Stavropoulos SN, Panagi SG, et al. Characteristics of adult celiac disease in the USA: results of a national survey. Am J Gastroenterol 2001;96:126-131.
• Rampertab SD, Pooran N, Brar P, Singh P, Green PH. Trends in the presentation of celiac disease. Am J Med 2006;119(4):355.e9-355.e14. Pavone L, Fiumara A, Bottaro G, Mazzone D, Coleman M. Autism and celiac disease: failure to validate the hypothesis that a link
• Fasano A, Catassi C. Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology 2001;120:636-651.
• Ventura A, Magazzu G, Greco L, SIGEP Study Group for Autoimmune Disorders in Celiac Disease. Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. Gastroenterology 1999;117:297-303.
• Larizza D, Calcaterra V, De Giacomo C, De Silvestri A, Asti M, Badulli C, Autelli M, Coslovich E, Martinetti M. Celiac disease in children with autoimmune thyroid disease. J Pediatr 2001;139:738-740.
• Catassi C, Fasano A. New developments in childhood celiac disease. Curr Gastroenterol Rep 2002;4:238-243.
• National Institutes of Health Consensus Conference on Celiac Disease. Available: www.consensus.nih.gov/cons/118/118cdc_intro.htm.
• Hill ID, Dirks MH, Liptak GS, Colletti RB, Fasano A, Guandalini S, Hoffenberg EJ, Horvath K, Murray JA, Pivor M, Seidman EG. Guideline for the diagnosis and treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr 2005;40:1-19.

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

• Bingley PJ et al. Avon Longitudinal Study of Parents and Children Study Team. BMJ 2004;328: 322-3
• Hogberg L et al. Familial prevalence of coeliac disease: a twenty year follow-up study. Scandinavian Journal of Gastroenterology 2003;38(1):61-5
• Mearin ML et al. Coeliac disease: is it time for mass screening? Best Practice & Research in Clinical Gastroenterology 2005;19(3):441-52
• Catassi C et al. Coeliac disease in the year 2000: exploring the iceberg. Lancet 1994;343:200-203
• Johnston SD et al. Prevalence of coeliac disease in Northern Ireland. Lancet 1997;350:1370
• Kolho KL et al. Undiagnosed coeliac disease is common in Finnish Adults. Scandinavian Journal of Gastroenterology 1998;33:1280-1283
• Csizmadia CG et al. An iceberg of childhood coeliac disease in the \Netherlands. Lancet 1999;353:813
• Catassi C et al. Risk of non-Hodgkin lymphoma in celiac disease. JAMA 2002;287:1413-9
• Riestra S et al. Prevalence of coeliac disease in the general population of northern Spain. Strategies of serologic screening. Scandinavian Journal of Gastroenterology 2000;35:398-402
• Hovell CJ et al. High prevalence of coeliac disease in a population based study from Western Australia: a case for screening? Medical Journal of Australia 2001;175:247-50
• Lagerqvist C et al. Screening for adult coeliac disease – which serologic marker(s) to use? Journal of International Medicine 2001;250:241-8
• Gomez JC et al. Prevalence of celiac disease in Argentina: screening of an adult population in the La Plata area. American Journal of Gastroenterology 2001;96:2700-4
• Pratesi R et al. Prevalence of coeliac disease: unexplained age-related variation in the same population. Scandinavian Journal of Gastroenterology 2003;38:747-750
• Fasano A et al. Prevalence of celiac disease in at-risk and non-at-risk groups in the United States: a large multicentre study. Archives of International Medicine 2003;163:286-92
• Maki M et al. Prevalence of coeliac disease among children in Finland. New England Journal of Medicine 2003;348:2517-24
• West J et al. Seroprevalence, correlates and characteristics of undetected coeliac disease in England. Gut 2003;52:960-5
• Schweizer JJ et al. Coeliac disease in the Netherlands. Scandinavian Journal of Gastroenterology 2004;39:359-64

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

The major causes of subfertility

• Subfertility is defined as a failure to conceive after one year of unprotected regular sexual intercourse. One in six couples have an unwanted delay in conception, with many factors being described as possible causes.
• The relationship between subfertiltiy and coeliac disease has been well described and may be the only presenting feature of coeliac disease

What is the relationship between untreated coeliac disease and subfertilily?

• Studies have shown that the prevalence of unrecognised coeliac disease (as a cause of subfertility) in women presenting to subfertility clinics is in the range of 2.7-3%, a significantly higher prevalence than that found in the general population (1.06%). Molteni et al found that menarche was significantly delayed among untreated patients with coeliac disease. Sher and Mayberry confirmed this and also reported significantly earlier age of menopause. Undiagnosed coeliac disease is also associated with a poorer outcome for the foetus.
• A cohort Danish study found that babies of patients with untreated coeliac disease had significantly lower birth weights than controls. This was not observed in newborns of treated patients, therefore suggesting treatment with a gluten-free diet is of importance in reducing the incidence of foetal growth restriction. The prevalence of low birth weight before and after a gluten-free diet prescribed to coeliac mothers fell from 29% to 0%.
• An increased incidence of miscarriage among patients with untreated coeliac disease has also been reported. Following a gluten free diet, the miscarriage rate among patients with untreated coeliac disease was similar to that of controls. Conversely Kolho et al found no difference in the incidence of coeliac disease among patients with recurrent miscarriage screened for coeliac disease and among healthy controls.
  

References

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

Dr. Widodo Judarwanto, SpA
· Picky Eaters Clinic Jakarta (Klinik Khusus Kesulitan Makan Pada Anak)

Orangtua seorang anak yang bertubuh mungil, sebut saja si Amang berusia 7 tahun, sempat frustasi karena anaknya tidak bisa gemuk dan sulit makan sejak usia 1 tahun. Setelah berkonsultasi dengan berbagai dokter ahli tak ada kemajuan yang dialami anaknya. Akhirnya seorang dokter memvonis anaknya menderita penyakit seliak, sehingga permasalahan anaknya bisa berkurang meskipun sudah terlambat.
Penyakit seliak atau juga sering disebut Celiak Disease, Nontropical Sprue, Enteropati Gluten, Celiac Sprue adalah merupakan suatu penyakit keturunan, dimana terjadi intoleransi terhadap gluten (sejenis protein), yang menyebabkan perubahan dalam usus halus sehingga terjadi gangguan penyerapan nutrisi yang masuk ke tubuh sehingga menyebabkan berbagai gangguan pada fungsi tubuh manusia.
Penyakit seliak terjadi pada 1% di antara populasi anak dan dewasa. Pada usia dewasa terdapat 2-3 kali lebih banyak perempuan dibandingkan laki-laki. Penyakit ini tidak hanya dikenal di Eropa tetapi juga di Timur Tengah, Asia, Amerika dan Afrika. Meskipun banyak manusia terkena penyakit ini dan angka kejadian semakin meningkat, tetapi masih banyak terjadi underdiagnosis, meskipun bahkan di salah satu negara di Eropa dilaporkan terjadi 1 penderita pada 77 orang.
Di Indonesia sampai sekarang masih belum diketahui pasti angka kejadiannya, tetapi diduga angkanya tidak jauh dari 1 dibandingkan 100 orang. Penulis mengadakan penelitian pada penderita kesulitan makan pada anak yang berobat di Picky Eaters Clinic Jakarta (Klinik Khusus Kesulitan Makan Pada Anak) diduga sekitar 34% dari populasi anak sulit makan tersebut adalah penderita penyakit seliak, karena saat dilakukan penghindaran terhadap diet gluten terdapat perbaikan klinis yang bermakna.

PENYEBAB
Penyakit seliak merupakan penyakit permanen yang bersifat jangka panjang. Beberapa faktor yang berpengaruh terhadap terjadinya penyakit, yaitu faktor genetik, lingkungan dan disebabkan oleh kepekaan terhadap gluten, yaitu protein yang terdapat dalam terigu dan gandum hitam, barley (jewawut) dan gandum. Makanan yang mengandung bahan tersebut adalah roti, biskuit, pasta, saos dan sebagainya. Proses terjadinya kelainan ini adalah adanya antibodi terhadap gluten yang dapat mengganggu permukaan usus halus. Gangguan ini menyebabkan lapisan usus yang berjonjot-jonjot menjadi rata. Permukaan yang rata ini kurang mampu mencerna dan menyerap makanan.

Usus Normal

Usus pada Penderita Penyakit Seliak
Berbagai faktor dapat mempengaruhi proses terjadinya penyakit ini, diantaranya adalah faktor genetik, faktor lingkungan dan faktor imunitas saluran cerna. Faktor genetik yang telah diidentifikasi adalah HLA-DQ2 or HLA-DQ8 proteins, yang merupakan produk dari gen HLA. Faktor lingkungan yang berpengaruh adalah pemberian ASI eksklusif, pemberian diet gluten terlalu dini atau terlalu banyak dan infeksi rotavirus saluran cerna pada usia bayi muda. Berbagai faktor inilah yang ikut menentukan mengapa gejala klinis pada penderita berbeda dan sangat bervariasi.

MANIFESTASI KLINIS
Penyakit seliak bisa mengenai berbagai usia dan setiap individu berbeda manifestasi klinis yang terjadi. Beberapa orang gejala mulai tampak saat usia anak pada orang lain timbul saat usia dewasa. Pada usia anak biasanya gejalanya timbul setelah pemberian makanan tambahan baru yaitu sekitar usia 4-6 bulan. Bila makanan tersebut mengandung gluten maka keluhan yang timbul adalah sulit buang air besar, diare, perut kembung dan sering rewel.
Pada anak yang lebih besar anak biasanya juga disertai keluhan nyeri perut. Beberapa anak mengalami sulit makan, kegagalan pertumbuhan, perut kembung yang terasa sakit, sering buang angin. Bentukan tinja biasanya banyak, berlemak, pucat dan sangat berbau busuk. Bila disiram di atas kloset terdapat bentukan benda padat yang melayang.
Di dalam mulut terlihat luka seperti sariwan atau disebut aphthus ulcers dan terdapat perubahan warna gigi atau kehilangan enamel gigi. Penderita seliak sering mengalami gigi caries atau gigi keropos. Pada kulit terjadi bintil kemerahan yang agak nyeri dan gatal terutama di daerah bokong, dada atau tangan dan kaki bagian luar yang sering disebut dermatitis herpertiformis.
Gangguan lain yang bisa terjadi adalah nyeri pada otot, tulang dan persendian atau kejang pada otot. Anak perempuan dengan penyakit seliak mungkin akan mengalami gangguan siklus menstruasi. Bahkan banyak laporan ilmiah menyebutkan gangguan infertilitas atau kesulitan punya anak sering terjadi pada penyakit ini.

KOMPLIKASI YANG TERJADI
Gangguan utama dalam penyakit ini adalah gangguan penyerapan nutrisi yang memasuki tubuh maka gangguan yang dapat terjadi adalah anemia kekurangan zat besi, kadar protein darah menurun drastis, akan terjadi penimbunan cairan dan pembengkakan jaringan atau edema. Pada beberapa penderita, gejala tersebut tidak nampak sampai mencapai usia dewasa. Bila gangguan sudah terjadi sejak usia anak resiko yang akan terjadi adalah gangguan pada tulang-tulang panjang atau osteopeni. Tergantung pada berat dan lamanya kelainan, akibat kadar protein, kalsium, natrium dan kalium darah yang rendah.
Akibat adanya malabsorbsi dapat terjadi karena kekurangan zat gizi yang menimbulkan gagal tumbuh atau gangguan peningkatan berat badan dan tinggi badan. Kekurangan protrombin yang diperlukan dalam proses pembekuan darah akan menyebabkan penderita mudah menjadi memar dan mudah mengalami perdarahan.
Beberapa peneliti menyebutkan penyakit seliak dapat mengakibatkan manifestasi neurologi atau gangguan persarafan, diantaranya adalah epilepsi, kejang, gangguan belajar, gangguan konsentrasi, depresi dan pada anak sering rewel yang tidak diketahui sebabnya. Juga dilaporkan adanya gangguan neuropati perifer dengan gejala kesemutan dan rasa kebas pada kaki dan tangan. Gangguan neurologis lain yang dilaporkan adalah “mielopati“, “ensefalitis brainstem“, “sindrom serebelar”, “myoclonic ataxia” (sindrom Ramsay-Hunt) dan “leukoencefalopati progresif kronik“.
Banyak peneliti mengungkapkan bahwa penderita seliak sering dikaitkan dengan terjadinya penyakit “autoimmune” lainnya seperti: penyakit thyroid, lupus, diabetes tipe 1, penyakit liver, penyakit pembuluh darah kolagen, reumatoid artritis atau sindrom Sjögren’s. Disebutkan penderita seliak akan 50 kali lebih mudah mengalami penyakit diabetes dibandingkan orang normal. Penderita juga 10 kali lebih mudah mengalami kekurangan Imunoglubulin A yang mengakibatkan daya tahan tubuh seseorang berkurang sehingga mudah terserang infeksi demam, batuk dan pilek. Penderita seliak yang tidak tertangani dengan baik akan beresiko menimbulkan proses keganasan (kanker) pada saluran cerna seperti adenocarcinoma dan “Enteropathy-Associated T-Cell Lymphoma“.

PENANGANAN PENDERITA
Diagnosis pasti harus dengan melakukan biopsi usus halus (duodenum), yang menunjukkan permukaannya yang mendatar dengan karakteristik adanya limfositosis intraepithelial, hiperplasia Kripta, atrofi dan pada pemeriksaan ulangan ditemukan perbaikan setelah makanan yang mengandung gluten dihentikan. Kriteria diagnostic yang dikembangkan oleh the European Society for Pediatric Gastroenterology and Nutrition hanya dibutuhkan kriteria perbaikan klinis dengan penghindaran diet gluten. Pemeriksaan darah standar yang dilakukan adalah pemeriksaan antibodi endomysial IgA yang mempunyai petanda spesifik yang tinggi pada penyakit ini dengan akurasi sekitar 100%, pemeriksaan lain adalah dengan antibodi gliadin dengan akurasi yang lebih rendah.
Penghindaran makanan yang mengandung gluten adalah penanganan terbaik yang harus dilakukan.Pemberian makanan di rumah juga harus diperhatikan dari berbagai jenis makanan yang mengandung gluten. Demikian pula bila membeli makanan kemasan harus membiasakan melihat label atau kandungan yang ada di dalam makanan tersebut. Banyak negara maju sudah mencantumkan kandungan bebas gluten dalam makanan kemasan bahkan beberapa restoran juga mencantumkan makanan yang bebas gluten.
Pemberian terapi suportif seperti pemberian kalsium, zat besi, vitamin B dan diet tinggi protein tampaknya harus dilakukan untuk mengurangi kekurangan yang ditimbulkan akibat gangguan penyakit ini.

MISDIAGNOSIS
Mendengar nama penyakitnya saja masih merupakan hal asing bagi telinga masyarakat Indonesia. Bahkan gangguan ini masih dianggap tidak ada atau sangat jarang oleh sebagian klinisi di Indonesia. Hal ini bisa dimaklumi karena di Amerika Serikat yang sudah demikian maju ilmu kedokterannyapun penyakit seliak merupakan penyakit gangguan saluran cerna kronis yang tidak popular dan sering diabaikan keberadaanya. Sehingga dalam penanganan seliak sering terjadi kesalahan diagnosis atau “misdiagnosis”. Apalagi di Indonesia, dengan tingkat pengetahuan dan sarana tehnologi medis yang ada tampaknya kejadian kesalahan diagnosis pada penyakit ini jauh lebih besar.
Dalam beberapa kasus keluhan anemia dan kelelahan dianggap sebagai gejala bukan gangguan saluran cerna seperti chronic fatigue syndrome, depression atau disebabkan berbagai penyakit lainnya. Menurut Reader’s Digest penyakit seliak merupakan salah satu dari 10 penyakit terbesar yang mengalami “misdiagnosed“. Sepuluh Penyakit yang sering terjadi kesalahan diagnosis tersebut adalah hepatitis C, lupus, penyakit seliak, hemochromatosis, aneurysm, penyakit lyme, hypothyroidism, polycystic ovary syndrome, klamidia, and “sleep apnea“.
Kesalahan diagnosis atau diagnosis alternatif yang diberikan pada penderita seliak karena kemiripannya adalah “Irritable Bowel Syndrome“, “Crohn’s disease“, Ulcerative colitis, Ulkus lambung, Divertikulosis, infeksi saluran cerna, Chronic fatigue syndrome, depresi, Diabetic Diarrhea, Diabetic Gastroparesis, alergi makanan, intoleransi makanan, Scleroderma and Ulcerative colitis. Permasalahan “underdiagnosis” di Amerika Serikat diakibatkan karena kesulitan diagnosis, gejala penyakit seliak sama dengan berbagai penyakit lainnya, banyak dokter belum mengetahui penyakit dengan baik, dan hanya beberapa laboratorium yang berpengalaman dan terlatih dalam penanganan penyakit seliak.
Melihat angka kejadian yang cukup tinggi serta resiko yang terjadi dalam gangguan ini sangat beragam dan sangat mengganggu dan berbahaya maka sebaiknya harus lebih mencermati berbagai gejala yang ditimbulkan pada tubuh sejak dini. Bila cermat dan tidak terlambat maka hanya dengan menghindari makanan yang mengandung gluten ternyata manusia bisa terbebaskan dari berbagai ancaman kesehatan yang dapat terjadi. Di Indonesia kasus ini belum banyak ditemukan diduga hanya karena banyak kasus belum terungkap karena banyak “misdiagnosis” yang terjadi. Ancaman besar yang tersembunyi ini ternyata mengintai setiap individu di dunia termasuk di Indonesia.

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

ILUSTRASI KASUS

• Orangtua seorang anak yang bertubuh mungil, berusia 7 tahun, sempat frustasi karena anaknya tidak bisa gemuk dan sulit makan sejak usia 1 tahun. Setelah berkonsultasi dengan berbagai dokter ahli diagnosis yang diberikan selalu berbeda. Dokter satu mendiagnosis tbc atau orang awan mengenal dengan penyakit “flek paru”, sedangkan dokter lain bilang hanya kurang enzim pencernaan, dokter lain lagui mengatakan wah anak ibu sehat2 aja hanya ibu kurang pandai merawat. Akhirnya seorang dokter memvonis anaknya menderita penyakit seliak, sehingga permasalahan anaknya bisa berkurang meskipun sudah terlambat.
  

BACKGROUND

• Mendengar nama penyakitnya saja masih merupakan hal asing bagi telinga masyarakat Indonesia. Bahkan gangguan ini masih dianggap tidak ada atau sangat jarang oleh sebagian klinisi di Indonesia. Hal ini bisa dimaklumi karena di Amerika Serikat yang sudah demikian maju ilmu kedokterannyapun penyakit seliak merupakan penyakit gangguan saluran cerna kronis yang tidak popular dan sering diabaikan keberadaanya. Sehingga dalam penanganan seliak sering terjadi kesalahan diagnosis atau “misdiagnosis”. Apalagi di Indonesia, dengan tingkat pengetahuan dan sarana tehnologi medis yang ada tampaknya kejadian kesalahan diagnosis pada penyakit ini jauh lebih besar.
• Penyakit seliak terjadi pada 1% di antara populasi anak dan dewasa. Pada usia dewasa terdapat 2-3 kali lebih banyak perempuan dibandingkan laki-laki. Penyakit ini tidak hanya dikenal di Eropa tetapi juga di Timur Tengah, Asia, Amerika dan Afrika. Meskipun banyak manusia terkena penyakit ini dan angka kejadian semakin meningkat, tetapi masih banyak terjadi underdiagnosis, meskipun bahkan di salah satu negara di Eropa dilaporkan terjadi 1 penderita pada 77 orang.
  Di Indonesia sampai sekarang masih belum diketahui pasti angka kejadiannya, tetapi diduga angkanya tidak jauh dari 1 dibandingkan 100 orang. Penulis mengadakan penelitian pada penderita kesulitan makan pada anak yang berobat di Picky Eaters Clinic Jakarta (Klinik Khusus Kesulitan Makan Pada Anak) diduga sekitar 34% dari populasi anak sulit makan tersebut adalah penderita penyakit seliak, karena saat dilakukan penghindaran terhadap diet gluten terdapat perbaikan klinis yang bermakna.
• Penyakit seliak merupakan penyakit permanen yang bersifat jangka panjang. Beberapa faktor yang berpengaruh terhadap terjadinya penyakit, yaitu faktor genetik, lingkungan dan disebabkan oleh kepekaan terhadap gluten, yaitu protein yang terdapat dalam terigu dan gandum hitam, barley (jewawut) dan gandum. Makanan yang mengandung bahan tersebut adalah roti, biskuit, pasta, saos dan sebagainya. Proses terjadinya kelainan ini adalah adanya antibodi terhadap gluten yang dapat mengganggu permukaan usus halus. Gangguan ini menyebabkan lapisan usus yang berjonjot-jonjot menjadi rata. Permukaan yang rata ini kurang mampu mencerna dan menyerap makanan.
  

MANIFESTASI KLINIS

• Penyakit seliak bisa mengenai berbagai usia dan setiap individu berbeda manifestasi klinis yang terjadi. Beberapa orang gejala mulai tampak saat usia anak pada orang lain timbul saat usia dewasa. Pada usia anak biasanya gejalanya timbul setelah pemberian makanan tambahan baru yaitu sekitar usia 4-6 bulan. Bila makanan tersebut mengandung gluten maka keluhan yang timbul adalah sulit buang air besar, diare, perut kembung dan sering rewel.
  Pada anak yang lebih besar anak biasanya juga disertai keluhan nyeri perut. Beberapa anak mengalami sulit makan, kegagalan pertumbuhan, perut kembung yang terasa sakit, sering buang angin. Bentukan tinja biasanya banyak, berlemak, pucat dan sangat berbau busuk. Bila disiram di atas kloset terdapat bentukan benda padat yang melayang.
• Di dalam mulut terlihat luka seperti sariwan atau disebut aphthus ulcers dan terdapat perubahan warna gigi atau kehilangan enamel gigi. Penderita seliak sering mengalami gigi caries atau gigi keropos. Pada kulit terjadi bintil kemerahan yang agak nyeri dan gatal terutama di daerah bokong, dada atau tangan dan kaki bagian luar yang sering disebut dermatitis herpertiformis.
• Gangguan lain yang bisa terjadi adalah nyeri pada otot, tulang dan persendian atau kejang pada otot. Anak perempuan dengan penyakit seliak mungkin akan mengalami gangguan siklus menstruasi. Bahkan banyak laporan ilmiah menyebutkan gangguan infertilitas atau kesulitan punya anak sering terjadi pada penyakit ini.
  

SERING SALAH DIAGNOSIS ATAU MISDIAGNOSIS

• Mendengar nama penyakitnya saja masih merupakan hal asing bagi telinga masyarakat Indonesia. Bahkan gangguan ini masih dianggap tidak ada atau sangat jarang oleh sebagian klinisi di Indonesia. Hal ini bisa dimaklumi karena di Amerika Serikat yang sudah demikian maju ilmu kedokterannyapun penyakit seliak merupakan penyakit gangguan saluran cerna kronis yang tidak popular dan sering diabaikan keberadaanya. Sehingga dalam penanganan seliak sering terjadi kesalahan diagnosis atau “misdiagnosis”. Apalagi di Indonesia, dengan tingkat pengetahuan dan sarana tehnologi medis yang ada tampaknya kejadian kesalahan diagnosis pada penyakit ini jauh lebih besar.
• Dalam beberapa kasus keluhan anemia dan kelelahan dianggap sebagai gejala bukan gangguan saluran cerna seperti chronic fatigue syndrome, depression atau disebabkan berbagai penyakit lainnya. Menurut Reader’s Digest penyakit seliak merupakan salah satu dari 10 penyakit terbesar yang mengalami “misdiagnosed“. Sepuluh Penyakit yang sering terjadi kesalahan diagnosis tersebut adalah hepatitis C, lupus, penyakit seliak, hemochromatosis, aneurysm, penyakit lyme, hypothyroidism, polycystic ovary syndrome, klamidia, and “sleep apnea“.
  Kesalahan diagnosis atau diagnosis alternatif yang diberikan pada penderita seliak karena kemiripannya adalah “Irritable Bowel Syndrome“, “Crohn’s disease“, Ulcerative colitis, Ulkus lambung, Divertikulosis, infeksi saluran cerna, Chronic fatigue syndrome, depresi, Diabetic Diarrhea, Diabetic Gastroparesis, alergi makanan, intoleransi makanan, Scleroderma and Ulcerative colitis.
• Permasalahan “underdiagnosis” di Amerika Serikat diakibatkan karena kesulitan diagnosis, gejala penyakit seliak sama dengan berbagai penyakit lainnya, banyak dokter belum mengetahui penyakit dengan baik, dan hanya beberapa laboratorium yang berpengalaman dan terlatih dalam penanganan penyakit seliak.
  Apalagi di Indonesia mungkin saja misdiagnosis tersebut bisa saja lebih besar lagi, bahkan sebagian dokter di Indonesia menganggap bahwa penyakit seliak di Indonesia tidak ada. Di Indonesia sering kasus seperti ini terjadi misdiagnosis dengan penyakit tuberkulosis paru.
• Melihat angka kejadian yang cukup tinggi serta resiko yang terjadi dalam gangguan ini sangat beragam dan sangat mengganggu dan berbahaya maka sebaiknya harus lebih mencermati berbagai gejala yang ditimbulkan pada tubuh sejak dini. Bila cermat dan tidak terlambat maka hanya dengan menghindari makanan yang mengandung gluten ternyata manusia bisa terbebaskan dari berbagai ancaman kesehatan yang dapat terjadi. Di Indonesia kasus ini belum banyak ditemukan diduga hanya karena banyak kasus belum terungkap karena banyak “misdiagnosis” yang terjadi. Ancaman besar yang tersembunyi ini ternyata mengintai setiap individu di dunia termasuk di Indonesia.

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.

Center for Celiac Disease at The Children’s Hospital of Philadelphia
The Center for Celiac Disease at The Children’s Hospital of Philadelphia is one of the largest of its kind in the United States. Our team of pediatric celiac experts give your child expert care, from initial testing and diagnosis through long-term disease management.
Visit the Celiac Center at CHOP

Celiac Disease Center at Columbia University
Seeks to redefine the future of celiac disease and treatment on an ongoing basis, through continuing advances in research, patient care, and physician and public education.
Visit the Celiac Disease Center at Columbia University

Celiac Sprue Clinic at the Allegheny Center for Digestive Health
In just one-four hour appointment at this clinic, clients meet one on one with a gastroenterologist, an internal medicine MD with a specialty in nutritional deficiencies, a dietician, a CAM practitioner, and a representative from the local support group, providing clients with a comprehensive evaluation and thorough education about this disease.  Contact – 412-359-8956
Visit the Allegheny Center for Digestive Health at Allegheny General

Kogan Celiac Center of the Saint Barnabas Health Care System
The Kogan Celiac Center, located at the Saint Barnabas Ambulatory Care Center, offers comprehensive testing and treatment for celiac disease for adults and children. The Center is dedicated to providing expert services that include early assessment and diagnosis, treatment, education and support to improve the health and well being of those who live with celiac disease.
Visit the Kogan Celiac Center

Northwestern Memorial Hospital (NMH)
Northwestern Memorial Hospital (NMH) is one of the country’s premier academic medical centers and is a major referral center for the Midwest and beyond. NMH provides at total of 897 beds in their Feinberg Pavilion and virtually every medical specialty is represented by the NMH medical staff of 1,545 physicians. NMH provides a range of healthcare services including acute and tertiary inpatient care, ambulatory care, wellness and prevention programs.
Visit Northwestern Memorial Hospital

The Mayo Clinic – Celiac Clinic
At Mayo Clinic, specialists from different medical specialties work together to diagnose and develop treatment plans for hundreds of adults and children who have celiac disease.
Visit the Mayo Clinic Celiac Center

University of Chicago Celiac Disease Center
The University of Chicago Celiac Disease Center is dedicated to raising diagnosis rates and meeting the critical needs of people affected by celiac disease through education, research and advocacy.
Visit the University of Chicago Celiac Disease Center

University of Maryland Center for Celiac Research
The University of Maryland Center for Celiac Research is an institution engaged in clinical care, diagnostic support, education, and clinical and basic science research in Celiac Disease.
Visit the University of Maryland Center for Celiac Research

University of Virginia Health System – The Digestive Health Center of Excellence
To provide excellence and innovation in the care of patients, the training of health professionals and the creation and sharing of health knowledge.
Visit the University of Virginia

William K. Warren Medical Research Center for Celiac Disease
The mission of the Center is to advance the knowledge of Celiac Disease pathogenesis, develop novel diagnostic and therapeutic advances, increase knowledge about celiac disease and provide state-of-the-art clinical care and education to adults and children.
Visit the William K Warren Medical Center

Supported  by
CLINIC FOR CHILDREN

Yudhasmara Foundation

JL Taman Bendungan Asahan 5 Jakarta Indonesia 102010

phone : 62(021) 70081995 – 5703646

http://childrenclinic.wordpress.com/

Clinical and Editor in Chief :

DR WIDODO JUDARWANTO

email : judarwanto@gmail.com

Copyright © 2009, Clinic For Children Information Education Network. All rights reserved.