Dr Widodo Judarwanto pediatrician
- 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 ?
- 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.
- 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 :
- NYERI KEPALA,
- SAKIT KEPALA,
- TANGAN DAN KAKI LEMA DAN KESEMUTAN,
- BADAN LEMAS
SPECIAL REFERENCE :
NEUROLOGY MANIFESTATION IN CELIAC DISEASE
A variety of neurological disorders have been reported in association with coeliac disease including epilepsy, ataxia, neuropathy, and myelopathy. The nature of this association is unclear and whether a specific neurological complication occurs in coeliac disease remains unproved. Malabsorption may lead to vitamin and trace element deficiencies. Therefore, patients who develop neurological dysfunction should be carefully screened for these. However, malabsorption does not satisfactorily explain the pathophysiology and clinical course of many of the associated neurological disorders. Other mechanisms proposed include altered autoimmunity, heredity, and gluten toxicity. This review attempts to summarise the literature and suggests directions for future research.
· Classical coeliac disease is a gluten sensitive enteropathy in which there is small bowel villous atrophy associated with malabsorption, steatorrhoea, and weight loss. However, most patients now present with non-specific or trivial complaints and the diagnosis is only suspected from abnormalities found in routine blood tests such as anaemia or from the results of specific serological tests. Asymptomatic patients with an enteropathy characteristic of coeliac disease are labelled “silent coeliac disease” while other patients who have an apparently normal small bowel biopsy but develop typical histological features later in life are regarded as having “latent coeliac disease”. These observations have led to the concept of a “coeliac iceberg” made up of a visible part of those who are diagnosed clinically and a far larger submerged portion that includes all individuals who are undiagnosed because of atypical, silent, or latent disease.1 Dermatitis herpetiformis is also a gluten sensitive disease and manifests as a blistering skin rash. Dermatitis herpetiformis and coeliac disease can be seen as part of a spectrum of illness characterised by heightened sensitivity to gluten.2 Gluten is found in foods containing wheat, barley, and rye. A gluten free diet (GFD) reverses villous atrophy and the skin changes associated with dermatitis herpetiformis. Although biopsy of small bowel and skin remain the diagnostic “gold standard” for coeliac disease and dermatitis herpetiformis respectively, antibody testing can be a useful supplementary investigation. A range of antibodies can be measured and include antireticulin, antigliadin, antiendomysial, and antitissue transglutaminase (tTG). In terms of sensitivity and specificity antiendomysial antibodies and tTG are the preferred tests for coeliac disease. Antigliadin antibodies occur in association with other conditions.3
· Population screening studies have shown that coeliac disease remains under-diagnosed in adults.4,5 Prevalence rates are as high as 1:82 in adults in New Zealand,6 and 1.3% in healthy Swedish children.7 The variable prevalence rates among different populations may be explained by genetic factors. Ninety per cent of patients with coeliac disease carry the histocompatibility locus antigen (HLA) Dqw2.8 The prevalence of this HLA haplotype varies enormously in different ethnic groups but in the UK population is estimated at 20%.
PREVALENCE OF NEUROLOGICAL COMPLICATIONS IN COELIAC DISEASE
· The true prevalence of neurological complications in coeliac disease is difficult to estimate because of differences in study criteria and variable definitions of “neurological disorder”. Moreover, most prevalence analyses have been performed in selected patient groups in tertiary referral centres.13
· Finelli et al estimated that 10% of patients with coeliac disease develop neurological complications.14
· Retrospective data obtained from our hospital found 263 neurological and psychiatric conditions occurring in 189 out of 620 patients with coeliac disease (some patients had more than one disturbance)
· The commonest three conditions in this series were depression (71 cases), epilepsy (25 cases), and migraine (20 cases). This was a heterogeneous group, including diverse conditions from self poisoning to transverse myelitis.
· Reunala et al found a low prevalence of neurological abnormalities in 305 patients with dermatitis herpetiformis from Finland.8 We recently took detailed histories and performed careful clinical examination in 35 patients with dermatitis herpetiformis and found no evidence for immune mediated neurological damage.15
PREVALENCE OF COELIAC DISEASE IN NEUROLOGICAL POPULATIONS
Luostarinen et al detected 10 new cases of coeliac disease in neurological clinics over a three year period, accounting for 7% of the total (144) new coeliac disease cases in their hospital.16 The spectrum of neurological disorders was heterogeneous, including neuropathy (3), myopathy (1), memory impairment (2), ataxia (1), epilepsy (1), tremor (1), and parkinsonism (1). Seven of the 10 cases had pre-existing gastrointestinal symptoms or vitamin deficiencies.
· In 1996, Hadjivassiliou et al looked for IgG and IgA antigliadin antibodies in two groups of neurological patients.17 The first group of 53 patients had a wide range of idiopathic neurological dysfunction and the second group of 94 patients had specific neurological diagnoses. They found a higher prevalence of positive antigliadin antibodies in the first group compared with the second (57% v 5%). A control group of healthy blood donors had a positive rate of 12%. Subsequently 26 patients from the first group consented to small bowel biopsy and nine had features consistent with coeliac disease. They have subsequently argued that IgG antigliadin antibody positivity is a sensitive marker of gluten sensitivity and may play an important part in the development of neurological illness.18 The high prevalence of antigliadin antibody positivity in their control population (12%) remains unexplained.
· Lahat and co-workers looked at the prevalence of coeliac disease in 167 children with various neurological disorders including migraine and epilepsy.19 Although they found positive IgG antigliadin antibodies in 22 (13%) of 167 patients compared with three (9%) in the control group, none had positive IgA antigliadin or antiendomysial antibodies so duodenal biopsies were not performed. They argued that there was no evidence to support a relationship between coeliac disease and neurological disorders in children and certainly no need to screen for coeliac disease in this population.
NEUROLOGICAL DISTURBANCES IN COELIAC DISEASE
· Spinocerebellar degeneration and cerebellar disease
· Myoclonic ataxia (Ramsay-Hunt syndrome)
· Peripheral neuropathy
· Other neuropsychiatric associations
The increased prevalence of epilepsy in patients with coeliac disease is well documented.33 A high prevalence of coeliac disease has been seen in patients with a curious combination of bilateral occipital calcifications and epilepsy,34–37 mainly from Italian centres. Gobbi et al looked at two groups of such patients and found a high incidence of coeliac disease in patients with unexplained cerebral calcifications and epilepsy (24/31) and a high incidence of cerebral calcifications in patients with coeliac disease and epilepsy (5/12).38 Low serum folate levels were also found which might be attributable either to malabsorption or chronic anticonvulsant therapy. Interestingly, cerebral calcifications have previously been reported in other folate deficiency states.39,40 Silica toxicity may play a part in the pathogenesis of the calcifications.41 This association of intracerebral calcifications with epilepsy and coeliac disease was not found in an Irish study.42 Although coeliac disease occurred with increased frequency in patients with epilepsy (one in 44), no patient had cerebral calcifications on computed tomography. The geographical distribution of patients with this syndrome is unexplained for it appears to be confined largely to Italian populations (fig 1 ).
AETIOLOGY : Role of nutritional deficiencies ?
Nutritional deficiencies may play a part in the development of neurological deficits in untreated coeliac disease because of overt or occult malabsorption. Some of these are briefly discussed below. However, it is now acknowledged that these deficiencies are not sufficient factors as vitamin replacement is rarely helpful22,24,45,54 and hypovitaminosis is not always detectable.25,44 Moreover, very often no neurological abnormality is detectable even in the presence of profound vitamin deficiency.
· Folic acid
· Pyridoxine (vitamin B6)
· Vitamin B12
Altered autoimmunity and inflammatory processes
o Ghezzi and co-workers described a man with coeliac disease whose small bowel biopsy revealed ulceration and an inflammatory infiltrate.21 However, two years after diagnosis, despite a GFD, his gastrointestinal symptoms deteriorated and he was given deflazacort. Gastrointestinal symptoms improved but he subsequently developed a relapsing-remitting brainstem and cerebellar syndrome considered to be due to an inflammatory process. Each relapse was treated with steroids and this appeared to improve his symptoms. Serial magnetic resonance imaging (MRI) during the course of his illness showed multiple enhancing lesions. At the start of his illness, corticosteroid administration improved the appearance of the lesions on MRI. Cerebrospinal fluid examination was initially normal but with subsequent relapses, the presence of oligoclonal IgG bands and an increased cerebrospinal fluid/serum albumin ratio was demonstrated, indicating damage to the blood-brain barrier. However, it could be argued that this patient had coeliac disease and multiple sclerosis, occurring in the same individual by chance.
o An immune mediated mechanism was also suggested in a patient with chronic progressive leukoencephalopathy because of a cerebrospinal fluid lymphocytosis and raised serum immunoglobulin levels.48 A patient with treatment resistant seizures and coeliac disease was described by Rush et al.68 He was found to have an isolated central nervous system vasculitis on brain biopsy. There was clinical and radiographic improvement after treatment with prednisolone and cyclophosphamide.
· Gluten free diet
· Vitamin replacement
· Immunosuppressive treatment
- 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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