PENYAKIT SELIAK DAN MANIFESTASI GANGGUAN SISTEM SARAF PUSAT



Dr Widodo Judarwanto SpA
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

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
· EpilepsI
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 helpful
22,24,45,54 and hypovitaminosis is not always detectable.25,44 Moreover, very often no neurological abnormality is detectable even in the presence of profound vitamin deficiency.
· Calcium
· Folic acid
· Pyridoxine (vitamin B6)
· Vitamin B12
· Biopterin
· Carnitine

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.

TREATMENT POTENTIAL
· Gluten free diet
· Vitamin replacement
· Immunosuppressive treatment

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.
     

    REFERENCES

     

    1. Catassi C, Ratsch IM, Fabiani E, et al. Coeliac disease in the year 2000: exploring the iceberg. Lancet 1994;343:200–3.
    2. Marsh MN. The natural history of gluten sensitivity: defining, refining and re-defining. Q J Med 1995;88:9–13.
    3. Rostoker G, Laurent J, Andre C, et al. High levels of IgA antigliadin antibodies in patients who have IgA mesangial glomerulonephritis but not coeliac disease. Lancet 1988;i:356–7.

    4. Unsworth DJ, Brown DL. Serological screening suggests that adult coeliac disease is underdiagnosed in the UK and increases the incidence by up to 12%. Gut 1994;35:61–4.
    5. Hin H, Bird G, Fisher P, et al. Coeliac disease in primary care: case finding study. BMJ 1999;318:164–7.

    6. Cook HB, Burt MJ, Collett JA, et al. Adult coeliac disease: prevalence and clinical significance. J Gastroenterol Hepatol 2000;15:1032–6

    7. Carlsson AK, Axelsson IE, Borulf SK, et al. Serological screening for celiac disease in healthy 2.5-year-old children in Sweden. Pediatrics 2001;107:42–5.

    8. Reunala T. Dermatitis herpetiformis: coeliac disease of the skin. Ann Med 1998;30:416–8.
    9. Holmes GKT. Coeliac disease and type 1 diabetes mellitus—the case for screening. Diabet Med 2001;18:169–77.
    10. Sategna-Guidetti C, Volta U, Ciacci C, et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am J Gastroenterol 2001;96:751–7
    11. Sorensen HT, Thulstrup AM, Blomqvist P, et al. Risk of primary biliary liver cirrhosis in patients with coeliac disease: Danish and Swedish cohort data. Gut 1999;44:736–8.

    12. Iltanen S, Collin P, Korpela M, et al. Celiac disease and markers of celiac disease latency in patients with primary Sjogren’s syndrome. Am J Gastroenterol 1999;94:1042–6.
    13. Holmes GKT. Neurological and psychiatric complications of coeliac disease. In: Gobbi G, Andermann F, Naccarato S, et al, eds. Epilepsy and other neurological disorders in coeliac disease. London: John Libbey; 1997: 251–64.

    14. Finelli PF, McEntee WJ, Ambler M, et al. Adult celiac disease presenting as cerebellar syndrome. Neurology 1980;30:245–9.

    15. Wills AJ, Turner B, Lock RJ, et al. Dermatitis herpetiformis and neurological dysfunction. J Neurol Neurosurg Psychiatry 2002;72:259–61.

    16. Luostarinen L, Pirttila T, Collin P. Coeliac disease presenting with neurological disorders. Eur Neurol 1999;42:132–5.
    17. Hadjivassiliou M, Gibson A, Davies-Jones GA, et al. Does cryptic gluten sensitivity play a part in neurological illness? Lancet 1996;347:369–71.
    18. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity: a many headed hydra. BMJ 1999;318:1710–1.
    19. Lahat E, Broide E, Leshem M, et al. Prevalence of celiac antibodies in children with neurologic disorders. Pediatr Neurol 2000;22:393–6.
    20. Cooke WT, Smith WT. Neurological disorders associated with adult coeliac disease. Brain 1966;89:683–722.

    21. Ghezzi A, Filippi M, Falini A, et al. Cerebral involvement in celiac disease: a serial MRI study in a patient with brainstem and cerebellar symptoms. Neurology 1997;49:1447–50.
    22. Ward ME, Murphy JT, Greenberg GR. Celiac disease and spinocerebellar degeneration with normal vitamin E status. Neurology 1985;35:1199–201.
    23. Beversdorf D, Moses P, Reeves A, et al. A man with weight loss, ataxia, and confusion for 3 months. Lancet 1996;347:446.
    24. Lu CS, Thompson PD, Quinn NP, et al. Ramsay Hunt syndrome and coeliac disease: a new association? Mov Disord 1986;1:209–19.
    25. Bhatia KP, Brown P, Gregory R, et al. Progressive myoclonic ataxia associated with coeliac disease. The myoclonus is of cortical origin, but the pathology is in the cerebellum. Brain 1995;118:1087–93.

    26. Chinnery PF, Reading PJ, Milne D, et al. CSF antigliadin antibodies and the Ramsay Hunt syndrome. Neurology 1997;49:1131–3.
    27. Smith GD, Saldanha G, Britton TC, et al. Neurological manifestations of coeliac disease. J Neurol Neurosurg Psychiatry 1997;63:550.

    28. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet 1998;352:1582–5.

    29. Pellecchia MT, Scala R, Filla A, et al. Idiopathic cerebellar ataxia associated with celiac disease: lack of distinctive neurological features. J Neurol Neurosurg Psychiatry 1999;66:32–5.
    30. Bushara KO, Goebel SU, Shill H, et al. Gluten sensitivity in sporadic and hereditary cerebellar ataxia. Ann Neurol 2001;49:540–3.

    31. Burk K, Bosch S, Muller CA, et al. Sporadic cerebellar ataxia associated with gluten sensitivity. Brain 2001;124:1013

    32. Combarros O, Infante J, Lopez-Hoyos M, et al. Celiac disease and idiopathic cerebellar ataxia. Neurology 2000;54:2346.
    33. Chapman RW, Laidlow JM, Colin-Jones D, et al. Increased prevalence of epilepsy in coeliac disease. BMJ 1978;2:250–1.

    34. Sammaritano M, Andermann F, Melanson D, et al. The syndrome of intractable epilepsy, bilateral occipital calcifications, and folic acid deficiency. Neurology 1988;38(suppl 1):239.

    35. Ventura A, Bouquet F, Sartorelli C, et al. Coeliac disease, folic acid deficiency and epilepsy with cerebral calcifications. Acta Paediatr Scand 1991;80:559–62.
    36. Magaudda A, Dalla Bernardina B, De Marco P, et al. Bilateral occipital calcification, epilepsy and coeliac disease: clinical and neuroimaging features of a new syndrome. J Neurol Neurosurg Psychiatry 1993;56:885–9.
    37. Lea ME, Harbord M, Sage MR. Bilateral occipital calcification associated with celiac disease, folate deficiency, and epilepsy. Am J Neuroradiol 1995;16:1498–500.
    38. Gobbi G, Bouquet F, Greco L, et al. Coeliac disease, epilepsy, and cerebral calcifications. The Italian Working Group on Coeliac Disease and Epilepsy. Lancet 1992;340:439–43.
    39. Kay HE, Knapton PJ, O’Sullivan JP, et al. Encephalopathy in acute leukaemia associated with methotrexate therapy. Arch Dis Child 1972;47:344–54.

    40. Flament-Durand J, Ketelbant-Balasse P, Maurus R, et al. Intracerebral calcifications appearing during the course of acute lymphocytic leukemia treated with methotrexate and X-rays. Cancer 1975;35:319–25.

    41. Toti P, Balestri P, Cano M, et al. Celiac disease with cerebral calcium and silica deposits: x-ray spectroscopic findings, an autopsy study. Neurology 1996;46:1088–92.
    42. Cronin CC, Jackson LM, Feighery C, et al. Coeliac disease and epilepsy. Q J Med 1998;91:303–8.
    43. Binder HJ, Solitare GB, Spiro HM. Neuromuscular disease in patients with steatorrhoea. Gut 1967;8:605–11.

    44. Kaplan JG, Pack D, Horoupian D, et al. Distal axonopathy associated with chronic gluten enteropathy: a treatable disorder. Neurology 1988;38:642–5.

    45. Simonati A, Battistella PA, Guariso G, et al. Coeliac disease associated with peripheral neuropathy in a child: a case report. Neuropediatrics 1998;29:155–8.
    [Medline]
    46. Polizzi A, Finocchiaro M, Parano E, et al. Recurrent peripheral neuropathy in a girl with celiac disease. J Neurol Neurosurg Psychiatry 2000;68:104–5.
    [Free Full Text]
    47. 4Brucke T, Kollegger H, Schmidbauer M, et al. Adult coeliac disease and brainstem encephalitis. J Neurol Neurosurg Psychiatry 1988;51:456–7.
    [Medline]
    48. Beyenburg S, Scheid B, Deckert-Schluter M, et al. Chronic progressive leukoencephalopathy in adult celiac disease. Neurology 1998;50:820–2.
    [Abstract]
    49. Goldberg D. A psychiatric study of patients with diseases of the small intestine. Gut 1970;11:459–65.
    [Medline]
    50. Hallert C, Derefeldt T. Psychic disturbances in adult coeliac disease. I. Clinical observations. Scand J Gastroenterol 1982;17:17–9.

    51. Dohan FC. Cereals and schizophrenia data and hypothesis. Acta Psychiatr Scand 1966;42:125–52.

    52. Rudin DO. The choroid plexus and system disease in mental illness. III. The exogenous peptide hypothesis of mental illness. Biol Psychiatry 1981;16:489–512.

    53. Marson C, Micchetti R, Volterra V. Coeliac disease and schizophrenia. In: Gobbi G, Andermann F, Naccarato S, et al, eds. Epilepsy and other neurological disorders in coeliac disease. London: John Libbey, 1997: 239–43.

    54. Muller AF, Donnelly MT, Smith CM, et al. Neurological complications of celiac disease: a rare but continuing problem. Am J Gastroenterol 1996;91:1430–5.

    55. Rubinstein A, Liron M, Bodner G, et al. Bilateral femoral neck fractures as a result of coeliac disease. Postgrad Med J 1982;58:61–2.

    56. Hardoff D, Sharf B, Berger A. Myopathy as a presentation of coeliac disease. Dev Med Child Neurol 1980;22:781–3.

    57. Bye AM, Andermann F, Robitaille Y, et al. Cortical vascular abnormalities in the syndrome of celiac disease, epilepsy, bilateral occipital calcifications, and folate deficiency. Ann Neurol 1993;34:399–403.
    [Medline]
    58. Reinken L, Zieglauer H. Vitamin B-6 absorption in children with acute celiac disease and in control subjects. J Nutr 1978;108:1562–5

    59. Morris JS, Ajdukiewicz AB, Read AE. Neurological disorders and adult coeliac disease. Gut 1970;11:549–54.

    60. Hallert C, Astrom J, Walan A. Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol 1983;18:299–304

    61. Dahele A, Ghosh S. Vitamin B12 deficiency in untreated celiac disease. Am J Gastroenterol 2001;96:745–50.

    62. Muller DP, Lloyd JK, Wolff OH. Vitamin E and neurological function. Lancet 1983;1:225–8.

    63. Muller DP, Harries JT, Lloyd JK. The relative importance of the factors involved in the absorption of vitamin E in children. Gut 1974;15:966–71.

    64. Mauro A, Orsi L, Mortara P, et al. Cerebellar syndrome in adult celiac disease with vitamin E deficiency. Acta Neurol Scand 1991;84:167–70.

    65. Battisti C, Dotti MT, Formichi P, et al. Disappearance of skin lipofuscin storage and marked clinical improvement in adult onset coeliac disease and severe vitamin E deficiency after chronic vitamin E megatherapy. J Submicrosc Cytol Pathol 1996;28:339–44.

    66. Cooke WT. The neurological manifestations of malabsorption. Postgrad Med J 1978;54:760–2.

    67. Lerner A, Gruener N, Iancu TC. Serum carnitine concentrations in coeliac disease. Gut 1993;34:933–5.

    68. Rush PJ, Inman R, Bernstein M, et al. Isolated vasculitis of the central nervous system in a patient with celiac disease. Am J Med 1986;81:1092–

    69. Pellecchia MT, Scala R, Perretti A, et al. Cerebellar ataxia associated with subclinical celiac disease responding to gluten-free diet. Neurology 1999;53:1606–8.

    70. Holmes GKT, Prior P, Lane MR, et al. Malignancy in coeliac disease—effect of a gluten free diet. Gut 1989;30:333–8.
    ]
    71. Bardella MT, Molteni N, Prampolini L, et al. Need for follow up in coeliac disease. Arch Dis Child 1994;70:211–3

    72. De Santis A, Addolorato G, Romito A, et al. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med 1997;242:421–3

    73. Wills AJ. The neurology and neuropathology of coeliac disease. Neuropathol Appl Neurobiol 2000;26:493–6

     

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3 thoughts on “PENYAKIT SELIAK DAN MANIFESTASI GANGGUAN SISTEM SARAF PUSAT

  1. Leonardo P

    Halo teman-teman,

    Kalau mungkin teman-teman pernah dengar kata “Rice Cake”, ingin mencoba tapi tidak tahu dimana tempat/toko yang menjualnya, saya bisa membantu teman-teman untuk mendapatkannya (Hub.: Debbie di 021-30731010 atau 70131825). Rice cake ini cocok juga untuk penderita penyakit Celiac yang tidak bisa memakan roti yang terbuat dari gandum dan mengandung glutten.

    Mungkin ada juga yang belum pernah dengar atau belum tau, apa sih “Rice Cake” itu? “Rice Cake” adalah semacam snack sehat yang renyah (Kriuk) dengan bahan dasar beras, tanpa bahan pengawet, pemanis buatan dan proses pembuatannya tidak digoreng sehingga “Rice Cake” ini rendah kalori dan dapat dinikmati tanpa perlu khawatir sakit tenggorokan.

    “Rice cake” (“N_asiKriuk”) bisa langsung dinikmati setiap saat, praktis dan sehat.

    - Sebagai snack : bisa dinikmati dengan topping sesuai selera Anda sambil minum kopi/teh/susu.
    - Sebagai nasi : bisa dinikmati dengan berbagai hidangan kesukaan Anda.

    Rasa kriuk kriuk gurih nikmat akan membuat siapa saja akan ketagihan makan “N_asiKriuk”.

    Bila teman-teman ingin mengadakan pesta, “N_asiKriuk” ini juga bisa dijadikan alternative untuk menu pondokan. Hanya dengan menambah topping saja, “N_asiKriuk” ini sudah renyah (tanpa perlu di panggang/goreng) dan siap untuk disajikan sehingga tamu tidah perlu lama menunggu/antri .

    “N_asiKriuk” sangat praktis untuk sumbangan sembako, karena tidak perlu dimasak lagi sudah bisa langsung dimakan.

    “N_asiKriuk” ini bisa disimpan dalam jangka waktu yang cukup lama (sekitar 6 bulan), jadi teman-teman bisa menyimpannya untuk stock di rumah dan nikmati “N_asiKriuk” setiap saat.

    Note:
    1 dus isi 25 bungkus. Harga Rp. 10.000 per bungkus (isi: 15 pcs/bungkus).

    Terima kasih.

    Debbie

    Reply

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