Page 345 - Abstract Book KONIKA 18

Neurology

P-NEU-017
Intestinal Tuberculosis Mimicking Crohn’s Disease: A Case Report

Agustina Kadaristiana, Wahyuni Indawati, Fatima Safira Alatas
Department of Child Health, Dr Cipto Mangunkusumo Tertiary General Hospital,
Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia

Abstract
Background Intestinal tuberculosis (ITB) and Crohn’s disease (CD) are chronic granulomatous disease
which shares similar characteristics.The prevalence of CD is increasing in countries where TB is endemic.
Confirming ITB in children is also difficult as bactriological or histological evidence are rarely found.
Objective To demonstrate a practical approach to diagnose ITB and highlighting key differences from CD.
Case A 16-year-old boy presented with chronic recurrent abdominal pain, diarrhea, and weight loss for
three months. He has no clear contact history of TB. Both TB and CD were suspected based on similar
epidemiology and symptomatology. However, he had no stomatitis and rectal bleeding which are often found
in CD. Colonoscopy with ileoscopy is crucial for differentiating CD and ITB. In ITB, linear ulceration and
polypoid lesions is common, while in CD longitudinal aphthous stomatitis, anal fissure and cobblestones
mucosa are frequent.The patient was finally diagnosed with pulmonary and intestinal TB. Nodular infiltrate
in the right apical lung was seen from chest radiography and Mycobacterium tuberculosis was detected from
the gastric aspirate. Colonoscopy showed ulcerative lesions on the large intestine. Once adult fixed dose
anti-tuberculosis was commenced, the patient gained weight and ulcerative lesions on the colonic mucosa
were no longer seen. Conclusion Distinguishing ITB from CD is challenging as tubercle lesion may not
always found. A high index of suspicion ITB guided by TB score, positive respons to therapy, and exclusion
of CD symptoms might aid ITB diagnosis.
Keywords: intestinal TB; crohn’s disease; child; colonoscopy

P-NEU-018
Plasma Exchange as Second-Line Therapy for Pediatric Neuromyelitis Optica
Spectrum Disorder: A Case Report

Achmad Rafli, Agustina Kadaristiana, Cahyani Gita Ambarsari, Irawan Mangunatmadja
Department of Child Health, Faculty of Medicine Universitas Indonesia/Dr. Cipto Mangunkusumo Hospital,
Jakarta, Indonesia
Abstract
Background Neuromyelitis optica spectrum disorder (NMOSD) is a rare antibody-mediated disease of
the central nervous system, affecting the spinal cord and optic nerve. Half of the untreated NMOSD cases
will be wheelchair dependent and blind. High-dose steroids have become a mainstay therapy, nevertheless,
the result may not be satisfying. Therapeutic plasma exchange (TPE) has been reported to be beneficial in
NMOSD cases failed to resolve with steroid treatment. Objective To demonstrate the favorable outcome of
TPE in a child with steroid-resistant NMOSD. Case A 12-year-old girl presented with sudden vision loss and
generalized limb weakness for 3 weeks. She had bilateral optic atrophy, paralysis of cranial nerves III and
IV, and tetraparesis. Her upper and lower extremities somatosensory evoked potentials revealed an axonal
sensorimotor polyneuropathy. She was diagnosed with aquaporin-4 seronegative NMOSD based on the white
matter hyperintensities on a T2 MRI image in the bilateral frontoparietal, bilateral periventricular, and left
occipital lobe with negative anti-aquaporin-4 immunoglobulin G. She was treated with high dose intravenous
methylprednisolone, 1 g daily for 3 days. However, she was unresponsive to it and complicated by sepsis.
Subsequently, five TPE procedures on alternate days were commenced and were tolerated well. Her nerve
function and weakness were gradually improving. She was maintained on azathioprine. Three months after
the TPE courses completion, she was able to sit and has not developed exacerbation. Conclusion TPE is
effective in treating severe acute attacks of NMOSD, particularly as a second-line therapy in children who
have not responded well to steroids.
Keywords: Plasmapheresis; steroids; muscle weakness; paresis; optic atrophy; white matter

KONIKA XVIII Abstract Book 297