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      • Poster Session : PS 0314 ; Hematology : Acute Psychosis: A Presentation of Cyanocobalamin Defi ciency Megaloblastic Anemia

        ( Anurag Bahekar ),( Girish Bhageshwar Ramteke ),( Sanjay Dubey ),( Amith R ),( Ankit Meshram ),( Amit Agarwal ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Mental disturbances due to vitamin B12 deficiency have been reported previously as chief or sole symptoms, occasionally even preceding decrease of cobalamin in serum. Frank psychosis related to vitamin B12 defi ciency is considered very rare and has received little attention. We report a 28 yrs young female presenting with acute psychosis due to cyanocobalamine deficiency which reversed with treatment. Presentation was irrelevant talking, picking of clothes, inability to recognize people for 3 days. No fever, headache, vomiting, weakness, head trauma, drug intake, stressor or addiction. No past major illness, psychiatric illness or memory loss. Pt. had weaknes easy fatigability since 2 years was on vegetarian diet. Bladder bowel habits were regular. Hb 2. 9 gm/dl, thrombocytopenia 1 lakh/cumm, normal leucocytes, MCV-142. 7 fi , smear showed dimorphic picture, pencil cells, tear drop cells, anisopoikilocytosis, hypersegmented neutrophils. Diagnosis of megaloblastic anemia was made. CSF, CT head, electrolytes were normal. B12 level 77. 12 pmol/l (N200-800 pmol/l). Endoscopy- atrophic gastritis. Histology-atrophic gastriris. Antiparietal cell antibody-negative. Patient recovered fully within 3 days therapy with Inj. cyanacobalamin 1000 microgm i. m. with no need of antipsychotics at discharge. Biermer`s disease, also called acquired pernicious anemia, disorder of vitamin B12 absorption characterized by megaloblastic anemia, gastrointestinal symptoms, can lead to neurological abnormalities. Frequent in elderly, less in adults(15%), extremely rare inchildren, adolescents. It is asymptomatic for years, non-specifi c symptoms of anemia, atrophic gastritis. Possible mechanism for psychotic behaviour suggested by Hutto, reported cobalamin and folate participate in synthesis of monoamine neurotransmitters in brain by increasing BH4(tetrahydrobiopterin) synthesis. Treatment:Oral administration of high-dose vitamin B(12) (1-2 mg daily) as effective as intramuscular administration in correcting defi ciency. We recommend consideration be given to B-12 defi ciency as an etiological possibility in some cases of depression, organic psychosis, certain childhood-disorders and dementia.

      • Poster Session : PS 0152 ; Neurology : Subacute Sclerosing Pan Encephalitis(SSPE): A Rare Presentation

        ( Amith Ram ),( Bhageshwar Girish Ramteke ),( Anjali Matani ),( Apoorva Paurank ),( Archana Verma ),( Anurag Bahekar ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Subacute Sclerosing Pan-Encephalitis is a prototype neurodegenerative disease of childhood characterised by onset of neurological symptoms between 5 and 15 years of age with a progressive downhill course and death within 2-4 years. Incidence of adult onset SSPE has been reported between 1-1.75% and 2.6%. To-date less than 140 cases of adult onset SSPE have been published, the majority being case reports. A 24 year old male presented with progressive neurological syndrome characterised by very frequent myoclonic jerks associated with brief dystonic posturing of upper limbs for 8 months. No history of seizures, cognitive decline or personality changes, no history-of measles in childhood but immunized. Routine blood investigations normal. EEG-periodic complexes, CSF- mild increase in proteins, normal sugar, cell count. Measles antibody titre elevated, serum as well as CSF levels, CSF/serum antibody quotient 2.62 which was strongly suggestive of SSPE. Other antibody titres were unremarkable. MRI-bilateral & near symmetrical T2 hyperintense signal in posterior putamen, slightly larger on right, restriction of diffusion & are hypo on T1. No cortical or white matter changes seen. Our patient is not classical case of SSPE. Atypical for age, late-onset, qualifi es as adult-onset of SSPE (defi ned onset after 18 years), well preserved cognition. He did not have seizures, spasticity or visual complaints which are common. Imaging fi ndings are also atypical as common fi ndings early in disease are white matter changes and cortical atrophy mainly in the posterior region of brain and the hyperintense signals seen in late course of the disease are seen early in this patient. EEG Stereotyped periodic complexes with normal background and is strongly suggestive SSPE. MRI reveals T2 hyperintense lesions in bilateral putaminal region slightly larger on right side. Treatment: No curative-therapy is available, few disease-modifying agents have been tried which may delay progression.

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