The Gut Offending the Brain: An Unusual Presentation of Pernicious Anemia Mimicking Catatonic Schizophrenia 2697
Pernicious anemia results from autoantibodies to intrinsic factor (IF), gastric parietal cells, or both which leads to impaired Vitamin B12 absorption and deficiency. Usually manifests with symptoms attributable to anemia, however, neuropsychiatric symptoms may precede commonly known clinical findin...
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Published in | The American journal of gastroenterology Vol. 113; no. Supplement; pp. S1504 - S1505 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
New York
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
01.10.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Pernicious anemia results from autoantibodies to intrinsic factor (IF), gastric parietal cells, or both which leads to impaired Vitamin B12 absorption and deficiency. Usually manifests with symptoms attributable to anemia, however, neuropsychiatric symptoms may precede commonly known clinical findings. We present the case of pernicious anemia with acute onset psychosis and rapid progression into catatonia. A 54-year-old African American woman with no significant medical history presented with hypothermia and cataplexy. Six months prior, she progressively developed social withdrawal and auditory hallucinations which was misdiagnosed as catatonic schizophrenia at two regional hospitals; a diagnosis initially supported by our psychiatry team and unresponsive to lorazepam therapy. Admission laboratory investigations revealed macrocytic anemia (Hemoglobin: 8.3 g/dL; Red blood Cell Mean Corpuscular Volume: 103 fL) and Vitamin B12 deficiency (serum vitamin B12 level < 50 pg/mL). Her serum folate level was normal (14.2 ng/mL). Antibody panel resulted positive for antibodies to intrinsic factor and parietal cells. MRI of her brain revealed subacute combined degeneration. Non - contrast CT abdomen showed gastric wall thickening with surrounding edema. She was started on subcutaneous Vitamin B12 injections 1000 mcg daily, then transitioned to intramuscular Vitamin B12 1000 mcg daily. She was also treated with intravenous Pantoprazole (proton pump inhibitor), 40 mg BID. Within twenty-four hours of therapy, patient became alert, and oriented to person and place and was able to follow commands appropriately and progressively improved with resolved abdominal pain and no manifestation of psychosis while inpatient and 3 months outpatient follow up. Pernicious anemia has been rarely reported in African Americans. This case supports existing evidence that vitamin B12 deficiency can manifest as catatonic schizophrenia. Our patient's clinical response to pantoprazole and CT findings suggest underlying gastritis from antibodies to parietal cells. Her misdiagnosis shows the need for improved awareness of the neuropsychiatric manifestations of Vitamin B12 deficiency among healthcare providers. This is particularly important because delayed diagnosis can lead to lack of reversibility. We therefore emphasize that clinicians include Vitamin B12 deficiency in the initial workup of patients presenting with neuropsychiatric and gastrointestinal symptoms. |
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ISSN: | 0002-9270 1572-0241 |
DOI: | 10.14309/00000434-201810001-02696 |