Vitamin B12 deficiency as a differential diagnosis of Systemic Lupus Erythematosus

Abstract

BACKGROUNDSystemic lupus erythematosus (SLE) is a multifactorial, chronic inflammatory, autoimmune disease more common in women, with alternating periods of exacerbation and remission. It presents cutaneous, joint, cardiac, pulmonary, renal, hematological and neuropsychiatric manifestations, the latter being present in 25-70% of patients, and may be the initial manifestation of the disease and occur even in the absence of other symptoms. As a differential diagnosis of neuropsychiatric alterations, vitamin B 12 deficiency should be considered, whose symptoms will be reversible if they have a short period of evolution, but may have permanent sequelae if treatment is not indicated early. CASE REPORTFemale patient, 56 years old, with a history of previous hospitalization due to inflammatory polyarthralgia, dyspnea on moderate exertion, visual hallucinations and psychomotor agitation. The psychiatric team started risperidone as symptomatic, with improvement of hallucinations. During the investigation, anemia, thrombocytopenia and serositis were evidenced, with negative ANA. The diagnostic hypothesis of SLE with lupus psychosis was raised and pulse therapy with methylprednisolone 3 g was performed in an external service. The patient evolved with an improvement in the condition, being discharged from the hospital with prednisone 40 mg/day and risperidone. After a short period, the psychiatric condition recurred with insomnia, psychomotor agitation, and hallucinations even when using risperidone. Neurology team hypothesized Parkinsonism secondary to risperidone and recommended replacement with quetiapine. The symptoms improved and she was discharged with an outpatient return. After reassessment of the case, hydroxychloroquine was introduced and the other medications were maintained due to the diagnostic hypothesis of probable SLE, but the patient was lost to follow-up. After one year, she returned to the emergency room with severe anemia, and 4 packed red blood cells were transfused. Complementary tests showed pancytopenia and vitamin B 12 55 (VR 114-890) deficiency. During hospitalization, she again presented visual hallucinations, psychomotor agitation and disorientation, and replacement of this vitamin was performed, without immunosuppression or use of steroids, and the patient showed improvement of the initial complaints and normalization of leukocytes and platelets, maintaining anemia. Thus, the diagnosis of SLE was ruled out and it was confirmed that the manifestations were only due to vitamin B 12 deficiency. CONCLUSIONNeuropsychiatric manifestations may result from SLE as long as other causes are ruled out, mainly metabolic disorders and infections. In this case, the patient showed improvement in clinical symptoms and laboratory tests after vitamin B 12 replacement, and the behavioral disorder was attributed to the deficiency of this vitamin.