RESUMO
Vitamin B12 deficiency is known to cause a variety of symptoms, including megaloblastic anemia, glossitis, and neuropsychiatric disorders. This case report describes a patient who presented with cognitive decline, psychosis, and seizures due to a severe vitamin B12 deficiency. Following treatment with vitamin supplementation therapy, the patient's condition significantly improved. The literature has also documented similar neuropsychiatric manifestations of vitamin B12 deficiency, highlighting the potential for symptom reversal with prompt and appropriate treatment. Therefore, early diagnosis and treatment of vitamin B12 deficiency are critical to preventing potentially irreversible neurological damage.
RESUMO
B-cell prolymphocytic leukemia (B-PLL) is a rare malignancy of mature B-cells with characteristic morphologic, immunophenotypic, cytogenetic, and molecular features characterized by late onset (median age 69 years), an aggressive clinical course, refractoriness to chemotherapy, and median survival of around three years. Treatment is influenced by the presence or absence of specific high-risk genetic mutations like 17P/TP53 deletion, the presence of which translates into poor prognosis. Patients without 17P deletion, who are <70 years, without significant co-morbidities, are initially treated with a combination chemotherapy regimen used for chronic lymphocytic leukemia (CLL) such as fludarabine, cyclophosphamide, and rituximab. On the other hand, patients with a 17P deletion, age >70 years, with multiple co-morbidities, receive ibrutinib or alemtuzumab as the initial therapy. Relapsed or refractory cases are managed with BCL-2 signaling inhibitors like venetoclax. We discuss the case of an 84-year-old male with B-PLL (positive TP53 mutation), resistant to ibrutinib therapy, with extremely high white blood cell (WBC) counts, thus creating a dilemma regarding the best treatment in the second-line setting.