INTRODUCTION: Subacute combined degeneration of the spinal cord associated with vitamin B12 deficit is well known. However a paraneoplastic induced cyanocobalamin malabsorption responsible for either subacute combined degeneration of the spinal cord, has not been reported. Moreover, the possibility of either subacute combined degeneration of the spinal cord may be manifestation of a cancer, it's unknown. CLINICAL CASE: We present the case of a 73-year-old woman with cutaneous paleness and clinical manifestations of a subacute combined degeneration of the spinal cord. Laboratory analysis showed a megaloblastic anemia and Schilling test showed cyanocobalamin malabsorption corrected by intrinsic factor. Anti-intrinsic factor antibodies were positive. Chronic atrophic gastritis and immunological diseases associated with pernicious anemia or with anti-intrinsic factor positive, were excluded. A hidden esophageal squamous cell carcinoma was discovered. Necropsy confirmed both, subacute combined degeneration of the spinal cord and esophageal carcinoma in the absence of chronic atrophic gastritis. CONCLUSIONS: Anti-intrinsic factor antibodies were the only found factor which could explain cyanocobalamin malabsorption. A esophageal squamous cel carcinoma was discovered. In our case, vitamin B12 malabsorption had a paraneoplastic origin mediated by anti-intrinsic factor antibodies. Subacute combined degeneration of the spinal cord may be the manifestation of a hidden esophageal squamous cell carcinoma.
INTRODUCTION: Subacute combined degeneration of the spinal cord associated with vitamin B12 deficit is well known. However a paraneoplastic induced cyanocobalaminmalabsorption responsible for either subacute combined degeneration of the spinal cord, has not been reported. Moreover, the possibility of either subacute combined degeneration of the spinal cord may be manifestation of a cancer, it's unknown. CLINICAL CASE: We present the case of a 73-year-old woman with cutaneous paleness and clinical manifestations of a subacute combined degeneration of the spinal cord. Laboratory analysis showed a megaloblastic anemia and Schilling test showed cyanocobalaminmalabsorption corrected by intrinsic factor. Anti-intrinsic factor antibodies were positive. Chronic atrophic gastritis and immunological diseases associated with pernicious anemia or with anti-intrinsic factor positive, were excluded. A hidden esophageal squamous cell carcinoma was discovered. Necropsy confirmed both, subacute combined degeneration of the spinal cord and esophageal carcinoma in the absence of chronic atrophic gastritis. CONCLUSIONS: Anti-intrinsic factor antibodies were the only found factor which could explain cyanocobalaminmalabsorption. A esophageal squamous cel carcinoma was discovered. In our case, vitamin B12malabsorption had a paraneoplastic origin mediated by anti-intrinsic factor antibodies. Subacute combined degeneration of the spinal cord may be the manifestation of a hidden esophageal squamous cell carcinoma.