Treatment of pancreatic cancer with intravenous vitamin C: a case report

Jeanne A Drisko, Oscar K Serrano, Lisa R Spruce, Qi Chen, Mark Levine, Jeanne A Drisko, Oscar K Serrano, Lisa R Spruce, Qi Chen, Mark Levine

Abstract

Pancreatic ductal adenocarcinoma (PDA) has a dismal prognosis and is often discovered at an advanced stage with few therapeutic options. Current conventional regimens for PDA are associated with significant morbidity, decreased quality of life, and a considerable financial burden. As a result, some patients turn to integrative medicine therapies as an alternate option after a diagnosis of PDA. Intravenous pharmacologic ascorbic acid (PAA) is one such treatment. The use of PAA has been passionately debated for many years, but more recent rigorous scientific research has shown that there are significant blood concentration differences when ascorbic acid is given parenterally when compared to oral dosing. This pharmacologic difference appears to be critical for its role in oncology. Here, we report the use of PAA in a patient with poorly differentiated stage IV PDA as an exclusive chemotherapeutic regimen. The patient survived nearly 4 years after diagnosis, with PAA as his sole treatment, and he achieved objective regression of his disease. He died from sepsis and organ failure from a bowel perforation event. This case illustrates the possibility of PAA to effectively control tumor progression and serve as an adjunct to standard of care PDA chemotherapy regimens. Our patient's experience with PAA should be taken into consideration, along with previous research in cell, animal, and clinical experiments to design future treatment trials.

Figures

Fig. 1
Fig. 1
Initial CT/PET at biopsy in April 2007. (a) CT/PET and (b) CT scan: metabolically active (SUV 16) hypodense 4.5×3.7×3.7 cm lesion in the uncinate process of the pancreas (arrows). (c) CT/PET and (d) CT scan: multiple metabolically active lesions throughout liver parenchyma, with the largest measuring 2.8×1.8 cm (SUV 7) (arrows). CT, computed tomography; SUV, standardized uptake value.
Fig. 2
Fig. 2
Follow-up CT/PET in November 2007, 8 months after the initial imaging. (a) CT/PET and (b) CT scan: metabolically active lesion in the uncinate process of the pancreas with decrease in activity (SUV 13) and stable measurement 5.3×3×3.3 cm (arrows). (c) CT/PET and (d) CT scan: hepatic parenchymal lesions identified with a decrease in metabolic activity (SUV 3) and resolving a large anterior right hepatic lobe mass (arrows). CT, computed tomography; SUV, standardized uptake value.
Fig. 3
Fig. 3
Follow-up CT/PET performed in June 2008 over 1 year after diagnosis. (a) CT/PET and (b) CT scan: metabolically active lesion in the uncinate process of the pancreas with a further decrease in metabolic activity (SUV 9) and stable in size from the previous scan with a necrotic central portion (arrows). (c) CT/PET and (d) CT scan: resolution of metabolic activity throughout hepatic parenchyma, with only small foci of residual disease identified consistent with improvement in metastatic disease. CT, computed tomography; SUV, standardized uptake value.
Fig. 4
Fig. 4
CT/PET follow-up performed in November 2008 at 18 months after diagnosis. (a) CT/PET and (b) CT scan: interval decrease in the size of the pancreatic uncinate process mass measuring 3.9×3.6×3.1 cm with increased necrotic components. The metabolic activity showed decreased activity (SUV 6.4). (c) CT/PET and (d) CT scan: no residual metabolic activity and no discrete lesions identified throughout the hepatic parenchyma. No biliary dilatation noted. CT, computed tomography; SUV, standardized uptake value.
Fig. 5
Fig. 5
Follow-up CT/PET in November 2009 now 2.5 years after diagnosis. (a) CT/PET and (b) CT scan: interval decrease in the size of the pancreatic uncinate process mass measuring 2.6×2.2×2.3 cm. Hypermetabolic activity showed increase from the previous scan (SUV 10) (arrows). The hepatic parenchyma remained free of hypermetabolic activity or focal lesions (not pictured). No biliary dilatation noted. CT, computed tomography; SUV, standardized uptake value.
Fig. 6
Fig. 6
Follow-up CT/PET in November 2010 now 3.5 years after diagnosis. (a) CT/PET and (b) CT scan: no significant change in the pancreatic mass size. Hypermetabolic activity was stable (SUV 9.3) and interpreted as stable disease (arrows). Hepatic parenchyma remained free of metastatic disease (not pictured). No biliary dilatation noted. CT, computed tomography; SUV, standardized uptake value.
Fig. 7
Fig. 7
February 2011 presentation to the emergency room, where the patient was found to be in septic shock 2 weeks after biliary stent placement. (a) Contrast-enhanced CT scan: stable size of mass in the uncinate process of pancreas (arrow) and no apparent tumor progression. There was mild diffuse induration of the mesentery consistent with third spacing of fluid. (b) Contrast-enhanced CT scan: hepatic parenchyma with air in the biliary tree (arrow), but no parenchymal lesions identified. CT, computed tomography.

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