[Document describing a Special Order from Brig. Genl L. B. M. Adoo]

Document describing a special order made by Brig. Genl L. B. M. Adoo allowing leave of absence to Fred A. Rice

Immunomodulation in surgical practice

Background. Immunomodulation may represent a potential way to improve surgical outcome. These types of interventions should be based on detailed knowledge of the underlying mechanisms involved. The aim of the present review is to summarize some experience on the acute phase response, potential ways of intervention and experiences from critical illness and HPB disease. Discussion. Mechanisms of the acute phase response are discussed including the individual parameters and local changes that take part. Mechanisms involved in failure of the gut barrier are presented and include changes in gut barrier permeability, effects on gut-associated immunocompetent cells, and systemic implications. As examples of HPB disease, mechanisms of the acute phase response and potential ways of intervention in obstructive jaundice and acute pancreatitis are discussed. Nutritional pharmacology and lessons learned from immunomodulation and immunonutrition in critical illness and major abdominal surgery, including upper GI and HPB surgery, are referred to. Overall, immunomodulation represents a potential tool to improve results but requires a thorough mapping of underlying mechanisms in order to achieve individualized treatment or prevention based on patients' specific needs

Transsulfuration Pathway Defects and Increased Glutathione Degradation in Severe Acute Pancreatitis.

noGlutathione depletion is a consistent feature of the progression of mild to severe acute pancreatitis. In this study, we examined the temporal relationship between cysteine, homocysteine, and cysteinyl-glycine levels; total reduced erythrocyte glutathione; gamma-glutamyl transpeptidase activity; and disease severity. Initially, cysteine concentration was low, at levels similar to those of healthy controls. However, glutathione was reduced whilst cysteinyl glycine and gamma-glutamyl transpeptidase activity were increased in both mild and severe attacks. As the disease progressed, glutathione and cysteinyl glycine were further increased in mild attacks and cysteine levels correlated with homocysteine (r = 0.8, P < 0.001) and gamma-glutamyl transpeptidase activity (r = 0.75, P < 0.001). The progress of severe attacks was associated with glutathione depletion, reduced gamma-glutamyl transpeptidase activity, and increased cysteinyl glycine that correlated with glutathione depletion (r = 0.99, P = 0.01). These results show that glutathione depletion associated with severe acute pancreatitis occurs despite an adequate cysteine supply and could be attributed to heightened oxidative stress coupled to impaired downstream biosynthesis