I believe this patient is diagnosable with combined marasmus-kwashiorkor. He has all the classic signs of marasmus, including depleted subcutaneous fat stores evidenced by a TSF in less than the 5th percentile, depleted somatic stores evidenced by an upper arm muscle area in less than the 5th percentile, and a 30 lb weight loss over the past 6 months (which is an 18% loss over 6 months, definitely clinically significant). Furthermore, he is 78% of desirable body weight based upon the latest NHANES data. Given the medical diagnosis of the patient, it is not unexpected at all that this patient might present with a picture of marasmus. Long-term (chronic) inflammation, with episodic acute exacerbation will influence dietary intake; will increase nutrient losses via exudative protein loss from the inflamed GI mucosa, as well as via frequent diarrhea; and will increase nutrient requirements (increased protein losses by the GIT coupled with at least episodic hypermetabolism due to inflammation will increase energy requirements). The patient also exhibits signs of kwashiorkor. Namely, depressed albumin, transferrin, TLC, and total protein indicate depressed visceral protein status. This patient could be suffering from kwashiorkor as a result of long-term protein deficit induced by inadequate intake, but it is also highly likely that kwashiorkor could be induced by the metabolic stress associated with acute disease exacerbation and namely, the occurrence of an enterocutaneous fistula. The metabolic stress response causes a depression of visceral protein synthesis with the shift to the synthesis of acute phase proteins, as well as a shift of albumin from the extracellular space (out of plasma). The fact that the patient is hypermetabolic, with fever, and with a high output enterocutaneous fistula all support the notion that a metabolic stress state is present in this patient. The imposition of metabolic stress on a patient that already has underlying marasmus results in combined marasmus-kwashiorkor.