Table 1.
Decrease in oral intake | (i) Restrictive diets (ii) Therapeutic fasting (iii) By the disease itself due to diarrhea, abdominal pain, nausea, and vomiting [9] (iv) Alteration in taste due to drugs, vitamin and mineral deficiencies, and proinflammatory mediators [7] (v) Anorexigenous effect of proinflammatory cytokines [7] |
| |
Gastrointestinal losses | (i) Diarrhea (ii) Rectorrhagia/hematochezia (iii) Loss of mucus and electrolytes (iv) Protein-losing enteropathy |
| |
Metabolic disorders | (i) Increase in resting energy expenditure due to inflammation, fever, and sepsis (ii) Enhanced fat oxidation |
| |
Increase in nutritional requirements | (i) Inflammatory states [7] (ii) Increased basal oxidative metabolism (iii) Infectious complications (iv) Postsurgery |
| |
Drug interaction | (i) Corticosteroids and calcium reabsorption (ii) Corticosteroids and protein catabolism (iii) Salazopyrin and folates [11] (iv) Methotrexate and folates [11] (v) Cholestyramine and liposoluble vitamins [11] (vi) Antimicrobials and vitamin K [12, 13] (vii) Antisecretors and iron [14] |
| |
Poor absorption of nutrients | (i) Reduction of the absorptive surface due to intestinal resection and enteric fistulas [8] (ii) Blind loops and bacterial overgrowth (iii) Poor absorption of bile salts in ileitis or resection [8] (iv) Mucosal inflammation |