Confounding Effects of Infection on Laboratory Assessment

As already indicated, many confounding effects of infection have been observed in many laboratory tests for nutritional status. For protein status, confounding effects of infection are reported for almost all laboratory tests, excluding that for total serum protein. In particular, serum albumin, plasma transport protein, and fibronectin levels decrease because of the increase of acute phase proteins.

For vitamin A, severe systemic infections (e.g., pneumonia, bronchitis, diarrhoea, septicaemia, rheumatic and scarlet fever, malaria, and measles) cause a marked decrease in serum retinol level. This decrease may be due to various factors (e.g., increased retinol excretion in urine and reduced liver release of retinol and RBP to plasma). A reduction of vitamin A liver reserves assessed by the RDR test has been observed in children with chickenpox.

Plasma vitamin E is reduced in malaria-infected patients. This influence is retained via the lipopro-teins and not directly. Tests for thiamin status can be confounded by infections that prevent normal absorption (diarrhea and dysentery) or increase the requirement (fever).

For vitamin B12, fish tapeworm or hookworm infestations give a low level of serum vitamin B12 because of their preferential consumption of this vitamin. For vitamin C, acute and chronic infections can depress markedly the serum ascorbic acid level due to a decrease in vitamin C reserves.

For iron status tests, infection induces an increase in serum ferritin and blood protoporphyrin levels and a decrease in serum iron binding capacity, serum iron, and hemoglobin. Zinc status tests are influenced by acute and chronic infections. A decrease in plasma zinc has been reported, due initially to redistribution of zinc within the body tissues and then to a negative body balance. This is due to anorexia, which reduces dietary intake, and also to increased losses via the faeces (diarrhea), sweat, and urine.

Regarding copper status tests, infection results in an increase in serum copper level because the leucocytic endogenous mediator induces an increase in serum cer-uloplasmin. Jodine status can be influenced by infection because the synthesis of TTR is markedly suppressed.

In nutrition surveys, to correct misclassification of laboratory values due to positive acute phase proteins, the concurrent serum determination of these proteins has been suggested.

Table 2 Tentative cutoff points for interpretation of results of micronutrient tests in adults

Severe deficiency Marginal deficiency Physiological level or range

Table 2 Tentative cutoff points for interpretation of results of micronutrient tests in adults

Severe deficiency Marginal deficiency Physiological level or range

Lv retinol (|mrnolg~1)


P retinol (iimolr1)




RBP:TTR ratio


Relative dose response (%)



S 25-OHD (nmol l-1)




P/S a-tocopherol (iimolr1)




P a-tocopherol (iimolr1)




E TPP (nmolr1)




U thiamin (mg/24 h)








E FAD (nmolr1)


U riboflavin (mg/g creatinine)












P PLP (nmol T1)



U 4-PA (nmol/nmol creatinine)






P vitamin B12 (pmolr1)0



STCII (pmolr1)


S methylmalonic acid (iimolr1)



P homocysteine (mmol l-1)




P folate (nmolr1)


P folate (nmolr1)0




RBC folate (nmolr1)




L lobe average




P biotin (nmolr1)0




P ascorbic acid (iimolr1)




B ascorbic acid (iimolr1)




L ascorbic acid (nmol/108 cells)



S/P ferritin (i g)




S iron (iimolr1)



S TIBC (imolr1)


Transferrin saturation (%)


e PP (imolr1)


Haemoglobin (gl-1)

M <130 F <120

Haematocrit (%)

M <40 F < 36



P Zn (imolr1)


S caeruloplasmin (iimolr1)


P Se (imolr1)




E Se (imolr1)



aThe percentage stimulation is now very seldom used. It can be calculated as follows: (AC x 100) - 100.

bFrom Benton D, Haller J and Fordy J (1997) The vitamin status of young british adults. International Journal for Vitamin and Nutrition Research 67: 34-40, with permission.

Lv, liver; P, plasma; S, serum; E, erythrocyte; U, urine; L, leucocytes; B, whole blood; RBP, retinol binding protein; TTR, transthyretin; TPP, thiamin pyrophosphate; ETK-AC, erythrocyte transketolase activation coefficient; FAD, flavinadeninedinucleotide; EGR-AC, erythrocyte glutathione reductase activation coefficient; PLP, pyridoxal-5'-phosphate; 4-PA, 4-pyroxic acid; EAST-AC, erythrocyte aspartate aminotransferase activation coefficient; TCII, transcobalamin II, RBC, red blood cell; TIBC, total iron-binding capacity; PP, protoporphyrin; MCV, mean cell volume.

Adapted with permission from Flair Concerted Action No. 10 Status Papers (1993) International Journal for Vitamin and Nutrition Research 63: 252-316, with changes suggested by C.J. Bates (personal communication).

See also: Ascorbic Acid: Physiology, Dietary Sources and Requirements. Carotenoids: Chemistry, Sources and Physiology. Cobalamins. Copper. Fatty Acids: Omega-3 Polyunsaturated; Omega-6 Polyunsaturated. Folic Acid. Iron. Magnesium. Niacin. Nutritional

Assessment: Anthropometry; Clinical Examination. Potassium. Riboflavin. Selenium. Sodium: Physiology. Thiamin: Physiology. Vitamin A: Physiology. Vitamin B6. Vitamin E: Metabolism and Requirements. Vitamin K. Zinc: Physiology.

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