Most of these data come from controlled studies in which primaquine was given to G6PD deficient volunteers or normal recipients after transfusion of 51Cr-labelled GPD-deficient red cells, and from case reports of patients who developed hemolytic anaemia after receiving primaquine. Therefore, beyond the routine use of primaquine, comprehensive knowledge of the epidemiology of the G6PD deficiency by using reliable methods is needed. In this study, we have determined, for the first time, the normal reference values of G6PD enzymatic activity for both Cambodian males and females adults by using the quantitative spectrophotometric assay. Reference ranges generally used are derived from North American or European populations which may not be applicable to the Cambodian population. For this purpose, healthy individuals were selected with a normal range of hemoglobin concentration and a wild-type sequence in their G6PD gene. Surprisingly, we found that globally G6PD enzymatic activity was significantly higher in males compared to females while SB431542 previous reports showed no difference using the same methodology. Using these values, the global prevalence of G6PD deficiency in our sample population was 10.7%, ranging from 9.3% in the most southern village to 20% in the most northern village of the Pailin province. The cut-off point to diagnose G6PD deficiency both in Cambodian males and females was around 30% of the normal mean value. As expected, we found that the prevalence of G6PD deficiency was almost 2-fold higher in males compared to females. This proportion was similar to previous reports from Cambodia and in the bordering countries of Vietnam, Laos and Thailand.. Clinical manifestations include early onset of dry skin, pruritus, eczema with typical age-dependent distribution, and personal or family history of atopic disease. Knowledge of the pathophysiology behind the disease is emerging, several common genetic, environmental disease mechanisms and individual trigger factors being of importance. Central in the pathogenesis are combinations of inherited and acquired insults thought to alter epidermal structure. Which in turn has negative consequences for skinbarrier homeostasis. Impaired homeostasis of the skin leads to increased trans-epidermal water loss and changes in gene expression patterns and enzymatic activity. The most common monogenic disorder of keratinisation, ichthyosis vulgaris, is associated with AD and related atopic manifestations in up to 50%. This contrasts with X-linked recessive ichthyosis, which is due to mutations in the STS gene leading to accumulation of cholesterol sulphate in the stratum corneum. XLI occurs almost exclusively in males and may look almost indistinguishable from IV. However, skin histology and surface pH differ in the two conditions and no association to AD has been reported in XLI. In 2006, it was found that mutations in the FLG gene resulting in filaggrin dysfunction are the causative genetic factor for IV.