Role of linoleic acid in arsenical palmar keratosis.

BACKGROUND: Chronic arsenic exposure can lead to palmoplantar keratosis. In the stratum corneum of skin, linoleic acid is of the utmost importance to the inflammation, keratinization, and regeneration processes. OBJECTIVES: The aims of this study were: (i) to present quantitative information on the linoleic acid fraction of intercorneocyte lipids, and (ii) to elucidate the role of linoleic acid in the pathophysiology of arsenical keratosis. METHODS: Lipid extracts were collected from keratotic lesions in seven patients, seven arsenic-exposed subjects, and seven non-exposed control subjects. Linoleic acid levels of the specimens were estimated by reverse-phase high-performance liquid chromatography (RP-HPLC). RESULTS: There was a significant (P < 0.001) increase in mean ± standard error (SE) linoleic acid levels in arsenical keratosis patients (palm: 25.66 ± 4.95 µg/cm(2); dorsum: 28.25 ± 6.20 µg/cm(2)) compared with arsenic-exposed (palm: 2.75 ± 0.85 µg/cm(2); dorsum: 1.96 ± 0.64 µg/cm(2)) and non-exposed (palm: 1.52 ± 0.61 µg/cm(2); dorsum: 1.28 ± 0.39 µg/cm(2)) control subjects. There was no significant difference (P = 0.556) in linoleic acid concentration in the non-affected skin of the dorsum of the hand (28.25 ± 6.20 µg/cm(2)) compared with that in the palmar sites (25.66 ± 4.95 µg/cm(2)) in the patient group. The change in linoleic acid levels in the arsenic-exposed control group did not differ from that in non-exposed controls (P = 1.000). CONCLUSIONS: Linoleic acid concentration is elevated in arsenical keratosis; this finding warrants further investigation to ascertain whether linoleic acid plays a direct role in the pathophysiology of arsenical keratosis.

Congenital erythropoietic porphyria affecting two brothers.

We report two brothers, aged 5 and 2 years, with typical features of congenital erythropoietic porphyria. The elder did not receive medical attention until the age of 2 years, even though his urine had been red almost from birth, and despite severe scarring of the hands and face. The younger brother suffered haemolysis at birth. The uroporphyrinogen III cosynthase (URO IIIS) enzyme activity of red blood cells was 2% and 1.2% in the brothers, and genetic studies showed two different mutations of the URO IIIS gene, C73R and P248Q. The latter is a recently described mutation.

Nickel-sensitive patients with vesicular hand eczema: oral challenge with a diet naturally high in nickel.

Oral challenge with nickel sulphate indicated that vesicular hand eczema in nickel-sensitive patients may be exacerbated by nickel occurring naturally in the diet. Twelve nickel-sensitive females with vesicular hand eczema were challenged with a supplementary high nickel diet for 4 days in a single-blind cross-over study. The diet had about five times the average nickel content of the daily Danish diet. An aggravation of the hand eczema was observed in six out of 12 patients on day 4 after the start of the challenge. By day II, the hand eczema was worse in 10 out of 12 patients, and remained unchanged in two.