Serum levels of lead and selenium in patients with premature graying of the hair.

BACKGROUND: The exact etiology of premature hair graying (PHG) remains unknown; however, oxidative stress is shown to be involved. Selenium, as an antioxidant, is widely known for its antiaging potentials. Moreover, PGH is more prevalent among addicts and because Lead is a common impurity found in illegal drug. AIMS: We evaluated the serum levels of lead and selenium in patients with PHG and compared it with a control group. PATIENTS/METHODS: In this cross-sectional study, 60 patients referred to Dermatology Clinic of Imam-Reza Hospital of Mashhad, Iran in 2015 were evaluated in two groups with and without PHG. Demographic information and disease characteristics, skin phenotype, and family history of PHG were recorded. Furthermore, 5 mL of brachial blood was drawn for measuring selenium and lead levels. RESULTS: The mean patients' age was 28.1 ± 4.8 years. Age, sex, occupation, and skin phenotype in individuals with and without PHG were not significantly different (P > .05) but family history of PHG was significantly higher in the patients with PHG (P = .001). Similarly, the number of white hairs was significantly higher (P < .001), and the age of onset of hair graying was significantly lower in patients with PHG (P < .001). Serum levels of selenium and lead were not significantly different between two groups (P < .05). However, the serum levels of lead in the patients with PHG were slightly higher. CONCLUSIONS: The results of this study showed that there was no significant difference in lead and selenium serum levels in patients with and without PHG.

Bronze baby syndrome. Report of a case.

A newborn female infant suddenly developed a generalized gray-brown discoloration of her skin while receiving phototherapy for hyperbilirubinemia. The discoloration waned over the succeeding weeks. Her serum contained an unknown pigment that had a characteristic absorbance on spectrophotometry. The distinctive findings and some possible causes of the bronze baby syndrome are discussed. The findings are compared to other causes of dusky-hued skin in the neonate. The bronze baby syndrome is usually innocuous but can signal life-threatening disease.

Low reserve albumin for binding of bilirubin in neonates with deficiency of bilirubin excretion and bronze baby syndrome.

The plasma reserve albumin concentration for binding of bilirubin was found to be low in four newborn infants with deficiency of bilirubin excretion, of whom two had the bronze baby syndrome. Thus, the risk of bilirubin encephalopathy was increased. Also the ratio of binding fraction of albumin, i.e. unconjugated bilirubin plus reserve albumin, to total albumin was low. Possible causes of the low reserve albumin concentration and the ratio are discussed.

Mechanism of development of bronze baby syndrome in neonates treated with phototherapy.

Comparisons of serum concentrations of unknown pigment and photobilirubin IX alpha , the two main bilirubin photoproducts, were made during phototherapy in infants with and without bronze baby syndrome who were treated similarly. The serum concentrations of unknown pigment estimated by high-pressure liquid chromatography in infants with the bronze baby syndrome were significantly increased in comparison with those in the control hyperbilirubinemic neonates during phototherapy. However, there was no difference in the serum concentrations of photobilirubin IX alpha between infants with bronze baby syndrome and the control groups. The unknown pigment separated from bilirubin photoproducts obtained from experiments in vitro by high-pressure liquid chromatography was gradually decomposed into brown products that showed the absorption spectrum similar to that of the serum of infants with bronze baby syndrome. This fact is probably due to reduction in hepatic excretory function of bilirubin photoproducts, especially in known pigment, because its main excretory pathway is the biliary route. The pigment accumulated in the body may be polymerized and forms bilifuscin-like substances following a free radical reaction. It is concluded that the brown pigment is formed via unknown pigment.