Single Nucleotide Polymorphism of Tumor Necrosis Factor-Alpha Gene with Sudden Deafness in Korean Population / 항공우주의학회지

BACKGROUND: Infections and vascular disorders are the two most widely accepted probable causes of sudden hearing loss. Tumor necrosis factor alpha (TNF-alpha) is major pro-inflammatory cytokine that is thought to be important in the pathogenesis of sudden deafness. However, the functions of genetic polymorphism in this cytokine have not been throughly examined in the context of sudden deafness pathology. In an effort to discover polymorphism in genes whose variants have been implicated in sudden deafness phenotypes, we examined the genetic effects of TNF-alpha polymorphisms in Koreans with sudden deafness. METHODS: Two common single nucleotide polymorphism (SNP) in TNF-alpha gene were genotyped in a Korean sudden deafness. Ninety nine patients with sudden deafness (45 males and 54 females) were selected from Keimyung University Dongsan Medical Center. The control subjects consisted of healthy 285 males and 319 females. RESULTS: Human genomic DNA was extracted from peripheral blood sample. The SNP at position -863 C/A and -857 C/T of TNF-alpha promoter were analyzed by PCR and pyrosequencing. Genotype distribution and allele frquencies in subjects were in Hardy-Weinberg equilibrium (p>0.05). No significant association was found between TNF-alpha -863 C/A and -857 C/T polymorphism and sudden deafness. We examined whether the relation between TNF-alpha polymorphism and sudden deafness varied according to tinnitus. Statistical analysis of TNF-alpha polymorphism at -857 C/T showed that there was a significant difference between SD without tinnitus and the control in both genotype distribution (p<0.05) and allele frequency [OR (95% CI)=2.63 (1.29-5.34)], but not between SD with tinnitus. CONCLUSION: These findings suggest TNF-alpha polymorphisms at -863C/A, -857 C/T are likely to play a role in SD.

A Case of Argyria from Silver in Cellular Phone Case Manufacture / 대한산업의학회지

BACKGROUND: Skin contact with, and the breathing in of air containing silver compounds can occur in the workplace. Occupational exposure to silver and its compounds is mainly via airborne dust, metal fumes, and mists of solutions containing silver compounds. Argyria results from increased serum silver levels and the deposition of silver-containing particles in the dermis and mucous membranes. The author reports a patient with generalized argyria, who worked on the manufacture of cellular phone cases. CASE REPORT: The patient was a 30 year-old male, with extensive blue-gray discoloration of the whole body, especially sun-exposed area, of 3 years duration. He had been exposed to silver in the processing of EMI for the past 4 years and gaskets for 1 year. EMI is the process by which the internal electromagnetic wave in cellular phone cases are shielded, and gaskets play an important role in shielding the electric clashes between electronic circuits, as well as increasing the durability of cellular phone cases to impact. EMI had been processed manually but this was changed to automatic spraying by robots in 2003. On physical examination, the patient had diffuse blue-gray discoloration of the skin, which was most prominent in the sun-exposed areas of his face, neck and V of the chest. Histopathological examination of a punch biopsy specimen from the posterior neck revealed fine, minute, round, and brown-black granules deposited in the basement membrane zone surrounding the eccrine glands. The laboratory findings were positive for hepatitis B antigen, with a serum silver concentration of 150.3 ppb. From this evidence, he was diagnosed with argyria due to silver exposure. DISCUSSION: The author reports a case of occupational systemic argyria due to inhalation exposure of silver compounds.