Introduction Onychomyosis is a common infection of the nails, caused by dermatophytes, nondermatophyte moulds or yeasts. There are four main types of onychomycosis which include lateral and distal onychomycosis, proximal onychomycosis, superficial white and total dystrophic onychomycosis. We performed a retrospective analysis looking into the recent trends of onychomycosis in a University Hospital in Malaysia. Materials and methods Data was collected from all patients who had their nail clippings cultured for fungal infection from January 2004 to December 2008, and were analysed. Results There were 272 nail specimens in total. The majority of specimens were from adults (65.8%), followed by the elderly (23.9%) and children and adolescents made up 10.3%. The mean age of the study population was 49.9 ± 19SD years. Of the 189 specimens with positive fungal culture, 110 (40.4%) were non-dermatophyte moulds, followed by yeasts predominantly Candida species (17.6%), 3 (1.1%) were dermatophytes, and 28 (10.3%) were a mixed infection of dermatophytes, non-dermatophyte moulds and yeasts. Conclusion From this study, it was found that onychomycosis in our hospital from 2004 to 2008 were mainly caused by non-dermatophyte moulds. Treatment may be challenging as nondermatophyte onychomycosis are more resistant to treatment.

Apart from clinical, histological and biochemical indices, genomics are now being employed to unravel the pathogenetic mechanisms in the disease progression of IgA nephritis (IgAN). The results of angiotensin converting enzyme (ACE) gene polymorphism have been controversial. Those patients with the DD genotype seem to have a poorer prognosis. However, with high dose angiotensin receptor blocker (ARB) therapy, the ACE gene polymorphism status of a patient may no longer be a matter for concern as those with the DD genotype would also respond favourably to high dose ARB therapy. Association studies with gene sequencing and haplotypes have suggested that multiple genes are involved in the pathogenesis of IgAN. Some workers have reported a synergistic effect in the combined analysis of AGT-M235T and ACE I/D polymorphism. With the use of deoxyribo nucleic acid (DNA) microarray, tens of thousands of gene expressions genome-wide can be examined together simultaneously. A locus of familial IgAN has been described with strong evidence of linkage to IgAN1 on chromosome 6q22-23. Two other loci were reported at 4q26-31 and 17q12-22. DNA microarray techniques could also help in the identification of specific pathogenic genes that are up- or down-regulated and this may allow genome wide analyses of these genes and their role in the pathogenesis and progression of IgAN. Recently, using genome-wide association studies (GWAS) more loci for disease susceptibility for IgAN have been identified at 17p13, 8p23, 22q12, 1q32 and 6p21.
Angiotensin Receptor Antagonists ; administration & dosage ; Disease Progression ; Dose-Response Relationship, Drug ; Genomics ; methods ; Glomerulonephritis, IGA ; drug therapy ; genetics ; pathology ; Haplotypes ; Humans ; Molecular Sequence Data ; Polymorphism, Single Nucleotide