HLA-A*31:01 and carbamazepine-induced DRESS syndrom in a sample of North African population.

PURPOSE: Drug rash with eosinophilia and systemic symptoms (DRESS) is a serious adverse drug reaction. Carbamazepine is the most common causes of this syndrome. The HLA-A*31:01 allele has been shown to be strongly correlated with carbamazepine-induced DRESS syndrome in European, Japanese, Han Chinese and other asian population but not in African populations. So, our purpose is to study there is a correlation between HLA-A*31:01 and carbamazepine-induced DRESS syndrome in africain population? METHODS: HLA class I (A and B) typing was performed on 7 subjects with carbamazepine-DRESS syndrome and 25 tolerants controls subjects. DNA typing HLA class I (A) alleles was checked by the polymerase chain reaction amplification Sequence Specific Oligonucleotide Probes (SSO) (reverse-SSO assay). High resolution HLA DNA Kit based on the Luminex technology (One Lambda®) was used according to the manufacturer's protocol. RESULTS: The HLA-A*31:01 allele, which has a prevalence of 1% in Tunisian population, was significantly associated with DRESS syndrome. It was detected in 57.14% of cases (4/7) and only 4% of controls subjects (1/25). Thus, the carrier frequency of HLA-A*31:01 allele in the cases group was also significantly higher than in the controls group (57, 14% vs 4% P = 0,004). Odds ratio is estimated 32 (OR = 32 [2.6; 389.2]) CONCLUSION: Similarly to other ethnicities, the presence of the HLA-A*31:01 allele was associated with carbamazepine-DRESS syndrome in a sample of North African population. Future study must be conducted on a larger sample in order to confirm these results.

HLA association with nasopharyngeal carcinoma in southern Tunisia.

In order to study the association of HLA-A, -B and/or DRB1, DQB1 and the nasopharyngeal carcinoma (NPC), 141 patients affected with NPC were typed for the HLA class I by serology method of microlymphocytotoxicity. Among these patients 101 were genotyped for HLA class II system by the PCR-SSP technique. HLA typing results were compared to those of 116 controls. We found that the HLA-A31 and -A33 antigens were significantly more expressed in patients than in the controls (P = 0.016 and 0.010, respectively) and the HLA-A19 antigen, was significantly more frequent in patients when compared to the controls (P = 0.007). The HLA-DRB1*03 and DRB1*13 alleles were significantly more frequent in patients as compared to the controls. The DRB1*01 allele was expressed with a frequency of 20.69% in the controls whereas it was only detected in 3.96% of the NPC patients. Furthermore, the DQB1*05 allele was expressed at a frequency which was significantly less important in affected patient (P = 0.03), whereas, the DQB1*02 allele was more frequent in patients (P = 0.643 x 10(-4)). Thus our study revealed a significant increase of HLA-A31, A33, A19, B16, B53 and DRB1*03, DRB1*13 and DQB1*02 alleles in our patients. These markers could play a predisposing role in the development of NPC. In contrast, a decrease of HLA-B14, -B35 and DRB1*01 and DQB1*05 alleles was found suggesting a likely protective effect.

HLA- A, B, DR and DQ alleles study in Tunisian patients with atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disease resulting from the interaction between envirommental and genetic factors. Many genes are involved in the etiopathology of AD, such as HLA genes. OBJECTIVES: Study the association between HLA-A, B, DR and DQ genes and the AD. METHODS: HLA A and B genotyping were practised for 53 atopic dermatitis patients and 76 healthy controls using the microlymphotoxicity complement dependent technique, while HLA DR and DQ genetyping were practised for only 20 patients with AD and all the controls by PCR-SSP method. RESULTS: Allelic frequency of HLA A32 was significantly increased in healthy individuals compared to patients affected with AD (p = 0.02, RR = 0.24). HLA-B, DR and DQ showed no differences in distrubition between patients and controls. CONCLUSION: Our study suggested that HLA-A32 could be a protective marker against atopic dermatitis for Tunisian patients, in contrast to HLA-B, DR and DQ alleles which seemed to have no importance in AD pathogenis.