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Objectives: This study aimed to compare the clinical effectiveness of oral hydroxyzine and chloral hydrate to topical lidocaine/prilocaine 2.5% cream as premedication in pediatric leukemia patients. Materials & Methods: This double-blind clinical trial study was conducted on 70 leukemic and nonleukemic patients aged 3-11 years. The patients were divided into four groups. In group A, chloral hydrate solution was given to 18 patients. In group B, hydroxyzine syrup was used for 18 patients. In group C, chloral hydrate solution and lidocaine/prilocaine cream were used for 17 patients. In group D, hydroxyzine syrup and lidocaine/prilocaine cream were used for 17 patients. These groups were assessed and judged based on the visual analog scale (VAS). The side effects of the drugs were also recorded. Results: In this study, 54.3% (n=38) and 45.7% (n=32) of the cases were female and male, respectively. Furthermore, 77%, 7.2%, and 15.8% of the cases were reported with acute lymphocytic leukemia, acute myeloid leukemia, and infectious disease, respectively. The VAS results showed no difference in these four groups. Nontraumatic lumbar puncture (LP) (red blood cell<50) was observed in 97.1% of the cases. Conclusion: Although premedications for LP with hydroxyzine syrup and chloral hydrate solution were not statistically effective in pain relief, they increased patient and parent satisfaction. Moreover, adding lidocaine/prilocaine cream does not improve the effectiveness of the drugs.
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Background The nucleotide excision repair (NER) system is one of the most important deoxyribonucleic acid (DNA) repair mechanisms and is critical for chemotherapy resistance. We conducted the present study to investigate the association between two polymorphisms of excision of repair cross-complementing group 1 (ERCC1), the key component of the NER pathway, and the clinicopathological features of patients with non-small cell lung cancer (NSCLC). Methods A total of 38 patients with confirmed NSCLC were included in our study. DNA was extracted from peripheral blood. ERCC1 rs3212986 (8092) and rs11615 (118) were genotyped using molecular assays including polymerase chain reaction (PCR) with restriction fragment length polymorphism (by MboII and HpyCH4 enzymes) and sequencing. Results The PCR results indicated the correct performance of the genomics extraction and molecular protocols. The distribution of C/C, C/A and A/A genotypes at position 8092 was 42.10%, 47.36%, and 10.52% respectively (P=0.03). Multivariate regression analysis showed that there was a significant correlation between C8092A (rs3212986) polymorphism and metastasis, grade of the tumor, and response to treatment. Individuals carrying the rs3212986 CA genotype and A allele had a significantly worse response to the treatment. Also, the correlation between alteration at this genomics location and patients with NSCLC who used to smoke cigarettes was positive. However, no significant association was detected between rs11615 C118>T polymorphism and demographic characteristics of patients with NSCLC. Conclusion We concluded that in lung cancer patients there is a relationship between tumor stage and rs3212986C>A polymorphism.
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BACKGROUND: The nucleotide changes in different genetic loci increased the incidence risk of breast cancer. AIM: The aim of present study was to investigate genotype distribution at codon 72 of the TP53 gene (rs1042522) in breast cancer patients to achieve a potential diagnostic marker related to some demographic feathers. METHODS: In our case-control study, blood samples were collected from a total of 34 patients harboured breast cancer. DNA was extracted, and nested-PCR was performed. Products were digested with AccII and subsequently were sequenced. Results were compared with samples characteristics. RESULTS: The PCR results indicated the correct implementation of extraction and amplification protocol. The genotypic distribution at codon 72 of TP53 in control group was 20%, 62.4% and 16.6% for Arg (wildtype), Arg/Pro (heterozygous) and Pro (homozygous variant) respectively. Also, this distribution in the patient group was 23.52% homozygous, 50% heterozygous, and 26.47% another homozygous variant (Adjusted odds ratio: 1.12 and 95%CI = 0.57 to 2.2, P = 0.03). The absence of Arg at codon 72 of TP53 is relevant with age higher than 40 years and metastasis to other organs. CONCLUSION: Polymorphism at codon 72 of TP53 was associated with high-grades of breast cancer risk and different responses to chemotherapy treatment. It is recommended genotype distribution of codon 72 of TP53 before chemotherapy.
