ABSTRACT
Objective:To observe the clinical effect of tranexamic acid radiofrequency introduction combined with Q-switched laser comprehensive treatment of moderate to severe melasma.Methods:From December 2019 to September 2021, ninety-six female patients with melasma [age 24-59 years old, average age (37.8±6.0) years old] were admitted to the Plastic and Aesthetic Department of the First Affiliated Hospital of Henan University of Chinese Medicine. They were divided into the Q-switched laser group and the combined group by random number table method, with 48 cases respectively. The Q-switched laser group received Q-switched laser therapy, while the combined group received tranexamic acid radiofrequency introduction combined with Q-switched laser comprehensive therapy. The melasma area and severity index (MASI) scores were compared between the two groups before and after treatment. The clinical efficacy, adverse reactions and recurrence rates of the two groups were compared.Results:The MASI scores of the Q-switched laser group and the combined treatment group were (28.28±1.24) points and (28.52±4.25) points respectively before treatment, and (13.38±7.96) points and (9.11±5.48) points respectively after treatment. The MASI scores of the two groups were decreased after treatment, which of the combined group was lower than that of the Q-switched laser group ( t=3.06, P<0.05). The total clinical effective rate of the combination group (93.75%) was higher than that of the Q-switched laser group (79.17%) (χ 2=4.36, P<0.05). The incidence rate of hyperpigmentation (2.08%) and recurrence rate (2.08%) of the combination group were lower than those of the Q-switched laser group (14.58%, 16.67%) (χ 2=6.01, P<0.05). Conclusions:Tranexamic acid radiofrequency introduction combined with Q-switched laser comprehensive treatment can improve skin lesions and clinical efficacy in patients with moderate to severe melasma, and reduce pigmentation and recurrence.
ABSTRACT
<p><b>OBJECTIVE</b>To study the relationship between SNP rs17401966 at the KIF1B gene and the genetic susceptibility to Hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>All study objects were recruited from two Grade A hospitals of Amoy from January 2011 to October 2014.They were surveyed in individual matching case-control study. Accepting criterias in the cases: HCC was first diagnosed based on diagnostic basis during the investigations, over 18 years old, present addresses were as same as surveyed areas in the district (county) level range, no past history of cancers; Exclusion criterias: patients with other liver diseases. The tumor patients without HCC, patients with autoimmune hepatitis or toxic hepatitis, patients who refused to be investigated or too ill to be investigated. Accepting criterias in the controls: the control who passed the physical examination matched the case in ages (no more than 3 years old), sex, health screening in the same hospital over the same period and district (county); Exclusion criterias: people with liver disease or any history of cancers. This study consisted of 376 HCC patients and 403 controls, 5 ml morning fasting venous blood of all subjects were obtained to isolate cells and distribute genotype. The differences in general information between cases and controls were tested by χ² test and t-test. The association between SNP rs17401966 and the risk of developing HCC were assessed by using the multiple factors logistic regression.</p><p><b>RESULTS</b>The mean age and standard deviation for case and control groups were (61.7 ± 12.8) years and (60.6 ± 12.7) years (t = 1.15, P = 0.251), respectively. The proportion of family history of cancer [28.7% (108/376)] and the HBsAg positive rate [26.9 % (101/376)] in case group were higher than these in control group [15.9% (64/403), 2.7% (11/403)] (χ² = 18.65, 92.02, P < 0.001). In HBsAg carriers, GG genotype genetic susceptibility to HCC is 0.12 (0.02-0.75) times for AA genotype, and G allele susceptibility to HCC is 0.38 (0.15-0.98) times for A allelc. In HBsAg negative group, it showed no statistical significance in the relationship between SNP rs17401966 and susceptibility to HCC, and compared with the A allele, the risk for HCC of G allele is 0.79 (0.62-1.01).</p><p><b>CONCLUSION</b>The results demonstrated that the presence of the GG genotype, the GA genotype and the G allele at rs17401966 of the KIF1B gene might decrease the risk for HCC.</p>