Background: Recently, several studies have reported an association between lipid profiles and sudden sensorineural hearing loss (SSNHL), yet there is considerable variability between the individual studies in defining the precise association between serum lipids levels and SSNHL. This study sought to identify a possible relationship between dyslipidemia and the prevalence and prognosis of SSNHL.Methods: A case‐control study was carried out at two independent medical centers, including 2,288 SSNHL patients and 2,288 healthy controls. Clinical characteristics and serum lipid parameters were assessed, including total cholesterol (CHOL), high‐density lipoprotein (HDL), low‐density lipoprotein (LDL), triglycerides (Trig), apolipoprotein AI (ApoAI), apolipoprotein B (ApoB), and lipoprotein a (Lpa). Multivariate logistic regression analysis was performed to assess the relationship between lipid profiles and SSNHL in the 4,576 subjects.Results: Significant differences were identified in several conventional serum lipid markers including CHOL, Trig, HDL, LDL, ApoAI, ApoB, and Lpa, between SSNHL patients and healthy controls. Serum ApoAI levels were significantly lower in patients with bilateral SSNHL compared to unilateral SSNHL. Binary logistic regression analysis revealed that higher levels of ApoB, LDL, Trig, and lower levels of ApoAI and HDL were all associated with an increased risk of SSNHL. After clinical characterization, multivariate analysis showed that only low levels of ApoB predicted likelihood of a recovery of more than 30 dB among patients with SSNHL.Conclusions: Serum lipids are associated with the incidence and prognosis of SSNHL. Identification of dyslipidemia may improve early evaluation and management of SSNHL risks.

Objective: To gain further insights into the predisposing risk factors for central nervous system (CNS) involvement in patients with acute lymphocytic leukemia (ALL), the impact of CD56 expression in these patients was investigated. Methods: We reviewed the clinical features of CD56 expression in 588 consecutive ALL patients treated with systemic chemotherapy regimens between 2000 and 2014. The categorical data from CD56⁺ ALL patients were compared with those from CD56⁻ ALL patients. Results: Among the 588 patients studied, 18.9% showed CD56 expression. The expression was significantly associated with CD33⁺, CD10⁻, CD15⁺, TdT⁻, and CD5⁺ immunophenotypes. After systemic chemotherapy, 8.8% patients showed CNS involvement, of which 3.2% exhibited combined recurrences and 5.6% exhibited isolated CNS involvement. The 5-year event-free survival was significantly lower for patients with CD56⁺ immunophenotype compared with patients with CD56⁻ immunophenotype (22.5% vs. 32.7%, P = 0.04). Cumulative incidences of CNS involvement were significantly greater in the CD56⁺ cohort compared with the CD56⁻ cohort (14.4% vs. 7.5%, P = 0.02). Multivariate analysis revealed CD56 expression to be statistically significant risk factors for CNS involvement. Conclusion: CD56 expression should be regarded as an independent risk factor for ALL with CNS involvement in adults.

Despite the outstanding advances made over the past decade regarding our knowledge of acute leukemia (AL), relapsed AL remains to be associated with a dismal prognosis. A better understanding of AL relapse and monitoring of the D‑dimer and lactate dehydrogenase (LDH) plasma levels following chemotherapy may aid clinicians in determining whether relapse may occur in the subsequent phases of the disease. The present study evaluated D‑dimer and LDH levels in 204 patients with relapsed AL. Data were collected at the initial onset of AL, at complete remission (CR) and in patients with relapsed AL. D‑dimer plasma levels were significantly increased in patients with initial AL and in patients with relapsed AL (P=0.005 and P=0.007, respectively) but not in those with CR. LDH levels were significantly increased in AL patients at the initial onset of disease and at relapse compared with patients achieving CR, irrespective of cell type. Plasma prothrombin time, activated partial thromboplastin time and fibrinogen levels were not significantly different across patients (with the exception of acute promyelocytic leukemia patients) at the initial onset, relapsed AL or CR. Routine hematological parameters (white blood cell count, hemoglobin, platelet count) were significantly different at the initial onset of AL (P=0.002, P<0.001 and P=0.001, respectively) and during relapsed AL (P=0.009, P=0.003 and P<0.001, respectively) compared with patients achieving CR, suggesting an association between D‑dimer, LDH and relapsed AL. These results also indicate that determination of D‑dimer and LDH levels may be useful for predicting the probability of relapse during chemotherapy, but should also be combined with routine hematological parameters.

Background: The emergence of resistance to azithromycin complicates the treatment of Neisseria gonorrhoeae, the causative agent of gonorrhea. Objectives: The main objective of this study was to investigate the impact of mutations in different sites of the rplD gene on azithromycin resistance (AZM-R) and the molecular characteristics of N. gonorrhoeae. This study aimed to provide evidence for drug resistance and transmission. Methods: A total of 37 isolates of N. gonorrhoeae were collected within January 2018 to December 2020. These isolates were obtained from urine, semen, or vaginal secretions of different patients. Azithromycin resistance was assessed, and genes associated with AZM-R, namely rplD, and rplV, were analyzed using polymerase chain reaction (PCR) and deoxyribonucleic acid (DNA) sequencing. All clinical isolates were characterized through multi-locus sequence typing (MLST). Results: The study comprised 21 azithromycin-resistant N. gonorrhoeae isolates, with two of them demonstrating high resistance, indicated by a minimum inhibitory concentration (MIC) greater than 256 µg/mL. Additionally, 16 sensitive isolates were included in the study. Ten isolates were observed to have rplD point mutations, including mutations such as G70D, G70S, G68D, and A43T. No mutations were detected in rplV. The rate of point mutations in rplD was significantly different between the azithromycin-sensitive (AZM-S) group and the AZM-R group (P < 0.05). Among the 37 isolates studied, 12 distinct MLST types were identified and further grouped into four different MLST goeBURST groups. The two isolates with high-level AZM-R were ST1901 and ST1588, respectively. Conclusions: The clinical isolates of N. gonorrhoeae from Wenzhou, Eastern China, exhibit significant genetic diversity and a relatively high prevalence of AZM-R. Mutations in the rplD gene were identified, which reduced susceptibility to macrolides and were significantly associated with increased AZM-R.