Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Crohn's disease (CD) is a chronic progressive inflammatory bowel disease. With the introduction of the "treat-to-target (T2T) " concept, the treatment goals for CD have become clearer and more specific. Traditional surgical treatment for CD typically follows a "complication-driven" approach, in which surgery is usually performed only after severe complications, such as bowel obstruction, fistulas, perforation, or cancer have occurred. The emergence of the treat-to-target strategy and the concept of disease clearance has transformed the surgical treatment of CD from a "passive rescue" model to an "active intervention" approach. Treatment goals have shifted from merely addressing complications and improving symptoms to achieving both short and long-term therapeutic objectives within the framework of treat-to-target. Achieving these goals helps to prevent CD-related complications, delay disease progression, reduce the risk of recurrence and malignancy, and improve the quality of life.

Objective:To evaluate the clinical characteristics of Crohn's disease (CD) patients with secondary upper gastrointestinal fistulas and analyze risk factors for recurrence.Methods:A restrospective observational research method was performed. Clinical data of CD patients with secondary upper gastrointestinal fistulas treated at Eastern Theater General Hospital of PLA from January 2010 to August 2024 were analyzed. Based on postoperative recurrence of upper gastrointestinal fistulas, the patients were divided into recurrence group and non-recurrence group. Differences in clinical data between the two groups were compared, and further multivariate Logistic regression analysis was used to identify the risk factors for fistula recurrence.Results:A total of 72 CD patients with secondary upper gastrointestinal fistulas were included, consisting of 48 males and 24 females, with a mean age of 39±12 years and a disease duration of 97±56 months, accounting for 2.8% of all CD patients undergoing surgeries during the same period. Among these patients, 75 upper gastrointestinal fistulas from 72 patients were identified, including 67 patients of simple duodenal fistula, 2 of simple gastric fistula, and 3 of double fistulas (2 of double duodenal fistulas and 1 of duodenal fistula combined with gastric fistula) .The preoperative diagnostic positivity rates were 55.6% (40/72) for gastroscopy, 54.2% (39/72) for upper gastrointestinal contrast imaging, 22.2% (16/72) for abdominal CT, and 22.2% (16/72) for colonoscopy. A history of biologic therapy was present in 33.3% (24/72) of patients, but none achieved fistula healing. All 72 patients underwent surgical treatment, with primary lesion surgical approaches including resection with anastomosis (37 patients, 51.4%) and resection with stoma (35 patients, 48.6%). Except for one gastric fistula treated by resection, all other fistulas underwent primary repair. During a median follow-up of 69 (40, 113) months, 8 patients (11.1%) required reoperation due to recurrent upper gastrointestinal fistulas (classified as the recurrence group), while the remaining 64 patients were assigned to the non-recurrence group. Univariate analysis revealed that the recurrence group had a higher proportion of patients aged 30-40 years ( P = 0.003), malnutrition ( P = 0.040), and anastomosis near the duodenum ( P = 0.047), but a lower proportion of postoperative biologic use ( P = 0.007) .Multivariate Logistic regression analysis showed that malnutrition and anastomosis near the duodenum were not the risk factors for duodenal fistula recurrence (both P > 0.05) . Conclusions:Upper gastrointestinal fistulas secondary to CD are rare, predominantly presenting as simple duodenal fistulas. Diagnosis primarily relies on gastroscopy and gastrointestinal contrast imaging. Biologic therapy shows poor efficacy, and most patients do not recur after the primary repair surgery of duodenal fistulas.

Objective To evaluate the efficacy,safety and patient compliance of a quadruple therapy containing minocycline compared with the traditional quadruple therapy in the treatment of Helicobacter(H.)pylori.Methods This study included 200 H.pylori positive patients,with 100 assigned to the minocycline-containing bismuth quadruple therapy group(LBMC group)and the other 100 to the amoxicillin-containing bismuth quadruple therapy group(LBAC group).After matching the two groups of patients using the propensity score matching(PSM)method,there were 86 cases in each group.Telephone follow-up was conducted on the 14th day after the start of treatment to record patient medication compliance and adverse drug reactions.A 13C urea breath test was performed for re-examination at least one month after completing the treatment plan and discontinuing medication.The intention-to-treat(ITT)and per-protocol(PP)analyses were used to compare the H.pylori eradication rates between the two groups,and Chi-square test and t-test were used for intergroup comparison.Results In the ITT analysis,the eradication rates of the LBMC group and the LBAC group were 89.5%(77/86,95%CI:82.9%～96.1%)and 82.6%(71/86,95%CI:74.4%～90.7%),respectively.In the PP analysis,the eradication rates were 92.6%(75/81,95%CI:86.8%～98.4%)and 88.8%(71/80,95%CI:81.7%～95.8%),respectively.The adverse reaction rate of the LBMC group was 27.9%(24/86),and that of the LBAC group 31.4%(27/86),showing no statistically significant difference(P>0.05).In terms of compliance,the LBMC group was 94.2%(81/86),and the LBAC group 93.0%(80/86),revealing no statistically significant difference(P>0.05).Conclusion As a first-line treatment for eradicating H.pylori,regimens containing minocycline demonstrate equivalent eradication rates to those containing amoxicillin,with similar safety and compliance.They can be used as an alternative treatment for patients allergic to penicillin.

Objective:To identify factors influencing treatment-free remission (TFR) outcomes in children and adolescent patients with chronic myeloid leukemia (CML) after imatinib (IM) discontinuation.Methods:This multicenter retrospective study analyzed 36 children and adolescent patients with CML from eight hematology centers in China (December 1, 2016, to September 27, 2024) who discontinued IM therapy with documented post-cessation outcomes. Clinical characteristics and molecular response dynamics were assessed. Univariate analysis and multivariate Cox proportional hazards regression models were employed to assess factors associated with TFR outcomes.Results:A total of 36 patients were documented, comprising 17 males and 19 females. The median ages at CML diagnosis and IM discontinuation were 11 years ( IQR: 5,16) and 20 years ( IQR: 14,25), respectively. The median time from IM initiation to first deep molecular response (DMR) was 21 months ( IQR: 13, 38). Pre-discontinuation, patients received IM for a median duration of 96 months ( IQR: 84, 121) and maintained DMR for 74 months ( IQR: 63, 89). With a median post-discontinuation follow-up of 38 months ( IQR: 15, 68), cumulative TFR rates at 6, 12, 24, and 36 months were 74.1%, 60.7%, 60.7%, and 56.0%, respectively, generating an overall TFR rate of 58.3%. Fifteen patients lost major molecular response at a median of 5 months post-discontinuation ( IQR: 3, 11). All 15 patients resumed tyrosine kinase inhibitor therapy, comprising 13 who restarted IM and 2 who switched to dasatinib. By the last follow-up, 13 (86.7% ) patients regained DMR after a median treatment duration of 5 months ( IQR: 3, 17), and no disease progression occurred in any patient. Withdrawal syndrome occurred in 2 (5.6% ) patients. Univariate analysis revealed significantly higher TFR rates in patients with pre-discontinuation IM duration of ≥100 months vs <100 months (82.4% vs 36.8%, P=0.017) and pre-discontinuation DMR duration of ≥72 months vs <72 months (84.2% vs 29.4%, P=0.003). Multivariate Cox analysis identified pre-discontinuation DMR duration as an independent protective factor for TFR ( HR=5.419, 95% CI: 1.524–19.272, P=0.009) . Conclusion:DMR duration was identified as an independent protective factor influencing TFR outcomes in children and adolescent patients with CML after IM discontinuation. Patients who maintained DMR for ≥72 months before IM discontinuation demonstrated a significantly higher TFR rate.

Crohn's disease (CD) is a chronic progressive inflammatory bowel disease. With the introduction of the "treat-to-target (T2T) " concept, the treatment goals for CD have become clearer and more specific. Traditional surgical treatment for CD typically follows a "complication-driven" approach, in which surgery is usually performed only after severe complications, such as bowel obstruction, fistulas, perforation, or cancer have occurred. The emergence of the treat-to-target strategy and the concept of disease clearance has transformed the surgical treatment of CD from a "passive rescue" model to an "active intervention" approach. Treatment goals have shifted from merely addressing complications and improving symptoms to achieving both short and long-term therapeutic objectives within the framework of treat-to-target. Achieving these goals helps to prevent CD-related complications, delay disease progression, reduce the risk of recurrence and malignancy, and improve the quality of life.

Objective:To evaluate the clinical characteristics of Crohn's disease (CD) patients with secondary upper gastrointestinal fistulas and analyze risk factors for recurrence.Methods:A restrospective observational research method was performed. Clinical data of CD patients with secondary upper gastrointestinal fistulas treated at Eastern Theater General Hospital of PLA from January 2010 to August 2024 were analyzed. Based on postoperative recurrence of upper gastrointestinal fistulas, the patients were divided into recurrence group and non-recurrence group. Differences in clinical data between the two groups were compared, and further multivariate Logistic regression analysis was used to identify the risk factors for fistula recurrence.Results:A total of 72 CD patients with secondary upper gastrointestinal fistulas were included, consisting of 48 males and 24 females, with a mean age of 39±12 years and a disease duration of 97±56 months, accounting for 2.8% of all CD patients undergoing surgeries during the same period. Among these patients, 75 upper gastrointestinal fistulas from 72 patients were identified, including 67 patients of simple duodenal fistula, 2 of simple gastric fistula, and 3 of double fistulas (2 of double duodenal fistulas and 1 of duodenal fistula combined with gastric fistula) .The preoperative diagnostic positivity rates were 55.6% (40/72) for gastroscopy, 54.2% (39/72) for upper gastrointestinal contrast imaging, 22.2% (16/72) for abdominal CT, and 22.2% (16/72) for colonoscopy. A history of biologic therapy was present in 33.3% (24/72) of patients, but none achieved fistula healing. All 72 patients underwent surgical treatment, with primary lesion surgical approaches including resection with anastomosis (37 patients, 51.4%) and resection with stoma (35 patients, 48.6%). Except for one gastric fistula treated by resection, all other fistulas underwent primary repair. During a median follow-up of 69 (40, 113) months, 8 patients (11.1%) required reoperation due to recurrent upper gastrointestinal fistulas (classified as the recurrence group), while the remaining 64 patients were assigned to the non-recurrence group. Univariate analysis revealed that the recurrence group had a higher proportion of patients aged 30-40 years ( P = 0.003), malnutrition ( P = 0.040), and anastomosis near the duodenum ( P = 0.047), but a lower proportion of postoperative biologic use ( P = 0.007) .Multivariate Logistic regression analysis showed that malnutrition and anastomosis near the duodenum were not the risk factors for duodenal fistula recurrence (both P > 0.05) . Conclusions:Upper gastrointestinal fistulas secondary to CD are rare, predominantly presenting as simple duodenal fistulas. Diagnosis primarily relies on gastroscopy and gastrointestinal contrast imaging. Biologic therapy shows poor efficacy, and most patients do not recur after the primary repair surgery of duodenal fistulas.