ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

Merkel cell polyomavirus (MCV) was named thus because it is the causative agent of Merkel cell carcinoma (MCC), with 80% of MCC cases being MCV-positive. MCV has been classified as a 2A carcinogen. It promotes carcinogenesis by integrating T antigens into the cell genome. The anti-MCV seroprevalence in the general population is as high as 90%. Usually, MCV is latent after infection in immunocompetent patients, and the incidence of MCC in immunosuppressive or defective patients, such as those with organ transplants, chronic lymphocytic leukemia, and HIV infection, is remarkably high. Patients with HIV/AIDS are a typical population with acquired immunodeficiency. At present, the research on patients with HIV/AIDS and MCV infection, activation, and pathogenesis is limited. In this paper, the progress of previous research is reviewed and the relationship between HIV infection and MCV activation is systematically investigated to provide a reference for the prevention and treatment of MCC in key populations, such as patients with HIV/AIDS.

Objective:To explore the role of curcumin (Cur) in improving IgA nephropathy (IgAN) and its related mechanisms.Methods:Fifty 7-month-old miR-23b knockout (miR-23b -/-) mice weighing (25±5) g were used to establish an IgAN disease model, and were randomly divided into IgAN group, IgAN+Cur (150 mg/kg) group and IgAN+Cur (300 mg/kg) group using simple randomisation. Sixteen healthy 7-month-old weighing (25±3) g C57BL/6J wild-type mice served as the normal control group. IgAN+Cur (150 mg/kg) and IgAN+Cur (300 mg/kg) groups were respectively gavaged continuously with 150 mg/kg Cur and 300 mg/kg Cur for 8 weeks, and the normal control and IgAN groups were gavaged continuously with an equal dose of 0.9% sodium chloride solution for 8 weeks. The samples of urine, serum, intestinal fluid, intestinal tissues, kidney tissues and liver tissues were collected from each group. In vitro experiments, human cloned colon adenocarcinoma (Caco-2) cells were divided into blank control (Ctrl), Ctrl+Cur (10 μmol/L), Ctrl+ Cur (60 μmol/L), tumor necrosis factor-α（TNF-α), TNF-α+Cur (10 μmol/L) and TNF-α+Cur (60 μmol/L) groups. Enzyme-linked immunosorbent assay was used to detect serum alanine transaminase, aspartate transaminase, secretory IgA (sIgA), creatinine, blood urea nitrogen, 24 h urine microalbumin, as well as sIgA, TNF-α, interleukin（IL)-6 and IL-1β in the intestinal fluids. HE staining was used to observe the effect of Cur on liver tissues, the hyperplasia of glomerular mesangial zone in kidney tissues and the morphological and structural changes of intestinal epithelial barrier, and the histopathological damage scores were performed respectively. PAS staining was used to observe the changes of glomerular basement membrane and mesangial matrix. Immunofluorescence was used to observe the deposition of immune complexes in the glomerular mesangial zone. Real-time quantitative PCR was used to detect the mRNA expression levels of B-cell activating factor ( BAFF) and a proliferation inducing ligand ( APRIL). Western blotting was used to detect the protein expression levels of tight junction proteins zonula occluden-1 (ZO-1) and occludin in the mouse intestinal tissues. The potential targets of Cur in IgAN were predicted. Western blotting was used to detect the protein expression levels of tight junction proteins, as well as Toll-like receptor 9 (TLR9), myeloid differentiation primary response protein (MyD88), nuclear factor-κB p65 (NF-κB p65) and p-NF-κB p65. Results:Genetic identification results revealed that all IgAN model mice exhibited the miR-23b -/- genotype, confirming successful model establishment. Seven-month-old mice were subsequently selected for Cur treatment. Histopathological analysis demonstrated no significant differences in hepatic tissue morphology across groups, with comparable liver histopathological injury scores and unaltered liver function parameters, thereby validating the safety of Cur administration. Compared with the normal control group, IgAN mice displayed elevated levels of serum sIgA, serum creatinine, blood urea nitrogen and 24 h urine microalbumin (all P<0.05). Renal pathological results revealed severe mesangial hypercellularity in glomeruli, higher glomerular injury scores, and notable glomerular mesangial deposits of IgA, IgG and complement C3 in IgAN mice (all P<0.05). Additionally, intestinal pathological alterations were observed, including structural changes in intestinal epithelium and Peyer's patches, accompanied by significantly higher intestinal histopathological injury scores in IgAN mice ( P<0.05). Intestinal epithelial expression levels of ZO-1 and occludin were significantly reduced, while sIgA, TNF-α, IL-1β and IL-6 in intestinal fluid were elevated (all P<0.05). Serum FITC fluorescence intensity was markedly increased, and intestinal tissue exhibited upregulated mRNA expression of BAFF and APRIL (all P<0.05). Following Cur treatment, serum sIgA level and renal function indices in mice showed partial recovery (all P<0.05). Renal pathological improvements included alleviated mesangial hypercellularity, reduced glomerular injury scores, and diminished glomerular immune complex deposition (all P<0.05). Intestinal pathologies, including epithelial and Peyer's patch lesions, were mitigated, with decreased intestinal histopathological injury scores ( P<0.05). Additionally, intestinal tight junction protein expression levels were upregulated, intestinal fluid sIgA level was reduced, inflammatory markers were attenuated, serum FITC fluorescence intensity was declined, and intestinal BAFF and APRIL mRNA expression levels were downregulated (all P<0.05). In vitro experiments demonstrated that TNF-α exposure reduced tight junction protein expression in Caco-2 cells, whereas Cur treatment reversed the effect (all P<0.05). Target prediction analysis revealed that Cur effectively bound to TLR9 structural domain in IgAN. Experimental validation confirmed that Cur treatment suppressed the upregulated protein expression levels of TLR9, MyD88, NF-κB p65 and p-NF-κB p65 in intestinal tissues of IgAN mice (all P<0.05). Conclusion:Cur has a significant effect in the treatment of IgAN and can regulate intestinal mucosal immunity by inhibiting the TLR9/MyD88/NF-κB signaling pathway, thereby reducing renal injury and protecting the kidneys.

Objective:To investigate the efficacy and safety of obinutuzumab combined with short-course dexamethasone in patients with relapsed immune thrombocytopenia (ITP) who had previously been treated with rituximab.Methods:A retrospective case series study was conducted. A total of 8 patients with relapsed ITP after treatment with rituximab who received obinutuzumab combined with short-course dexamethasone between January 2023 and January 2024 in the First Affiliated Hospital of Harbin Medical University were collected. The clinical characteristics, changes in platelet counts, changes in peripheral blood B-lymphocyte counts, treatment outcome and treatment-related adverse events were analyzed.Results:There were 1 male and 7 females in 8 patients with relapsed ITP after treatment with rituximab. The median age [ M ( Q1, Q3)] of the 8 enrolled patients was 52.5 (40.5, 56.0) years. The median relapsed times was 2.0 (2.0, 2.5) times and the median course of disease was 16.0 (13.0, 18.5) months. The platelet count increased from 8.73 (5.79, 11.65)×10 9/L pre-treatment to 180.00 (83.40, 255.00)×10 9/L post-treatment, and the difference was statistically significant ( Z = -2.37, P = 0.018); conversely, peripheral blood B-lymphocyte count decreased from 322.59 (148.29, 403.07) × 10 9/L pre-treatment to 1.23 (0.57, 1.76) ×10 9/L post-treatment, and the difference was statistically significant ( Z = -2.52, P = 0.012). After obinutuzumab and short-course dexamethasone treatment, 6 patients achieved complete remission, 1 case showed response, and 1 case had no response. No severe adverse events were observed during treatment and follow-up in all patients. Conclusions:Obinutuzumab combined with short-course dexamethasone appears to be effective in treating relapsed ITP patients after treatment with rituximab, and its safety is good.

Objective:To explore the role of curcumin (Cur) in improving IgA nephropathy (IgAN) and its related mechanisms.Methods:Fifty 7-month-old miR-23b knockout (miR-23b -/-) mice weighing (25±5) g were used to establish an IgAN disease model, and were randomly divided into IgAN group, IgAN+Cur (150 mg/kg) group and IgAN+Cur (300 mg/kg) group using simple randomisation. Sixteen healthy 7-month-old weighing (25±3) g C57BL/6J wild-type mice served as the normal control group. IgAN+Cur (150 mg/kg) and IgAN+Cur (300 mg/kg) groups were respectively gavaged continuously with 150 mg/kg Cur and 300 mg/kg Cur for 8 weeks, and the normal control and IgAN groups were gavaged continuously with an equal dose of 0.9% sodium chloride solution for 8 weeks. The samples of urine, serum, intestinal fluid, intestinal tissues, kidney tissues and liver tissues were collected from each group. In vitro experiments, human cloned colon adenocarcinoma (Caco-2) cells were divided into blank control (Ctrl), Ctrl+Cur (10 μmol/L), Ctrl+ Cur (60 μmol/L), tumor necrosis factor-α（TNF-α), TNF-α+Cur (10 μmol/L) and TNF-α+Cur (60 μmol/L) groups. Enzyme-linked immunosorbent assay was used to detect serum alanine transaminase, aspartate transaminase, secretory IgA (sIgA), creatinine, blood urea nitrogen, 24 h urine microalbumin, as well as sIgA, TNF-α, interleukin（IL)-6 and IL-1β in the intestinal fluids. HE staining was used to observe the effect of Cur on liver tissues, the hyperplasia of glomerular mesangial zone in kidney tissues and the morphological and structural changes of intestinal epithelial barrier, and the histopathological damage scores were performed respectively. PAS staining was used to observe the changes of glomerular basement membrane and mesangial matrix. Immunofluorescence was used to observe the deposition of immune complexes in the glomerular mesangial zone. Real-time quantitative PCR was used to detect the mRNA expression levels of B-cell activating factor ( BAFF) and a proliferation inducing ligand ( APRIL). Western blotting was used to detect the protein expression levels of tight junction proteins zonula occluden-1 (ZO-1) and occludin in the mouse intestinal tissues. The potential targets of Cur in IgAN were predicted. Western blotting was used to detect the protein expression levels of tight junction proteins, as well as Toll-like receptor 9 (TLR9), myeloid differentiation primary response protein (MyD88), nuclear factor-κB p65 (NF-κB p65) and p-NF-κB p65. Results:Genetic identification results revealed that all IgAN model mice exhibited the miR-23b -/- genotype, confirming successful model establishment. Seven-month-old mice were subsequently selected for Cur treatment. Histopathological analysis demonstrated no significant differences in hepatic tissue morphology across groups, with comparable liver histopathological injury scores and unaltered liver function parameters, thereby validating the safety of Cur administration. Compared with the normal control group, IgAN mice displayed elevated levels of serum sIgA, serum creatinine, blood urea nitrogen and 24 h urine microalbumin (all P<0.05). Renal pathological results revealed severe mesangial hypercellularity in glomeruli, higher glomerular injury scores, and notable glomerular mesangial deposits of IgA, IgG and complement C3 in IgAN mice (all P<0.05). Additionally, intestinal pathological alterations were observed, including structural changes in intestinal epithelium and Peyer's patches, accompanied by significantly higher intestinal histopathological injury scores in IgAN mice ( P<0.05). Intestinal epithelial expression levels of ZO-1 and occludin were significantly reduced, while sIgA, TNF-α, IL-1β and IL-6 in intestinal fluid were elevated (all P<0.05). Serum FITC fluorescence intensity was markedly increased, and intestinal tissue exhibited upregulated mRNA expression of BAFF and APRIL (all P<0.05). Following Cur treatment, serum sIgA level and renal function indices in mice showed partial recovery (all P<0.05). Renal pathological improvements included alleviated mesangial hypercellularity, reduced glomerular injury scores, and diminished glomerular immune complex deposition (all P<0.05). Intestinal pathologies, including epithelial and Peyer's patch lesions, were mitigated, with decreased intestinal histopathological injury scores ( P<0.05). Additionally, intestinal tight junction protein expression levels were upregulated, intestinal fluid sIgA level was reduced, inflammatory markers were attenuated, serum FITC fluorescence intensity was declined, and intestinal BAFF and APRIL mRNA expression levels were downregulated (all P<0.05). In vitro experiments demonstrated that TNF-α exposure reduced tight junction protein expression in Caco-2 cells, whereas Cur treatment reversed the effect (all P<0.05). Target prediction analysis revealed that Cur effectively bound to TLR9 structural domain in IgAN. Experimental validation confirmed that Cur treatment suppressed the upregulated protein expression levels of TLR9, MyD88, NF-κB p65 and p-NF-κB p65 in intestinal tissues of IgAN mice (all P<0.05). Conclusion:Cur has a significant effect in the treatment of IgAN and can regulate intestinal mucosal immunity by inhibiting the TLR9/MyD88/NF-κB signaling pathway, thereby reducing renal injury and protecting the kidneys.

Objective To review the literatures about ability in management of perioperative frailty in the elderly cancer patients and to provide references for clinical development of perioperative frailty management.Methods The methodological framework proposed by Arskey and O'Malley was used to retrieve studies on perioperative management of frailty in elderly cancer patients through the databases of CNKI,Wanfang Data,Chinese Biomedical Literature,PubMed,CINAHL,Embase,Cochrane and Scopus,from inception of the databases to May 2023.The included literatures were summarised and analysed by two independent researchers.Results A total of 23 studies were included,with 14 randomised controlled trials,6 reviews,1 expert consensus and 2 quasi-experimental studies.Perioperative frailty management abstracted from the retrieved literatures included preoperative frailty management,early postoperative frailty management,continuous frailty management after discharge,and hospice care management.Conclusions Perioperative fateful management of elderly cancer patients is diversified,including management of perioperative frailty,early postoperative frailty,continuous frailty after discharge and hospice care.The results of this study provide references in perioperative frailty management of elderly cancer patients.

Objective:To evaluate the effect of Qishi Tongguan Prescription on pregnancy outcomes after interventional recanalisation in patients with tubal infertility (TFI).Methods:This was a retrospective study based on real-world and propensity score matching. Totally 260 patients with TFI from January 2020 to October 2021 in Shuguang Hospital of Shanghai University of Traditional Chinese Medicine and Maternal and Child Health Hospital of Pudong New Area were selected as observation subjects, and were divided into 123 cases in the TCM combination group and 137 cases in the control group based on whether they were treated with Qishi Tongguan Prescription in combination with interventional revascularization. Propensity score matching (PSM) was used as a covariate to obtain a new sample of inter group covariate equilibrium, and confounding factors that may affect the pregnancy outcome of TFI patients undergoing interventional recanalization surgery were used as covariates. The intrauterine pregnancy rate, ectopic pregnancy rate, biochemical pregnancy rate, early abortion rate and adverse reactions of the two groups of patients within 12 months of follow-up were compared, and the influence of TFI intervention and recanalization combined with Qishi Tongguan Prescription on intrauterine pregnancy rate was evaluated.Results:Age, years of infertility, type of infertility, history of miscarriage, history of ectopic pregnancy, history of biochemical pregnancy, history of uterine surgery, history of pelvic laparotomy, and degree of tubal patency had an effect on whether intrauterine pregnancy was achieved after interventional reversal in patients with TFI ( P<0.05), with age [ OR (95% CI) was 0.843 (0.769, 0.926)], history of pelvic laparotomy [ OR (95% CI) was 0.477 (0.248, 0.920)] and the degree of tubal obstruction [ OR (95% CI) was 0.152 (0.046, 0.500)] were independent factors ( P<0.01 or P<0.05). 81 patients were seen in each of the 2 groups after PSM, of whom the intrauterine pregnancy rates in the combined herbal group at 9 and 12 months after recanalisation were 48.1% (39/81) and 58.0% (47/81) respectively, compared with 32.1% (26/81) and 35.8% (29/81) in the control group, with statistical significance between the 2 groups ( χ2 values of 4.34 and 8.03, respectively, P<0.01); there was no statistical significance in the ectopic pregnancy rate, biochemical pregnancy rate and early abortion rate between the 2 groups ( P>0.05). There were no significant adverse reactions during the treatment. Conclusion:Qishi Tongguan Prescription combined with interventional recanalization can effectively improve the intrauterine pregnancy rate and shorten the waiting time for pregnancy in patients with TFI with higher safety.

Objective:To explore the safety and efficacy of Obinutuzumab in the treatment of immune thrombotic thrombocytopenic purpura.Methods:Data from a case of immune thrombotic thrombocytopenic purpura (iTTP) admitted to the Department of haematology of the First Affiliated Hospital of Harbin Medical University were evaluated retrospectively and a literature review was performed.Results:A 66-year-old female patient was admitted to our hospital for thrombocytopenia. On admission, physical examination showed that yellow skin and sclera. The patient was fully conscious but had a decreasing ability to calculate. Laboratory examination revealed a platelet count of 7×10 9/L; liver function: alanine aminotransferase 55.2 U/L, azelaic aminotransferase 117.5 U/L; total bilirubin 142.7 μmol/L, direct bilirubin 64.6 μmol/L, indirect bilirubin 78.1 μmol/L; lactate dehydrogenase: 2362 U/L; creatinine: 260.7 μmol/L; peripheral blood smear showed 4% fragmented erythrocytes; ADAMTS13 activity 2.7% and positive inhibitor (1.12 BU). The patient is treated with plasma exchange and glucocorticoids, but the patient’s symptoms worsened. Rituximab was permanently discontinued for severe infusion reactions. Treatment with Obinutuzumab (1000 mg, qw×2 w) and she achieved a complete remission for 18 months. The treatment was well tolerated with no adverse events related to Obinutuzumab. Conclusion:For iTTP patients with rituximab intolerance, obinutuzumab is a safe and effective alternative treatment option.

Objective:To explore the safety and efficacy of Obinutuzumab in the treatment of immune thrombotic thrombocytopenic purpura.Methods:Data from a case of immune thrombotic thrombocytopenic purpura (iTTP) admitted to the Department of haematology of the First Affiliated Hospital of Harbin Medical University were evaluated retrospectively and a literature review was performed.Results:A 66-year-old female patient was admitted to our hospital for thrombocytopenia. On admission, physical examination showed that yellow skin and sclera. The patient was fully conscious but had a decreasing ability to calculate. Laboratory examination revealed a platelet count of 7×10 9/L; liver function: alanine aminotransferase 55.2 U/L, azelaic aminotransferase 117.5 U/L; total bilirubin 142.7 μmol/L, direct bilirubin 64.6 μmol/L, indirect bilirubin 78.1 μmol/L; lactate dehydrogenase: 2362 U/L; creatinine: 260.7 μmol/L; peripheral blood smear showed 4% fragmented erythrocytes; ADAMTS13 activity 2.7% and positive inhibitor (1.12 BU). The patient is treated with plasma exchange and glucocorticoids, but the patient’s symptoms worsened. Rituximab was permanently discontinued for severe infusion reactions. Treatment with Obinutuzumab (1000 mg, qw×2 w) and she achieved a complete remission for 18 months. The treatment was well tolerated with no adverse events related to Obinutuzumab. Conclusion:For iTTP patients with rituximab intolerance, obinutuzumab is a safe and effective alternative treatment option.