B-cell lymphoma with cytokine storm in serosal effusion: A case report and literature review.

RATIONALE: Cytokine storm is now considered to be a systemic inflammatory response, but local cytokine storm may exist in systemic diseases of the blood system. Monitoring of regional cytokine storm is an important clue for the diagnosis of systemic diseases. PATIENT CONCERNS: A 72-years-old male presented to our hospital with multiple serosal effusion without solid mass or enlarged lymph nodes. We found that the level of cytokines in ascites was tens to hundreds of times higher than that in plasma, mainly IL-6 and IL-8. DIAGNOSES: The patient was diagnosed with multiple serous effusion, hemophagocytic syndrome, B-cell lymphoma, Epstein-Barr virus infection, and hypoproteinemia. INTERVENTIONS: During hospitalization, the patient was treated with 5 courses of R-CVEP therapy and supportive treatment. OUTCOMES: After the first R-CVEP regimen, the patient's condition was evaluated as follows: hemophagocytic syndrome improved: no fever; Serum triglyceride 2.36 mmol/L; Ferritin 70.70 ng/L; no hemophagocyte was found in the bone marrow; the lymphoma was relieved, ascites disappeared, and bone marrow cytology showed: the bone marrow hyperplasia was reduced, and small platelet clusters were easily seen. Bone marrow flow cytometry showed that lymphocytes accounted for 13.7%, T cells increased for 85.7%, CD4/CD8 = 0.63, B cells decreased significantly for 0.27%, and NK cells accounted for 10.2%. Blood routine returned to normal: WBC 5.27 × 109/L, HB 128 g/L, PLT 129 × 109/L; Epstein-Barr virus DNA < 5.2E + 02 copies/mL; correction of hypoproteinemia: albumin 39.7 g/L. LESSONS: Cytokines in ascites are significantly higher than those in plasma by tens to hundreds of times, suggesting that "regional cytokine storms" may cause serosal effusion.

[Inhibitory Effect of Cinobufotalin on Macrophage Inflammatory Factor Storm and Its Mechanism].

OBJECTIVE: To investigate the inflammatory effects of Cinobufotalin on monocytes in resting state and macrophages in activated state and its molecular mechanism. METHODS: THP-1 cells were stimulated with Phorbol 12-myristate 13-acetate to induce differentiation into macrophages. Lipopolysaccharides was added to activate macrophages in order to establish macrophage activation model. Cinobufotalin was added to the inflammatory cell model for 24 h as a treatment. CCK-8 was used to detect cell proliferation, Annexin V /PI double staining flow cytometry was used to detect cell apoptosis, flow cytometry was used to detect macrophage activation, and cytometric bead array was used to detect cytokines. Transcriptome sequencing was used to explore the gene expression profile regulated by Cinobufotalin. Changes in the significantly regulated molecules were verified by real-time quantitative polymerase chain reaction and Western blot. RESULTS: 1∶25 concentration of Cinobufotalin significantly inhibited the proliferation of resting monocytes(P<0.01), and induced apoptosis(P<0.01), especially the activated macrophages(P<0.001, P<0.001). Cinobufotalin significantly inhibited the activation of macrophages, and significantly down-regulated the inflammatory cytokines(IL-6, TNF-α, IL-1ß, IL-8) released by activated macrophages(P＜0.001). Its mechanism was achieved by inhibiting TLR4/MYD88/P-IκBa signaling pathway. CONCLUSION: Cinobufotalin can inhibit the inflammatory factors produced by the over-activation of macrophages through TLR4/MYD88/P-IκBa pathway, which is expected to be applied to the treatment and research of diseases related to the over-release of inflammatory factors.

[Establishment of a Patient-Derived T-Cell Acute Lymphoblastic Leukemia Xenograft Model in Novel Immunodeficient NCG Mice].

OBJECTIVE: The leukemia cells from patients with T-cell acute lymphoblastic leukemia (T-ALL) were inoculated into NCG mice to establish a stable human T-ALL leukemia animal model. METHODS: Leukemia cells from bone marrow of newly diagnosed T-ALL patients were isolated, and the leukemia cells were inoculated into NCG mice via tail vein. The proportion of hCD45 positive cells in peripheral blood of the mice was detected regularly by flow cytometry, and the infiltration of leukemia cells in bone marrow, liver, spleen and other organs of the mice was detected by pathology and immunohistochemistry. After the first generation mice model was successfully established, the spleen cells from the first generation mice were inoculated into the second generation mice, and after the second generation mice model was successfully established, the spleen cells from the second generation mice were further inoculated into the third generation mice, and the growth of leukemia cells in peripheral blood of the mice in each group was monitored by regular flow cytometry to evaluate the stability of this T-ALL leukemia animal model. RESULTS: On the 10th day after inoculation, hCD45+ leukemia cells could be successfully detected in the peripheral blood of the first generation mice, and the proportion of these cells was gradually increased. On average, the mice appeared listless 6 or 7 weeks after inoculation, and a large number of T lymphocyte leukemia cells were found in the peripheral blood and bone marrow smear of the mice. The spleen of the mice was obviously enlarged, and immunohistochemical examination showed that hCD3+ leukemia cells infiltrated into bone marrow, liver and spleen extensively. The second and third generation mice could stably develop leukemia, and the average survival time was 4-5 weeks. CONCLUSION: Inoculating leukemia cells from bone marrow of patients with T-ALL into NCG mice via tail vein can successfully construct a patient-derived tumor xenografts (PDTX) model.

Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF­1α.

The purpose of the present study was to evaluate cimigenol (Cim) treatment effects to cell proliferation by breaking bone marrow stromal cells (BMSCs) through C-X-C chemokine receptor type 4 (CXCR4)/stromal cell-derived factor-1α (SDF-1α) pathway. MV-4-11 and U937 cell lines were used. The present study was divided into two parts. First, the cell lines were divided into normal control (NC), BMSC (cells co-cultured with BMSCs), BMSC + DMSO, BMSC + Low (treated with 5 mg/ml Cim), BMSC + Middle (treated with 10 mg/ml Cim), BMSC + High (treated with 20 mg/ml Cim). In the second step, the cell lines were divided into NC, BMSC, BMSC + BL8040 (treated with BL8040 which inhibits CXCR4), BMSC + Cim and BMSC + Cim + BL8040. EdU positive cell numbers were measured by EdU assay and apoptosis rate by flow cytometry and TUNEL assay. Relative gene and protein expression was measured by reverse transcription-quantitative PCR and western blotting assay. BMSCs were able to protect proliferation of cancer cells and decreased cell apoptosis compared with the NC group (P<0.001, respectively). With Cim supplement, the cell proliferation was decreased with cell apoptosis increasing compared with NC group (P<0.001 respectively). However, the anti-tumor effects of Cim were not significantly different from the BL8040 treated groups (P<0.001, respectively). In conclusion Cim decreased acute myeloid leukemia cells protected by BMSCs through the CXCR4/SDF-1α pathway.

Shengma Biejia Decoction Inhibits Cell Growth in Multiple Myeloma by Inducing Autophagy-Mediated Apoptosis Through the ERK/mTOR Pathway.

Shengma Biejia decoction (SMBJD), a traditional Chinese formula recorded in the Golden Chamber, has been widely used for the treatment of malignant tumors. However, its underlying molecular targets and mechanisms are still unclear. This study showed that SMBJD inhibited tumor growth and stimulated hemogram recovery significantly in a multiple myeloma xenograft model. Western blot and immunohistochemistry assays of tumor tissues showed that SMBJD reduced the ratio of autophagy-related proteins LC3-II/LC3-I, while P62 and apoptosis-related proteins cleaved caspase-3/caspase-3 and Bax/Bcl-2 were upregulated. In vitro experiments demonstrated the time-dependent and dose-dependent cytotoxicity of SMBJD on multiple myeloma cell lines H929 and U266 through MTT assays. The LC3-II/LC3-I ratio and number of GFP-LC3 puncta showed that SMBJD inhibited the autophagy process of H929 and U266 cells. Moreover, both SMBJD and 3-methyladenine (3-MA) caused a decrease in LC3-II/LC3-I, and SMBJD could not reverse the upregulation of LC3-II/LC3-I caused by bafilomycin A1 (Baf-A1). Furthermore, the results of annexin V-FITC and propidium iodide double staining demonstrated that SMBJD treatment induced the apoptosis of H929 and U266 cells. These data prove that SMBJD inhibits autophagy and promotes apoptosis in H929 and U266 cells. The results also show that rapamycin could reduce the rate of SMBJD-induced apoptosis in H929 and U266 cells, at a concentration which had no effect on apoptosis but activated autophagy. In addition, analysis of the mechanism indicated that levels of phosphorylated ERK and phosphorylated mTOR were increased by treatment with SMBJD in vivo and in vitro. These results indicate that SMBJD, an old and effective herbal compound, could inhibit the viability of H929 and U266 cells and induce autophagy-mediated apoptosis through the ERK/mTOR pathway. Thus, it represents a potential therapy strategy for multiple myeloma.

Philadelphia chromosome-positive acute lymphoblastic leukemia: a case report.

Prognosis of patients with Philadelphia-positive acute lymphoblastic leukemia (Ph-ALL) relapsing after allogeneic hematopoietic stem cell transplantation (HSCT) is extremely poor. Therefore, effective alternative therapeutic measures are urgently needed. Recently, the use of antigen receptor-modified T cells holds great promise for relapsed and refractory ALL treatment. Prior to chimeric antigen receptor T-cell (CAR-T) infusion conditioning chemotherapy is used routinely to establish a favorable in vivo environment for CAR-T expansion, which has mostly involved fludarabine and cyclophosphamide. We report on a patient presented with extreme fatigue and anemia and was diagnosed with relapsed and refractory acute lymphoblastic leukemia (ALL) harbored T315I-BCR-ABL mutation, who had undergone allogeneic HSCT and multiple reinducing chemotherapy, but achieved complete hematologic remission (CHR) with CAR -T infusion as a later salvage treatment. Prior to CAR-T infusion there was no conditioning chemotherapy, but a bone marrow suppression period induced by ponatinib. CAR-T cell infusion was well tolerated and the patient achieved a CHR and maintained it for three months. At present, there is no relevant report on the use of tyrosine kinase inhibitors (TKI) as preconditioning protocols before CAR-T cells infusion. Our case indicated ponatinib not only reduces tumor burden but may also serve as a conditioning regimen for CAR-T therapy in the treatment of relapsed and refractory Ph-ALL.

[Curative Efficacy and Survival Analysis of Low-Intensity Traditional Chemotherapy Regimen in the Elderly Patients with Acute Myeloid Leukemia (non-M3)].

OBJECTIVE: To investigate the short-term and long-term curative efficacy of low-intensity traditional chemotherapy regimen for elderly patients with acute myeloid leukemia (AML, non-M3) and related adverse reactions, in order to explore whether low-intensity traditional chemotherapy regimen still has application value in the treatment of elderly AML patients today. METHODS: The clinical characteristics, treatment response and prognosis of 67 elderly patients with AML (non-M3) admitted to our hospital from June 2008 to December 2018 were retrospectively analyzed. All patients received low-intensity conventional chemotherapy (i.e. lower standard dose, and without new drugs listed in China since the 21st century), including DA, HA, CAG, etc. The CR rate, median survival time and 5-year cumulative survival rate of patients were evaluated, and the related indexes were compared with the data reported in domestic and foreign literatures at the same time. RESULTS: The CR rate was 55.2% (37/67), the median survival time was 13.7 months, and the 5-year cumulative survival rate was (24.4±6.3)% in patients received low-intensity tradional chemotherapeutic regimens. The CR rates of high-risk group and non-high-risk group were 38.7% (12/31) and 69.4% (25/36), respectively; the median survival time of high-risk group and non-high-risk group was 8.9 months and 25.2 months respectively; the 5-year cumulative survival rate of high-risk group was (10.2±6.6)% and that of non-high-risk group was (36.0± 9.4)%. Compared with the data reported in the literature at the same time, the data obtained from the low-intensity traditional chemotherapy regimen for the elderly AML did not have an obvious disadvantage, morever had relatively short bone marrow suppression time, low induction early mortality rate and low incidence of severe infection. CONCLUSION: At present, the low-intensity traditional chemotherapy regimen still has good curative effect and survival advantages for elderly AML patients, especially for non-high-risk patients. The adverse reactions are controllable, and the physical and economic conditions of the vast majority of patients can bear the treatment regimen.

Anti-angiogenic activity of ShengMaBieJia decoction in vitro and in acute myeloid leukaemia tumour-bearing mouse models.

Context: ShengMaBieJia decoction (SMBJD) is used to treat solid and hematological tumours; however, its anti-angiogenesis activity remains unclear.Objective: This study verified the anti-angiogenic effects of SMBJD in vitro and in tumour-bearing acute myeloid leukaemia (AML) mouse models.Materials and methods: In vivo, the chicken chorioallantoic membrane (CAM) and BALB/c null mouse xenograft models were treated with SMBJD (0, 2, 4, and 8 mg/mL) for 48 h and for 2 weeks, respectively. Anti-angiogenic activity was assessed according to microvessel density (MVD) and immunohistochemistry (IHC) targeting CD31 and VEGFR2. In vitro, proliferation viability, migratory activity and tube formation were measured. Western blots and polymerase chain reaction (PCR) assays were used to examine the levels of PI3K, Akt, and VEGF.Results: HPLC analyses revealed the active constituents of SMBJD such as liquiritin, cimifugin, ferulic, isoferulic, and glycyrrhizic acids. In vitro, SMBJD treatment decreased cellular migration, chemotaxis, and tube formation at non-cytotoxic concentrations (2, 4, and 8 mg/mL) in a time- and dose-dependent manner. The dosage of less than IC20 is considered safe. In vivo, CAM models exhibited a decrease in MVD, and the tissues of xenografted mice possessed reduced CD31 and VEGFR2 expression. Conditioned media (CM) from AML cells (HL60 and NB4 cells) treated with non-cytotoxic doses of SMBJD inhibited chemotactic migration and tube formation in vitro. Both CM (HL60) and CM (NB4) exhibited downregulated expression of PI3K, Akt, and VEGF.Discussion and conclusions: SMBJD inhibited angiogenesis in AML through the PI3K/AKT pathway, which might be combined with targeted therapy to provide more effective treatment.

Solasonine Suppresses the Proliferation of Acute Monocytic Leukemia Through the Activation of the AMPK/FOXO3A Axis.

Solasonine, the main active ingredient of Solanum nigrum L., has been reported to exert extensive antitumor activity. However, the antitumor effects in acute monocytic leukemia and the exact mechanisms involved are unknown. In this study, we investigated the role of solasonine on inhibiting the progression of acute monocytic leukemia. Our findings showed that solasonine inhibited the proliferation of acute monocytic leukemic cell lines (THP-1 and MV4-11) in vitro. Solasonine promoted apoptosis and induced cell cycle arrest in the G2/M phase. Analysis of RNA-seq data suggested that solasonine correlated with increased expression of genes in the AMPK/FOXO3A pathway. Inhibition of AMPK with compound C followed by treatment with solasonine showed that solasonine reduced apoptosis, caused less cell cycle arrest, and inactivated the AMPK/FOXO3A axis in THP-1 and MV4-11 cells. Solasonine also inhibited tumor growth by the activation of the AMPK/FOXO3A axis. In conclusion, solasonine inhibited the progress of acute monocytic leukemia in vitro and in vivo and triggered the apoptosis and cell cycle arrest in the G2/M phase by upregulating the AMPK/FOXO3A pathway.

Tenacigenin B Has Anti-Tumor Effect in Lymphoma by In Vitro and In Vivo Study.

BACKGROUND The aim of this study was to examine the effects and mechanisms of tenacigenin B in lymphoma treatment by in vitro and in vivo experiment. MATERIAL AND METHODS Raji cells were treated by difference methods. Measuring the cell proliferation of difference groups was done by MTT assay; cell apoptosis and cell cycle of difference groups were evaluated by flow cytometer; relative mRNA expression was evaluated by real-time polymerase chain reaction (RT-PCR), and relative protein expressions were measured by western blot assay in an in vitro study. In an in vivo study, we used a nude mice model to explore the anti-tumor effects and mechanism of tenacigenin B. Cell apoptosis was measured by TUNEL assay; relative protein expressions were evaluated by immunohistochemistry assay, and relative mRNA expression was evaluated by RT-PCR. In addition, the blood components of difference groups were measured. RESULTS Compared with the Normal control group, the cell proliferation rate was significantly downregulated, with cell apoptosis significantly increasing with G1 phase in the Drug group and the si-Aurora-A group (P<0.05, respectively). The PTEN, PI3K, AKT, P53, and P21 mRNA and protein expressions of the Drug group, the si-Aurora-A group, and the si-Aurora-A+Drug group were significantly different (P<0.01, respectively), The tumor volume and weight of the Drug group, the si-Aurora-A group, and the si-Aurora-A+Drug group were significantly suppressed compared with the Normal group (P<0.01, respectively). The positive apoptosis cell number in the Drug group, the si-Aurora-A group, and si-Aurora-A+Drug group were increased compared with that of Normal group (P<0.01, respectively). CONCLUSIONS Tenacigenin B had anti-tumor effects on lymphoma via regulation of Aurora-A in vitro and in vivo.

Suppression of murine B-cell lymphoma growth by trichosanthin through anti-angiogenesis.

Studies have suggested trichosanthin (TCS) exerts antitumor activity mainly through direct cytotoxicity toward cancer cells and immune regulation. In this study, we conducted the proliferation and apoptosis assay on A20 cells and endothelial cells (ECs) with different concentrations of TCS and investigated the levels of gene expression linked to angiogenesis. Herein, a new mechanism that TCS inhibits murine B-cell lymphoma growth by anti-angiogenesis was reported. First, TCS inhibit tumor growth and prolonged survival significantly in vivo, and TCS depressed the formation of new blood vessels around the tumor in a dose-dependent manner. Further studies showed that the platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31)-positive endothelial cell numbers, and the serum levels of MMP-2 and MMP-9 were also lower in the study group than controls. However, TCS did neither change the ratio of T cells and NK cells in the spleen of treated mice nor affect the proliferation and apoptosis of A20 cells in vitro. Additionally, the newly formed blood vessels in chorioallantoic membranes treated with TCS were significantly reduced. Last, TCS may suppress the proliferation, induce apoptosis and decrease tube formation and migration of endothelial cells (ECs). And, the mRNA and protein levels of VEGF in ECs treated with TCS were lower than that in the control group. These findings confirm that inhibitory effect of TCS on A20 murine B-cell lymphoma growth is mediated via anti-angiogenesis, and which may be associated with the down-regulation of VEGF and MMPs expression. This is an indication that TCS may represent a natural anti-angiogenic drug for lymphoma therapy.

Marsdenia tenacissima extract suppresses tumor growth and angiogenesis in A20 mouse lymphoma.

Marsdenia tenacissima (MT), a traditional Chinese medicine, has been utilized in the treatment of a variety of malignant conditions for decades, but the underlying mechanism remains unclear. Angiogenesis, new blood vessel formation by nearby endothelial cells (ECs) from pre-existing vessels, plays a key role in cancer growth. In the present study, the effects of MT extract (MTE) on EC proliferation and apoptosis in vitro, and on A20 mouse lymphoma growth and angiogenesis in vivo were investigated. MTE exhibited an anti-proliferative effect on the ECs, with a half maximal inhibitory concentration of 11.91±0.24 µl/ml. Acridine orange/propidium iodide staining indicated that cell apoptosis increased with MTE concentration. Flow cytometry revealed that the EC apoptosis rates induced by 0, 6.25, 12.5 and 25 µl/ml MTE were 4.8, 23.3, 49.8 and 92.3%, respectively. In vivo, the volume and weight of the A20 solid tumors were significantly inhibited following administration of 300 µl MTE per day for 14 days (P<0.05). MTE showed extended survivability and a satisfactory security. Subsequent to treatment with MTE, peritumorous angiogenesis was significantly reduced, with lower microvessel density (P<0.05) was quantified by hemotoxylin and eosin staining. Moreover, serum vascular endothelial growth factor, matrix metalloproteinase (MMP)-2 and MMP-9 expression at the protein level in the MTE-treated group, quantified using an ELISA, was significantly lower than that of the control (P<0.05). In a chick chorioallantoic membrane assay, 12.5 and 25 µl/ml MTE distinctly decreased the level of angiogenesis (P<0.05). In conclusion, MTE exhibited potent anti-lymphoma efficacy in vitro and this may be associated with its effects against tumor angiogenesis.

[Modified Shengma Biejia Decoction Combined with CAG Program for Elderly Acute Myeloid Leuke- mia Patients with Yin Deficiency Toxin Stasis Syndrome].

OBJECTIVE: To observe the efficacy and safety of modified Shengma Biejia Decoction (MSBD) combined with CAG program in treating elderly acute myeloid leukemia (AML) patients with yin deficiency toxin stasis syndrome (YDTSS). METHODS: Totally 46 elderly AML patients were assigned to the treatment group (24 cases; treated with MSBD + CAG) and the control group (22 cases; treated with CAG + placebos of Chinese medicine) according to random digit table. The therapeutic course of CM placebo or MSBD was 21 days. The clinical efficacy and adverse reactions were observed. Meanwhile, physical state (ECOG Score), transfusion dependency, and TCM syndrome score were compared before and after treatment. RESULTS: (1) The complete remission rate was 54% (13/24) and the objective response rate (ORR) was 71% (17/24) in the treatment group, obviously higher than those of the control group [36% (8/22); 54% (13/24)], with statistical difference (P = 0.036, 0.042). When comparing the efficacy based on risk level, the moderate and poor ORR was 71% (10/14) and 67% (6/9) in the treatment group, and 57% (8/14) and 33% (2/6) in the control group, with statistical difference between the two groups (P = 0.048; P = 0.010). (2) Compared with before treatment in the same group, the ECOG score significantly decreased, the average infusion time of red cells and platelets were markedly prolonged in the treatment group after treatment (P < 0.05). ECOG score, the average infusion time of red cells and platelets were significantly better in the treatment group than in the control group after treatment (P < 0.05). (3) Compared with before treatment in the same group, scores of fever, hemorrhage, and bone pain were markedly reduced in the control group (P < 0.05); scores of fever, fatigue, hemorrhage, dry mouth, and bone pain were markedly reduced in the treatment group (P < 0.05). Better effect in relief of fever, fatigue, hemorrhage, dry mouth, and so on was obtained in the treatment group than in the control group (P < 0.05). (4) In aspect of hematotoxicity, the incidence of neutropenia, anemia, thrombocytopenia was obviously lower in the treatment group than in the control group [29.2% (7/24) vs 54.5% (12/22); 16.7% (4/ 24) vs 45.5% (10/22); 33.3% (8/24) vs 63.6% (14/22); P < 0.05]. The incidence of fatigue and anorexia was obviously lower in the treatment group than in the control group [37.5% (9/24) vs 63.6% (14/22), 37.5% (9/24) vs 81.8% (18/22); P < 0.05]. CONCLUSION: MSBD combined with CAG program in treating elderly AML patients with YDTSS, with efficacy enhancing toxicity reducing effect, had distinct advantages in improving physical condition and clinical symptoms, and reducing transfusion dependency.

[Experience of Professor SUN Xue-mei in Treatment of Primary Thrombocythemia].

There is no radical cure for essential thrombocythemia currently. Professor SUN Xue-mei has extensive clinical experience in treating it by combined therapy of Chinese and Western medicine. In this paper, authors tried to summarize her experience from guiding ideology and therapeutic points. Authors insisted on the direction of integrative medicine on the basis of syndrome differentiation, paying attention to psychological counseling,and applied individual treatment in clinics.

Small-lymphoid cells and myeloid antigen expression in a patient with IgG myeloma: A case report.

Multiple myeloma is defined as a malignant proliferation of a single clone of plasma cells resulting in monoclonal immunoglobulin production. Due to the number of plasma cell morphological variants, difficulty is often faced during morphological diagnosis. The current study describes the case of a 49-year-old woman presenting with atypical plasma cell morphology detected by a bone marrow examination. Flow cytometric immunophenotyping determined the nature of the neoplastic cells as monoclonal myeloma cells with myeloid antigen expression. Serum electrophoresis with immunofixation and subsequent clinical findings confirmed this diagnosis. Therefore, the immunophenotyping of plasma cells in myelomas may be useful for the diagnosis of cases with atypical plasma cell morphology.

[Thinking on Treatment of Severe Aplastic Anemia by Detoxication, Blood Activating, and Yin Nourishing Method].

Chinese medicine therapy has advantages in treating aplastic anemia (AA) in depart- ments of Chinese medicine (CM) blood diseases. But there is no unified syndrome typing standard of CM for severe AA. Heat-toxin induced yin deficiency syndrome is one of severe AA syndrome types com- monly seen in authors' long-term clinical practice. This syndrome type has the features of asthenia in ori- gin and asthenia in superficiality. Therefore, authors put forward that detoxication, blood activating, and yin nourishing (DBAYN) method, taking detoxication as superficiality and Shen supplementing as origin. Meanwhile, blood activating and stasis removing was assisted. Detoxication aimed to eliminating evils and purifying blood, blood activating aimed to getting rid of evils and generating new blood, and yin nour- ishing aimed to strengthening vital qi and nourishing blood. Classical recipes such as Xijiao Dihuang De- coction and Erzhi Pill could be modified. This theory was of great significance in complementing and per- fecting CM theoretical systems of AA, which provided beneficial ideas and methods for clinical treatment of severe AA.

Guillain Barré Syndrome in a multiple myeloma patient after the first course of bortezomib therapy: A case report.

Bortezomib is approved for treating relapsed multiple myeloma (MM) and mantle cell lymphoma, and clinical evidence has shown complete clinical responses in MM patients. Peripheral neuropathy is one of the most common adverse effects of bortezomib. However, rare evidence has shown that bortezomib is associated with Guillain-Barré syndrome (GBS). In the present study, a case of GBS is reported in an MM patient finishing the first course of bortezomib therapy. Based on a bone marrow cell examination revealing 34% plasma cell infiltration and according to the International Staging System, the patient was diagnosed with stage III MM (λ type). Thus, a chemotherapy protocol was performed, which consisted of bortezomib and dexamethasone. However, 5 days after the first cycle, paresthesias of the upper and lower limbs developed. Standard nerve conduction studies revealed marked reduction of the motor conduction velocity of the median nerve bilaterally and of the right ulnar nerve, while sensory conduction was significantly slowed in the majority of the nerves of the upper and lower limbs. However, there was no evidence of demyelination. With this clinical evidence, a diagnosis of GBS was considered. The patient was subsequently treated with high-dose intravenous immunoglobulins (IVIGs; 400 mg/kg/day for 5 days). Following IVIG treatment, the symptoms were largely relieved. This study suggested that GBS may occur when administering bortezomib, and that high-dose IVIGs could treat the symptoms of GBS.