BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant sour...BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant source to trigger and sustain the pathophysiology has been proposed to come from the altered gut microbiota and chronic intestinal inflammation. In this case, our serendipitous finding provides convincing evidence that the persistently dysregulated autoimmunity may be generated, at least in a significant proposition of AA patients, by the altered gut microbiota and compromised intestinal epithelium.CASE SUMMARY A 30-year-old Chinese male patient with refractory severe AA experienced a 3-month-long febrile episode, and his fever was refractory to many kinds of injected broad-spectrum antibiotics. When presenting with abdominal cramps, he was prescribed oral mannitol and gentamycin to get rid of the gut infection. This treatment resulted in a quick resolution of the fever. Unanticipatedly, it also produced an excellent hematological response. He had undergone three episodes of recurrence within the one-year treatment, with each recurrence occurring 7-8 wk from the gastrointestinal inflammation eliminating preparations. However,subsequent treatments were able to produce subsequent remissions and consecutive treatments were successful in achieving durative hematological improvements, strongly indicating an etiological association between chronic gut inflammation and the development of AA. Interestingly, comorbid diseases superimposed on this patient(namely, psychiatric disorders, hypertension,insulin resistance, and renal dysfunction) were ameliorated together with the hematological improvements.CONCLUSION Chronic gut inflammation may be responsible for AA pathogenesis. The comorbidities and AA may share a common etiological association.展开更多
Objective： To observe the clinical effect of Astragalus Injection （黄芪注射液, Al） and its immuno-regulatory action in treating chronic aplastic anemia （CAA）. Methods： Sixty patients with CAA were randomly assig...Objective： To observe the clinical effect of Astragalus Injection （黄芪注射液, Al） and its immuno-regulatory action in treating chronic aplastic anemia （CAA）. Methods： Sixty patients with CAA were randomly assigned to two groups equally, both were treated with Stanozolol three times a day, 2 mg each time through oral intake, but AI was given additionally to the patients in the treated group once a day via intravenous dripping. All were treated for 15 days as one therapeutic course and the whole medication lasted for more than 4 months totally, with follow-up adopted. The clinical efficacy was estimated and the changes of T-lymphocyte subsets in peripheral blood as well as the serum levels of tumor necrosis factor-α （TNF-α ） and interleukin-2 （IL-2） were observed. Results： The total effective rate in the treated group was 83.3% （25/30）, which was higher than that in the control group 66.7% （20/30）, showing significant difference between them （P〈0.05）. Levels of hemoglobin, WBC, reticular cell and platelet were elevated in both groups after treatment, but the improvement was significantly better in the treated group than that in the control group with respect to the former three indexes （P〈0.05）. The level of CD4^＋ increased and that of CD8^＋ decreased significantly after treatment in the treated group （P〈0.05）, which showed significant difference as compared with those in the control group （P〈0.05）. Levels of serum TNF-α and IL-2 lowered after treatment in both groups, but significance only showed in the treated group （P〈0.05）. The degree of proliferation in bone marrow got raised significantly and the percentage of non-hemopoietic cells reduced significantly in the treated group after treatment, also showing significant difference to those in the control group （P〈0.05）. Conclusion： AI could promote the recovery of hemopoietic function, which might be through improving T-lymphocyte subsets and reducing the release of negative regulatory factors such as TNF-α and IL-2 to alleviate the inhibition on hemopoietic function.展开更多
Objective： To analyze changes in gene amplification in the mitochondrial genome and in the ID4 gene promoter methylation region in patients with chronic aplastic anemia （CAA） suffering from Kidney （Shen） yin defi...Objective： To analyze changes in gene amplification in the mitochondrial genome and in the ID4 gene promoter methylation region in patients with chronic aplastic anemia （CAA） suffering from Kidney （Shen） yin deficiency or Kidney yang deficiency. Methods： Bone marrow and oral epithelium samples were collected from CAA patients with Kidney yin deficiency or Kidney yang deficiency （20 cases）. Bone marrow samples were collected from 20 healthy volunteers. The mitochondrial genome was amplified by polymerase chain reaction （PCR）, and PCR products were used for sequencing and analysis. Results： Higher mutational rates were observed in the ND1-2, ND4-6, and CYTB genes in CAA patients suffering from Kidney yin deficiency. Moreover, the ID4 gene was unmethylated in bone marrow samples from healthy individuals, but was methylated in some CAA patients suffering from Kidney yin deficiency （positive rate, 60%） and Kidney yang deficiency （positive rate, 55%）. Conclusions： These data supported that gene mutations can alter the expression of respiratory chain enzyme complexes in CAA patients, resulting in energy metabolism impairment and promoting the physiological and pathological processes of hematopoietic failure. Functional impairment of the mitochondrial respiration chain induced by gene mutation may be an important reason for hematopoietic failure in patients with CA,＆,. This change is closely related to maternal inheritance and Kidney yin deficiency. Finally, these data supported the assertion that it is easy to treat disease in patients suffering from yang deficiency and difficult to treat disease in patients suffering from yin deficiency.展开更多
文摘BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant source to trigger and sustain the pathophysiology has been proposed to come from the altered gut microbiota and chronic intestinal inflammation. In this case, our serendipitous finding provides convincing evidence that the persistently dysregulated autoimmunity may be generated, at least in a significant proposition of AA patients, by the altered gut microbiota and compromised intestinal epithelium.CASE SUMMARY A 30-year-old Chinese male patient with refractory severe AA experienced a 3-month-long febrile episode, and his fever was refractory to many kinds of injected broad-spectrum antibiotics. When presenting with abdominal cramps, he was prescribed oral mannitol and gentamycin to get rid of the gut infection. This treatment resulted in a quick resolution of the fever. Unanticipatedly, it also produced an excellent hematological response. He had undergone three episodes of recurrence within the one-year treatment, with each recurrence occurring 7-8 wk from the gastrointestinal inflammation eliminating preparations. However,subsequent treatments were able to produce subsequent remissions and consecutive treatments were successful in achieving durative hematological improvements, strongly indicating an etiological association between chronic gut inflammation and the development of AA. Interestingly, comorbid diseases superimposed on this patient(namely, psychiatric disorders, hypertension,insulin resistance, and renal dysfunction) were ameliorated together with the hematological improvements.CONCLUSION Chronic gut inflammation may be responsible for AA pathogenesis. The comorbidities and AA may share a common etiological association.
基金Supported by the Funds of Langfang Municipal Department of Science and Technology (No 2005050245)
文摘Objective： To observe the clinical effect of Astragalus Injection （黄芪注射液, Al） and its immuno-regulatory action in treating chronic aplastic anemia （CAA）. Methods： Sixty patients with CAA were randomly assigned to two groups equally, both were treated with Stanozolol three times a day, 2 mg each time through oral intake, but AI was given additionally to the patients in the treated group once a day via intravenous dripping. All were treated for 15 days as one therapeutic course and the whole medication lasted for more than 4 months totally, with follow-up adopted. The clinical efficacy was estimated and the changes of T-lymphocyte subsets in peripheral blood as well as the serum levels of tumor necrosis factor-α （TNF-α ） and interleukin-2 （IL-2） were observed. Results： The total effective rate in the treated group was 83.3% （25/30）, which was higher than that in the control group 66.7% （20/30）, showing significant difference between them （P〈0.05）. Levels of hemoglobin, WBC, reticular cell and platelet were elevated in both groups after treatment, but the improvement was significantly better in the treated group than that in the control group with respect to the former three indexes （P〈0.05）. The level of CD4^＋ increased and that of CD8^＋ decreased significantly after treatment in the treated group （P〈0.05）, which showed significant difference as compared with those in the control group （P〈0.05）. Levels of serum TNF-α and IL-2 lowered after treatment in both groups, but significance only showed in the treated group （P〈0.05）. The degree of proliferation in bone marrow got raised significantly and the percentage of non-hemopoietic cells reduced significantly in the treated group after treatment, also showing significant difference to those in the control group （P〈0.05）. Conclusion： AI could promote the recovery of hemopoietic function, which might be through improving T-lymphocyte subsets and reducing the release of negative regulatory factors such as TNF-α and IL-2 to alleviate the inhibition on hemopoietic function.
基金Supported by the National Natural Science Foundation of China(No.81202839/H2902)the Class General Financial Grant from the China Postdoctoral Science Foundation(No.2012M521356)+1 种基金the Natural Science Foundation of Shandong Province(No.ZR2012HQ023)the Shandong Province Technology Development Program of Traditional Chinese Medicine(No.2011-063)
文摘Objective： To analyze changes in gene amplification in the mitochondrial genome and in the ID4 gene promoter methylation region in patients with chronic aplastic anemia （CAA） suffering from Kidney （Shen） yin deficiency or Kidney yang deficiency. Methods： Bone marrow and oral epithelium samples were collected from CAA patients with Kidney yin deficiency or Kidney yang deficiency （20 cases）. Bone marrow samples were collected from 20 healthy volunteers. The mitochondrial genome was amplified by polymerase chain reaction （PCR）, and PCR products were used for sequencing and analysis. Results： Higher mutational rates were observed in the ND1-2, ND4-6, and CYTB genes in CAA patients suffering from Kidney yin deficiency. Moreover, the ID4 gene was unmethylated in bone marrow samples from healthy individuals, but was methylated in some CAA patients suffering from Kidney yin deficiency （positive rate, 60%） and Kidney yang deficiency （positive rate, 55%）. Conclusions： These data supported that gene mutations can alter the expression of respiratory chain enzyme complexes in CAA patients, resulting in energy metabolism impairment and promoting the physiological and pathological processes of hematopoietic failure. Functional impairment of the mitochondrial respiration chain induced by gene mutation may be an important reason for hematopoietic failure in patients with CA,＆,. This change is closely related to maternal inheritance and Kidney yin deficiency. Finally, these data supported the assertion that it is easy to treat disease in patients suffering from yang deficiency and difficult to treat disease in patients suffering from yin deficiency.
