摘要:

AbstractGranulocyte colony‐stimulating factor (G‐CSF) is a cytokine that mediates the clonal proliferation and differentiation of progenitor cells into mature granulocytes. The kinetics of G‐CSF production by human bone marrow fibroblasts (BMF) were investigated by quantitative immunoassays. The spontaneous production of G‐CSF by BMF was below the detectable level. Interleukin‐1 (IL‐1) induced a dose‐dependent production of G‐CSF, and the production reached a plateau at 50 U/ml of IL‐1. G‐CSF production by BMF stimulated with IL‐1 was cell concentration dependent. Detectable G‐CSF was produced by 5 × 102BMF in a 35 × 10‐mm plastic dish. The optimal range was 1 × 104−5 × 104BMF. Production of newly synthesized G‐CSF was detectable 6 hr after stimulation and continued for approximately 48 hr. A 6‐hr pulse exposure to IL‐1 was necessary to induce production of G‐CSF, and after 48 hr, the adherent BMF could not be restimulated. IL‐2, IL‐3, IL‐4, IL‐5, and IL‐6 were unable to induce G‐CSF production. However, IL‐4 promoted G‐CSF production after stimulation with IL‐1. These results provide useful data with regard to the mechanism

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<71::AID-AJH1>3.0.CO;2-2

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractMore effective and safer regimens are needed for patients who have advanced multiple myeloma resistant to or relapsing despite prior treatment with alkylating agents and VAD. We treated 58 such patients using the combination of twice daily cyclophosphamide (total dose 1.8 g/m2) and VAD (hyperCVAD). Treatment was given to outpatients followed by G‐CSF at 5 μg/kg/d until granulocyte recovery. Twenty‐three patients responded (40%), with a median duration of granulocyte depression to less than 500/μl of 4 days and a mortality rate of 2%. The median survival time for all patients was 15 months, and the median remission time of responding patients was 8 months. Patients who had low LDH, low B2M, or primary resistant disease lived significantly longer than patients without these features. The combination of fractionated cyclophosphamide and VAD provided an effective and safe rescue treatment for many patients who had advanced myeloma resistant to standard therapies. © 1996 Wiley‐L

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<77::AID-AJH2>3.0.CO;2-2

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractB cell reconstitution after bone marrow transplantation is slow in patients with chronic graft‐vs.‐host disease (cGVHD). Could this be secondary to decreased production of B cells in the bone marrow? We determined the relative amount of B cell precursors in the marrow of 26 patients at approximately 1 year after marrow transplant (10 patients with and 16 patients without clinical cGVHD) and 8 normal adult controls. In the controls (median), 3.1% of all marrow mononuclear cells were B cell precursors. The patients without cGVHD tended to have higher than normal percents of B cell precursors (median 6.5%; the difference from normal adults was not significant). In contrast, the patients with cGVHD had barely detectable B cell precursors (median 0.2%; the difference from normal adults was significant,P= 0.004). Therefore, delayed reconstitution of B cells in patients with cGVHD appears to be due at least in part to decreased B cell production by the marrow. © 1996 Wiley‐Lis

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<82::AID-AJH3>3.0.CO;2-1

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractThe incidence of antibodies to heparin‐PF4 complexes (H‐PF4) has been evaluated in patients who were under heparin therapy for more than 7 days: 109 patients treated with unfractionated heparin (UH) and 100 patients with low‐molecular‐weight heparin (LMWH). The presence of antibodies was identified in 17% of the former group and 8% of the latter. In both the UH and the LMWH groups, IgM antibodies were found in all but four patients who showed IgA antibodies. IgG isotypes were only detected in five patients and were consistently associated to either IgM or IgA antibodies. The follow‐up of H‐PF4 antibodies in 76 patients treated with UH from 1 to ≥ 12 days showed a relationship between the incidence of antibodies and the duration of therapy. Despite the presence of anti‐H‐PF4 antibodies there was no thrombocytopenia (150 109/L. Our study demonstrates that the induction of antibodies to H‐PF4 is a frequent phenomenon in patients treated with UH or with LMWH. The absence of thrombocytopenia and of clinical complications in these patients demonstrates that other conditions must be associated with H‐PF4 antibodies for inducing type II HIT: optimal concentrations of heparin and PF4 in the blood circulation to allow the formation of macromolecular H‐PF4 complexes, presence of activated platelets that present an increased binding of H‐PF4 complexes, increased expression of FcγRIIA receptors, or presence of their H 131 phenotype. We conclude that the measurement of antibodies to H‐PF4 complexes allows the detection of heparin‐treated patients at risk of developing type

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<90::AID-AJH4>3.0.CO;2-0

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractCardiac function was measured at rest and during exercise in 9 patients with sickle‐cell anemia (SS) and coexisting homozygous alpha thalassemia‐2 (alpha thal‐2). Results were compared with 18 sickle cell patients with normal alpha globin genes, who were matched to the study group by age, gender, and size, and to published normal values. SS alpha thal‐2 patients were less anemic: 9.9 ± 1.0 vs 8.2 ± 1.2 gm/dl for SS alone (P<.05). Left ventricular dimensions were normal in SS alpha thal‐2 (4.9 ± 0.7 cm), but increased in SS (5.4 ± 0.7, cmP= .05) (normal range, 3.7–5.6 cm). Left ventricular wall thickness was, however, dramatically increased in the SS alpha thal‐2 patients (free wall, 1.8 ± 0.6 cm; septum, 1.6 ± 0.4 cm), though SS controls had normal wall thickness (free wall, 1.0 ± 0.2 cm; septum, 1.0 ± 0.2 cm,P<.001) (normal range, 0.6–1.1 cm). At rest, Doppler indices of systolic function were not significantly different between sickle groups and normal values. SS alpha thal‐2 patients did have abnormal diastolic filling at rest, as evidenced by a reduced ratio of early/late diastolic filling, 1.4 ± 0.3 vs. 2.0 ± 0.5 for SS controls (P<.01), and 1.8 ± 0.4 for normals. An analysis of covariance suggested that this abnormality persisted after taking into account the previously demonstrated hypertrophy. During exercise, SS alpha thal‐2 patients had higher heart rates and blood pressures than SS controls in spite of performing the same or less work. This resulted in a higher double product (an estimate of oxygen consumption) in SS alpha thal‐2 patients (37,470 ± 2,310 mm Hg‐BPM) than in SS controls (33,310 ± 1,490 mm Hg‐BPM,P<.01). Work capacity, peak heart rate, and blood pressure were all abnormally decreased in both sickle‐cell groups when compared to normal. Cardiac abnormalities noted at rest and during exercise in SS alpha thal‐2 patients suggest a role of microvascular occlusion and a protective effect of de

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<96::AID-AJH5>3.0.CO;2-0

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractSickle‐cell disease (SCD) is the most common cause of avascular necrosis (AVN) of the hip in childhood. It results in significant physical impairment and chronic pain, and often progresses to require hip replacement. Conservative therapy is ineffective. We evaluated whether core decompression can arrest progression of AVN. We performed 13 coring procedures in 10 patients with SCD and AVN. Patients ranged from age 9–21 years at diagnosis (mean, median age, 15 years); five hips were stage I, six hips were stage II, and two hips were stage III. Mean follow‐up on these patients was 3.7 years. Efficacy of the procedure was evaluated by clinical improvement in pain, radiographic progression, and need for further surgery. All 5 stage I patients had substantial improvement in pain, and only one showed X‐ray progression. Five of the 6 (83%) stage II patients had improvement in pain, and 2 patients progressed on X‐ray. Both stage III patients progressed on X‐ray, but one was clinically improved. None of the 10 patients has required further surgery. Our results demonstrate that in early AVN, core decompression was beneficial for almost all patients, even with progression on X‐ray. Core decompression should be considered in the management of SCD patients with early AVN. © 1996 W

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<103::AID-AJH6>3.0.CO;2-Y

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractAplastic anemia is a disorder characterized by pancytopenia and bone marrow hypocellularity. There is some evidence that aplastic anemia may be due to suppression of hematopoiesis by activated T‐suppressor cells. Thus, immunosuppressive agents have been used as an alternative to bone marrow transplantation for treatment. We report on a unique case of a patient with aplastic anemia who was treated with a course of immunosuppression including cyclosporine (CSA), anti‐thymocyte globulin (ATG), and prednisone. Five months after this treatment, the patient developed a B cell lymphoproliferative disorder which was successfully treated with radiation therapy. Prior reports of CSA‐associated lymphoproliferative disorders have appeared in the literature as potential side effects of immunosuppression following transplantation. This is the first report of a lymphoproliferative disorder associated with immunosuppressive treatment of aplastic anemia in a nontransplant setting. Thus, when presenting options for treatment of aplastic anemia, lymphoproliferative disorders should be included as a rare complication of immunosuppressive therapy. © 1996 Wiley‐L

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<108::AID-AJH7>3.0.CO;2-Y

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractWe conducted this study to investigate whether antioxidized low‐density lipoprotein (a‐oxLDL) is an antibody to cryptic and/or neo‐antigen on β2‐glycoprotein I (GPI), which is introduced by binding to anionic phospholipid, similar to that of GPI‐dependent anticardiolipin antibody (aCL) employing a‐oxLDL ELISA. We found that no significant optical density differences existed among systemic lupus erythematosus patients, including cases with aCL and/or lupus anticoagulant positivity, before and after the addition of GPI. Our results suggest that a‐oxLDL is not an antibody to denatured GPI, but rather to oxLDL. © 1996

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<114::AID-AJH8>3.0.CO;2-X

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractSkin necrosis is a rare but serious complication of oral anticoagulation with coumarin derivatives. Frequently, the necrosis can be extensive and may result in major morbidity and mortality. The majority of these patients require prolonged anticoagulation for life‐threatening conditions such as deep venous thrombosis and pulmonary embolism. Resuming oral anticoagulants in the face of skin necrosis is a difficult decision for both the patient and the physician. Because long‐term heparin therapy is inconvenient and is associated with significant side effects, we reviewed the literature to find alternative treatment strategies. A Medline search was done, and all papers published in English since 1967 were reviewed. Of 58 cases with skin necrosis attributed to oral anticoagulants, oral anticoagulation was resumed in 7 patients with no resulting adverse effects. Warfarin is the most widely used coumarin derivative in the United States. Based on our review, we make recommendations for resuming warfarin in patients who have developed skin necrosis when the clinical condition absolutely requires prolonged anticoagulation. © 1996 Wiley‐Lis

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199606)52:2<117::AID-AJH9>3.0.CO;2-X

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

ISSN:0361-8609    

DOI:10.1002/1096-8652(199606)52:2<120::AID-AJH2830520202>3.0.CO;2-M

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY