***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE Behçet 's disease ( BD ) is a multisystem vasculopathy of unknown cause with variable clinical presentation and the outcome of current treatments is often unsatisfactory . There is evidence for T-cell autoreactivity in BD and this study explores the therapeutic response to lymphocyte depletion with a humanized anti-CD52 antibody , CAMPATH-1H . METHODS Eighteen patients with active BD received a single course of 134 mg of CAMPATH-1H . Immunosuppressives were withdrawn and prednisolone reduced according to clinical status . Treatment response was assessed by remission of clinical features of disease activity , erythrocyte sedimentation rate , C-reactive protein , prednisolone dose , the need for subsequent immunosuppressives and disease relapse . RESULTS By 6 months , 13/18 ( 72 % ) had entered remission and average , daily prednisolone dose was reduced from 17.7 to 6.7 mg/day ( P < 0.005 ) . At patient follow-up after 37 ( 6 - 60 ) months , seven had relapsed after an average of 25 months , five had required the introduction of an immunosuppressive drug and two had been retreated with CAMPATH-1H ; 10 were in stable remission and six were receiving no therapy . Moderate infusion-related adverse effects occurred in five and two developed hypothyroidism . Circulating CD4 + T cells fell to low levels after CAMPATH-1H and remained depressed for at least 1 yr ; no opportunistic infections were seen . CONCLUSIONS The therapeutic response to CAMPATH-1H suggests a central role for autoreactive lymphocytes in BD . The potential of CAMPATH-1H to induce sustained treatment-free remission in BD poorly controlled by conventional therapy requires further evaluation BACKGROUND The anti-CD52 monoclonal antibody alemtuzumab reduces disease activity in previously untreated patients with relapsing-remitting multiple sclerosis . We aim ed to assess efficacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite first-line treatment . METHODS In our 2 year , rater-masked , r and omised controlled phase 3 trial , we enrolled adults aged 18 - 55 years with relapsing-remitting multiple sclerosis and at least one relapse on interferon beta or glatiramer . Eligible participants were r and omly allocated in a 1:2:2 ratio by an interactive voice response system , stratified by site , to receive subcutaneous interferon beta 1a 44 μg , intravenous alemtuzumab 12 mg per day , or intravenous alemtuzumab 24 mg per day . Interferon beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baseline and for 3 days at 12 months . The 24 mg per day group was discontinued to aid recruitment , but data are included for safety assessment s. Co primary endpoints were relapse rate and time to 6 month sustained accumulation of disability , comparing alemtuzumab 12 mg and interferon beta 1a in all patients who received at least one dose of study drug . This study is registered with Clinical Trials.gov , number NCT00548405 . FINDINGS 202 ( 87 % ) of 231 patients r and omly allocated interferon beta 1a and 426 ( 98 % ) of 436 patients r and omly allocated alemtuzumab 12 mg were included in the primary analyses . 104 ( 51 % ) patients in the interferon beta 1a group relapsed ( 201 events ) compared with 147 ( 35 % ) patients in the alemtuzumab group ( 236 events ; rate ratio 0·51 [ 95 % CI 0·39 - 0·65 ] ; p<0·0001 ) , corresponding to a 49·4 % improvement with alemtuzumab . 94 ( 47 % ) patients in the interferon beta 1a group were relapse-free at 2 years compared with 278 ( 65 % ) patients in the alemtuzumab group ( p<0·0001 ) . 40 ( 20 % ) patients in the interferon beta 1a group had sustained accumulation of disability compared with 54 ( 13 % ) in the alemtuzumab group ( hazard ratio 0·58 [ 95 % CI 0·38 - 0·87 ] ; p=0·008 ) , corresponding to a 42 % improvement in the alemtuzumab group . For 435 patients allocated alemtuzumab 12 mg , 393 ( 90 % ) had infusion-associated reactions , 334 ( 77 % ) had infections ( compared with 134 [ 66 % ] of 202 patients in the interferon beta 1a group ) that were mostly mild-moderate with none fatal , 69 ( 16 % ) had thyroid disorders , and three ( 1 % ) had immune thrombocytopenia . INTERPRETATION For patients with first-line treatment-refractory relapsing-remitting multiple sclerosis , alemtuzumab could be used to reduce relapse rates and sustained accumulation of disability . Suitable risk management strategies allow for early identification of alemtuzumab 's main adverse effect of secondary autoimmunity . FUNDING Genzyme ( Sanofi ) and Bayer Schering Pharma BACKGROUND Multiple sclerosis results from T-cell-dependent inflammatory demyelination of the central nervous system . Our objective was long-term suppression of inflammation with short-term monoclonal antibody treatment . METHODS We depleted 95 % of circulating lymphocytes in 27 patients with multiple sclerosis by means of a 5-day pulse of the humanised anti-CD52 monoclonal antibody , Campath-1H . Clinical and haematological consequences of T-cell depletion , and in-vitro responses of patients ' peripheral-blood mononuclear cells were analysed serially for 18 months after treatment . FINDINGS Radiological and clinical markers of disease activity were significantly decreased for at least 18 months after treatment . However , a third of patients developed antibodies against the thyrotropin receptor and carbimazole-responsive autoimmune hyperthyroidism . The depleted peripheral lymphocyte pool was reconstituted with cells that had decreased mitogen-induced proliferation and interferon gamma secretion in vitro . INTERPRETATION Campath-1H causes the immune response to change from the Th1 phenotype , suppressing multiple sclerosis disease activity , but permitting the generation of antibody-mediated thyroid autoimmunity BACKGROUND The anti-CD52 monoclonal antibody alemtuzumab reduced disease activity in a phase 2 trial of previously untreated patients with relapsing-remitting multiple sclerosis . We aim ed to assess efficacy and safety of first-line alemtuzumab compared with interferon beta 1a in a phase 3 trial . METHODS In our 2 year , rater-masked , r and omised controlled phase 3 trial , we enrolled adults aged 18 - 50 years with previously untreated relapsing-remitting multiple sclerosis . Eligible participants were r and omly allocated in a 2:1 ratio by an interactive voice response system , stratified by site , to receive intravenous alemtuzumab 12 mg per day or subcutaneous interferon beta 1a 44 μg . Interferon beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baseline and once per day for 3 days at 12 months . Co primary endpoints were relapse rate and time to 6 month sustained accumulation of disability in all patients who received at least one dose of study drug . This study is registered with Clinical Trials.gov , number NCT00530348 . FINDINGS 187 ( 96 % ) of 195 patients r and omly allocated interferon beta 1a and 376 ( 97 % ) of 386 patients r and omly allocated alemtuzumab were included in the primary analyses . 75 ( 40 % ) patients in the interferon beta 1a group relapsed ( 122 events ) compared with 82 ( 22 % ) patients in the alemtuzumab group ( 119 events ; rate ratio 0·45 [ 95 % CI 0·32 - 0·63 ] ; p<0.0001 ) , corresponding to a 54·9 % improvement with alemtuzumab . Based on Kaplan-Meier estimates , 59 % of patients in the interferon beta 1a group were relapse-free at 2 years compared with 78 % of patients in the alemtuzumab group ( p<0·0001 ) . 20 ( 11 % ) of patients in the interferon beta 1a group had sustained accumulation of disability compared with 30 ( 8 % ) in the alemtuzumab group ( hazard ratio 0·70 [ 95 % CI 0·40 - 1·23 ] ; p=0·22 ) . 338 ( 90 % ) of patients in the alemtuzumab group had infusion-associated reactions ; 12 ( 3 % ) of which were regarded as serious . Infections , predominantly of mild or moderate severity , occurred in 253 ( 67 % ) patients treated with alemtuzumab versus 85 ( 45 % ) patients treated with interferon beta 1a . 62 ( 16 % ) patients treated with alemtuzumab had herpes infections ( predominantly cutaneous ) compared with three ( 2 % ) patients treated with interferon beta 1a . By 24 months , 68 ( 18 % ) patients in the alemtuzumab group had thyroid-associated adverse events compared with 12 ( 6 % ) in the interferon beta 1a group , and three ( 1 % ) had immune thrombocytopenia compared with none in the interferon beta 1a group . Two patients in the alemtuzumab group developed thyroid papillary carcinoma . INTERPRETATION Alemtuzumab 's consistent safety profile and benefit in terms of reductions of relapse support its use for patients with previously untreated relapsing-remitting multiple sclerosis ; however , benefit in terms of disability endpoints noted in previous trials was not observed here . FUNDING Genzyme ( Sanofi ) and Bayer Schering Pharma This study investigated the efficacy , safety , and clinical benefit of alemtuzumab ( Campath-1H ) for patients with relapsed or refractory B-cell chronic lymphocytic leukemia exposed to alkylating agents and having failed fludarabine therapy . Ninety-three patients received alemtuzumab in 21 centers worldwide , with the aim to obtain an overall response rate of at least 20 % . Dosage was increased gradually ( target 30 mg , 3 times weekly , for a maximum of 12 weeks ) . Infection prophylaxis was m and atory , beginning on day 8 , and continuing for a minimum of 2 months after treatment . Responses were assessed at weeks 4 , 8 , and 12 , and patients were followed for 34 months . Overall objective response in the intent-to-treat population ( n = 93 ) was 33 % ( CR 2 % , PR 31 % ) . Median time to response was 1.5 months ( range , 0.4 - 3.7 months ) . Median time to progression was 4.7 months overall , 9.5 months for responders . At data cut-off , 27 patients ( 29 % ) were alive ; overall median survival was 16 months ( 95 % CI : 11.8 - 21.9 ) and 32 months for responders . Nineteen responders survived more than 21 months . Clinical benefit was observed both in responders and in patients with stable disease . The most common adverse events were related to infusion , generally grade 1 or 2 in severity , occurring mainly in the first week . Grade 3 or 4 infections were reported in 25 patients ( 26.9 % ) . However , only 3 ( 9.7 % ) of 31 patients who responded to alemtuzumab treatment developed grade 3 or 4 infections on the study . Alemtuzumab induced significant responses in these patients with clinical benefit in the majority and with acceptable toxicity in a high-risk group CONTEXT Alemtuzumab , an anti-CD52 monoclonal antibody , increased the risk of thyroid dysfunction in CAMMS223 , a phase 2 trial in relapsing-remitting multiple sclerosis . OBJECTIVE The objective of the study was a detailed description of thyroid dysfunction in CAMMS223 . DESIGN Relapsing-remitting multiple sclerosis patients ( n=334 ) were r and omized 1:1:1 to 44 μg sc interferon-β-1a ( SC IFNB-1a , Rebif ) or annual courses of 12 or 24 mg iv alemtuzumab  . Thyroid function tests ( TSH , free T3 , free T4 ) and thyrotropin-binding inhibitory immunoglobulin ( TBII ) were assessed at screening , month 1 , and quarterly thereafter ; antithyroid peroxidase antibodies were assessed at screening and every 6 months . Thyroid dysfunction episodes were categorized post hoc by 
    Output:
    
In patients with relapsing-remitting MS , alemtuzumab 12 mg was better than subcutaneous interferon beta-1a for the following outcomes assessed at 24 months : relapse-free survival , sustained disease progression-free survival , number of participants with at least one adverse event and number of participants with new or enlarging T2-hyperintense lesions on MRI .
Alemtuzumab 24 mg seemed to be better than subcutaneous interferon beta-1a for relapse-free survival and sustained disease progression-free survival , at 36 months .