今日の臨床サポート

Kaposi肉腫

著者: 加藤哲朗 東京慈恵会医科大学附属病院 感染症科

監修: 味澤篤 がん・感染症センター 都立駒込病院

著者校正/監修レビュー済:2018/11/06

概要・推奨   

疾患のポイント
  1. カポジ肉腫はAIDS患者に発生する代表的な悪性腫瘍である。主に皮膚や粘膜および消化管や肺などの内臓臓器に発生する。
  1. 原因はヒトヘルペスウイルス8(human herpes virus-8: HHV-8)であり、潜伏感染していたHHV-8が免疫力の低下に伴ってカポジ肉腫を発症すると考えられている。
  1. HIV感染者において、CD4陽性リンパ球数が500個/μL未満で発症リスクが増加し、特に200個/μL未満でのリスクが高い。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
加藤哲朗 : 特に申告事項無し[2021年]
監修:味澤篤 : 特に申告事項無し[2021年]

病態・疫学・診察

疾患情報(疫学・病態)  
  1. カポジ肉腫はAIDS患者に発生する代表的な悪性腫瘍である。主に皮膚や粘膜および消化管や肺などの内臓臓器に発生する。
  1. 原因はヒトヘルペスウイルス8(human herpes virus-8: HHV-8)であり、潜伏感染していたHHV-8が免疫力の低下に伴ってカポジ肉腫を発症すると考えられている[1]
  1. HIV感染者において、CD4陽性リンパ球数が500個/μL未満で発症リスクが増加し、特に200個/μL未満でのリスクが高い[2]
  1. 疫学的な特徴として、カポジ肉腫患者のほとんどが男性同性間性的接触者(MSM)であることが挙げられる。
問診・診察のポイント  
HIV感染症のリスクの確認:
  1. リスクの高い性行為歴、特に同性間性交渉歴

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文献 

著者: G Rezza, M Andreoni, M Dorrucci, P Pezzotti, P Monini, R Zerboni, B Salassa, V Colangeli, L Sarmati, E Nicastri, M Barbanera, R Pristerà, F Aiuti, L Ortona, B Ensoli
雑誌名: J Natl Cancer Inst. 1999 Sep 1;91(17):1468-74.
Abstract/Text BACKGROUND: The incidence of Kaposi's sarcoma (KS) is increased severalfold in individuals infected with human immunodeficiency virus-1 (HIV). Human herpesvirus 8 (HHV8) has also been implicated in KS. We investigated several factors that may determine the onset of KS, particularly HHV8 infection in individuals after becoming seropositive for HIV.
METHODS: We studied 366 individuals belonging to different HIV-exposure categories (i.e., homosexual activity, intravenous drug use, and heterosexual contact) for whom a negative HIV serologic test and then a positive HIV serologic test were available within a 2-year period. HHV8 antibody testing was performed by use of an immunofluorescence assay on the first serum sample available after the first positive HIV test. Actuarial rates of progression of KS and of other acquired immunodeficiency syndrome (AIDS)-defining diseases were estimated by use of time-to-event statistical methods. All statistical tests were two-sided.
RESULTS: Twenty-one of the 366 study participants developed AIDS-related KS, and 83 developed AIDS without KS. One hundred forty (38.3%) participants had detectable anti-HHV8 antibodies. The actuarial progression rate to KS among persons co-infected with HIV/HHV8 was nearly 30% by 10 years after HIV seroconversion. Increasing HHV8 antibody titers increased the risk of developing KS (for seronegative versus highest titer [1:125 serum dilution], adjusted relative hazard [RH] = 51.82; 95% confidence interval [CI] = 6.08-441.33) but not of other AIDS-defining diseases (adjusted RH = 1.14; 95% CI = 0.72-1.80). HHV8-seropositive homosexual men compared with HHV8-seropositive participants from other HIV-exposure categories showed an increased risk of KS that approached statistical significance (adjusted RH = 6.93; 95% CI = 0.88-54.84).
CONCLUSIONS: Approximately one third of individuals co-infected with HIV/HHV8 developed KS within 10 years after HIV seroconversion. Progression to KS increased with time after HIV seroconversion. Higher antibody titers to HHV8 appear to be related to faster progression to KS but not to other AIDS-defining diseases.

PMID 10469747  J Natl Cancer Inst. 1999 Sep 1;91(17):1468-74.
著者: Sara Lodi, Marguerite Guiguet, Dominique Costagliola, Martin Fisher, Andrea de Luca, Kholoud Porter, CASCADE Collaboration
雑誌名: J Natl Cancer Inst. 2010 Jun 2;102(11):784-92. doi: 10.1093/jnci/djq134. Epub 2010 May 4.
Abstract/Text BACKGROUND: Despite the success of combination antiretroviral therapy (cART) in reducing the incidence of Kaposi sarcoma, HIV-infected individuals who have responded to treatment continue to be diagnosed with Kaposi sarcoma. We examine factors associated with the incidence of Kaposi sarcoma among cART-treated HIV-infected homosexual men and changes in their survival after its diagnosis over calendar time.
METHODS: Data were from HIV-infected homosexual men with well-estimated dates of HIV seroconversion (ie, change in status from being HIV negative to having HIV antibodies detected). Incidence of Kaposi sarcoma was calculated. We used Kaplan-Meier methods to determine survival after Kaposi sarcoma diagnosis in three calendar periods: before 1996, 1996-2000, and 2001-2006. Poisson models were used to examine the effect of risk factors such as current and nadir CD4 cell count (ie, the lowest CD4 cell count ever recorded for a person), duration of infection, and age at diagnosis for Kaposi sarcoma incidence in cART-treated men. All statistical tests were two-sided.
RESULTS: Among the 9473 men, 555 were diagnosed with Kaposi sarcoma in the period 1986-2006, of whom 319 died. The percentage surviving 24 months after Kaposi sarcoma diagnosis rose statistically significantly during the study period from 35% (95% confidence interval [CI] = 29% to 42%) before 1996 to 84% (95% CI = 76% to 90%) in 1996-2000 and to 81% (95% CI = 70% to 88%) in 2001-2006 (P < .001). Seventy men were diagnosed with Kaposi sarcoma after starting cART. Current (ie, within 6 months) CD4 cell count was associated with incidence of Kaposi sarcoma among cART-treated men (rate ratios [RRs] = 18.91, 95% CI = 8.50 to 42.09, for CD4 level category <200 cells per cubic millimeter; RR = 3.55, 95% CI = 1.40 to 9.00, for 200-349 cells per cubic millimeter; and RR = 4.11, 95% CI = 1.74 to 9.70, for 350-499 cells per cubic millimeter; all compared with > or = 500 cells per cubic millimeter). After adjustment for current CD4 cell count, HIV infection duration, age, or nadir CD4 cell count was not associated with Kaposi sarcoma incidence.
CONCLUSIONS: Among cART-treated HIV-infected homosexual men, current CD4 cell count was the factor most strongly associated with the incidence of Kaposi sarcoma. Survival estimates after Kaposi sarcoma diagnosis have improved over time.

PMID 20442214  J Natl Cancer Inst. 2010 Jun 2;102(11):784-92. doi: 10.・・・
著者: H Katano, Y Sato, T Kurata, S Mori, T Sata
雑誌名: Am J Pathol. 1999 Jul;155(1):47-52. doi: 10.1016/S0002-9440(10)65097-3.
Abstract/Text Human herpesvirus 8 (HHV-8) has been demonstrated previously in Kaposi's sarcoma (KS) tissues by immunohistochemistry, in situ polymerase chain reaction, and in situ hybridization. The HHV-8-encoded protein ORF73 is a 222- or 234-kd protein named latent nuclear antigen (LNA) or latency-associated nuclear antigen (LANA) that is identified in HHV-8-infected cell lines by immunofluorescence assay. In the present study, a rabbit antibody against a recombinant ORF73 protein was developed. Immunofluorescent staining of a HHV-8-infected cell line, TY-1, showed that the staining pattern of the anti-ORF73 antibody overlapped completely the LANA staining pattern obtained using KS patients' sera. Immunoblotting analysis showed that the anti-ORF73 antibody reacted specifically with 222- and 234-kd proteins that were present in TY-1 and BCBL-1 cell lysates. Immunohistochemistry using a catalyzed signal amplification system demonstrated that the anti-ORF73 antibody reacted exclusively with the majority of KS spindle-shaped cells, showing a nuclear dot-like staining pattern. Some of the ORF73 protein-positive cells also expressed CD34 and vimentin but not CD68 or factor-VIII-related antigen. These data indicate that the anti-ORF73 antibody recognizes LANA and that most KS cells are infected with HHV-8 in the latent phase. Our findings also suggest that ORF73 protein plays an important role in the pathogenesis of KS.

PMID 10393835  Am J Pathol. 1999 Jul;155(1):47-52. doi: 10.1016/S0002-・・・
著者: H T Turoglu, M F Akisik, S Y Naddaf, W S Omar, J S Kempf, H M Abdel-Dayem
雑誌名: Clin Nucl Med. 1998 Jul;23(7):446-59.
Abstract/Text Examples of Ga-67 and Tl-201 scans in AIDS patients performed at St. Vincent's Hospital and Medical Center of New York are presented. Use of these methods is the adopted approach at this institution in AIDS patients for localizing sites of tumor or infection involvement. A Ga-67 scan is the most common nuclear medicine examination performed on AIDS patients. Sequential Tl-201 and Ga-67 scans have a role in differentiating Kaposi's sarcoma from malignant lymphoma and opportunistic infections. For intracranial lesions, Tc-99m MIBI or Tl-201-201-201-201 chloride can differentiate malignant from benign inflammatory lesions.

PMID 9676950  Clin Nucl Med. 1998 Jul;23(7):446-59.
著者: B Holkova, K Takeshita, D M Cheng, M Volm, C Wasserheit, R Demopoulos, A Chanan-Khan
雑誌名: J Clin Oncol. 2001 Sep 15;19(18):3848-51. doi: 10.1200/JCO.2001.19.18.3848.
Abstract/Text PURPOSE: Kaposi's sarcoma (KS) is the most common AIDS-related malignancy. Pulmonary involvement by KS (PKS) has carried a poor prognosis with median reported survival ranging from 3 to 10 months. We studied whether the introduction of highly active antiretroviral therapy (HAART; triple antiretroviral therapy including a protease inhibitor and two reverse transcriptase inhibitors) has been associated with improved survival for AIDS patients with PKS.
PATIENTS AND METHODS: A retrospective study was performed of 37 consecutive patients with PKS and human immunodeficiency virus infection in the tumor registry at a large municipal hospital in New York City between 1994 to 1997. There were 16 patients from 1994 to 1995 (pre-HAART period) and 21 patients from 1996 to 1997 (post-HAART period). The primary end point was survival, which was defined as time from start of chemotherapy until death from any cause.
RESULTS: Patients were analyzed by the date of diagnosis (pre- v post-HAART period) and whether or not they received HAART. Kaplan-Meier analysis showed significantly better survival in patients diagnosed in the post-HAART period (P =.0025). Additional Kaplan-Meier analysis indicated that patients on HAART had substantially better survival (P <.0001). Cox multivariate analyses showed that HAART therapy was associated with a reduced risk of death (hazard ratio = 0.09; 95% confidence interval, 0.03 to 0.69).
CONCLUSION: In patients with AIDS-associated PKS and undergoing chemotherapy, administration of HAART was associated with increased survival.

PMID 11559722  J Clin Oncol. 2001 Sep 15;19(18):3848-51. doi: 10.1200/・・・
著者: M Bower, M Nelson, A M Young, C Thirlwell, T Newsom-Davis, S Mandalia, T Dhillon, P Holmes, B G Gazzard, J Stebbing
雑誌名: J Clin Oncol. 2005 Aug 1;23(22):5224-8. doi: 10.1200/JCO.2005.14.597.
Abstract/Text PURPOSE: A proportion of patients with HIV infection who subsequently receive highly active antiretroviral therapy (HAART) exhibit a deterioration in their clinical status, despite control of virologic and immunologic parameters. This clinical response, known as the immune reconstitution inflammatory syndrome (IRIS), occurs secondary to an immune response against previously diagnosed pathogens.
PATIENTS AND METHODS: From our cohort of 5,832 patients treated in the HAART era, we identified 150 therapy-naive patients with a first presentation of Kaposi's sarcoma (KS). Their clinicopathologic features and progress were recorded prospectively.
RESULTS: After commencing HAART, ten patients (6.6%) developed progressive KS, which we identify as IRIS-associated KS. In a comparison of these individuals with those whose KS did not progress, we found that IRIS-KS occurred in patients with higher CD4 counts (P = .03), KS-associated edema (P = .01), and therapy with both protease inhibitors and non-nucleosides together (P = .03). Time to treatment failure was similar for both groups, although the CD4 count declined more rapidly at first, in those patients with IRIS-associated KS. Despite this initial decline, in our clinical experience HAART could be successfully continued in those with IRIS-associated KS.
CONCLUSION: We have identified IRIS-KS in a cohort of HIV patients with KS who start HAART.

PMID 16051964  J Clin Oncol. 2005 Aug 1;23(22):5224-8. doi: 10.1200/JC・・・
著者: Thomas S Uldrick, Kathleen M Wyvill, Pallavi Kumar, Deirdre O'Mahony, Wendy Bernstein, Karen Aleman, Mark N Polizzotto, Seth M Steinberg, Stefania Pittaluga, Vickie Marshall, Denise Whitby, Richard F Little, Robert Yarchoan
雑誌名: J Clin Oncol. 2012 May 1;30(13):1476-83. doi: 10.1200/JCO.2011.39.6853. Epub 2012 Mar 19.
Abstract/Text PURPOSE: Alternatives to cytotoxic agents are desirable for patients with HIV-associated Kaposi's sarcoma (KS). Vascular endothelial growth factor-A (VEGF-A) contributes to KS pathogenesis. We evaluated the humanized anti-VEGF-A monoclonal antibody, bevacizumab, in patients with HIV-KS.
PATIENTS AND METHODS: Patients with HIV-KS who either experienced progression while receiving highly active antiretroviral therapy (HAART) for at least 1 month or did not regress despite HAART for at least 4 months were administered bevacizumab 15 mg/kg intravenously on days 1 and 8 and then every 3 weeks. The primary objective was assessment of antitumor activity using modified AIDS Clinical Trial Group (ACTG) criteria for HIV-KS. HIV-uninfected patients were also eligible and observed separately.
RESULTS: Seventeen HIV-infected patients were enrolled. Fourteen patients had been receiving effective HAART for at least 6 months (median, 1 year). Thirteen patients had advanced disease (ACTG T(1)), 13 patients had received prior chemotherapy for KS, and seven patients had CD4 count less than 200 cells/μL. Median number of cycles was 10 (range, 1 to 37 cycles); median follow-up was 8.3 months (range, 3 to 36 months). Of 16 assessable patients, best tumor responses observed were complete response (CR) in three patients (19%), partial response (PR) in two patients (12%), stable disease in nine patients (56%), and progressive disease in two patients (12%). Overall response rate (CR + PR) was 31% (95% CI, 11% to 58.7%). Four of five responders had received prior chemotherapy for KS. Over 202 cycles, grade 3 to 4 adverse events at least possibly attributed to therapy included hypertension (n = 7), neutropenia (n = 5), cellulitis (n = 3), and headache (n = 2).
CONCLUSION: Bevacizumab is tolerated in patients with HIV-KS and has activity in a subset of patients.

PMID 22430271  J Clin Oncol. 2012 May 1;30(13):1476-83. doi: 10.1200/J・・・
著者: Susan E Krown, Debasmita Roy, Jeannette Y Lee, Bruce J Dezube, Erin G Reid, Raman Venkataramanan, Kelong Han, Ethel Cesarman, Dirk P Dittmer
雑誌名: J Acquir Immune Defic Syndr. 2012 Apr 15;59(5):447-54. doi: 10.1097/QAI.0b013e31823e7884.
Abstract/Text PURPOSE: The mammalian target of rapamycin is activated in Kaposi sarcoma (KS) and its inhibitor, rapamycin, has induced KS regression in transplant-associated KS. This study aimed to evaluate rapamycin's safety and toxicity in HIV-infected individuals with KS receiving antiretroviral therapy (ART), investigate rapamycin interactions with both protease inhibitor (PI)-containing and nonnucleoside reverse transcriptase inhibitor (NNRTI)-containing ART regimens, and assess clinical and biological endpoints including KS response and mammalian target of rapamycin-dependent signaling.
METHODS: Seven participants, 4 on PI-based and 3 on NNRTI-based ART, had rapamycin titrated to achieve trough concentrations of 5-10 ng/mL. Patients were monitored for safety and KS response. KS biopsies were evaluated for changes in phosphoribosomal S6 protein, and phospho-Akt expression. Interleukin 6 and vascular endothelial growth factor levels, HIV and KS-associated herpesvirus viral loads, and CD4 counts were monitored.
RESULTS: Despite pharmacokinetic interactions resulting in >200-fold differences in cumulative weekly rapamycin doses between participants on PI-containing and NNRTI-containing regimens, treatment was well tolerated. There were no significant changes in viral loads or cytokine levels; modest initial decreases in CD4 counts occurred in some patients. Three participants, all on PI-containing regimens and with higher rapamycin exposure, showed partial KS responses. Three of 4 subjects whose biopsies were studied at ≥day 50 showed decreased phosphoribosomal S6 protein staining.
CONCLUSIONS: Rapamycin seems safe in HIV-infected individuals with KS and can, in some cases, induce tumor regression and affect its molecular targets. Significant pharmacokinetic interactions require careful titration to achieve target drug trough concentrations but may be exploited to achieve therapeutic benefit.

PMID 22067664  J Acquir Immune Defic Syndr. 2012 Apr 15;59(5):447-54. ・・・
著者: Valérie Pourcher, Aude Desnoyer, Lambert Assoumou, Céleste Lebbe, Angélique Curjol, Anne-Geneviève Marcelin, Fanny Cardon, Séverine Gibowski, Dominique Salmon, Jean-Marie Chennebault, Isabelle Poizot-Martin, Gilles Peytavin, François Boué, Dominique Costagliola
雑誌名: AIDS Res Hum Retroviruses. 2017 Jan;33(1):1-10. doi: 10.1089/AID.2016.0069. Epub 2016 Sep 7.
Abstract/Text Lenalidomide, an oral immunomodulating agent, has shown promising activity in HIV-infected individuals with Kaposi's sarcoma (KS). This single-arm, multicenter, open-label, Gehan's two-stage phase II trial evaluated the efficacy and safety of lenalidomide in HIV-infected patients with progressive KS despite previous chemotherapy (NCT01282047, ANRS 154 Lenakap trial). The primary endpoint was the rate of partial response (PR) or complete response (CR) at week 24, evaluated by both the study investigators and the patients using the Physical Global Assessment (PGA). AIDS Clinical Trials Group (ACTG) criteria for KS treatment evaluation were used as a secondary endpoint. The data and safety monitoring board recommended that enrollments be halted on April 24, 2013, because of lack of responses. We enrolled 12 antiretroviral-treated HIV-infected men with progressive KS despite previous chemotherapy. Their HIV plasma viral load was <50 copies/ml and their median CD4 cell count 444/mm3. One patient stopped taking lenalidomide because of hives at week 1 and a second patient died at week 7. The remaining 10 patients were assessable at week 24, when none had PGA-defined CR or PR and one had ACTG-defined PR. There were no additional PGA responses at week 48, but an additional three patients had ACTG responses, for a total of four patients with ACTG PR at week 48 (40%; 95% confidence interval: 12.2-73.8). Fourteen grade 3-4 adverse events were considered at least possibly related to lenalidomide during a total of 101 cycles. Lenalidomide was well tolerated in antiretroviral experienced patients with progressive KS previously treated with chemotherapy. The ACTG-defined response rate at week 48 was 40%, while it was 0% using PGA criteria.

PMID 27405442  AIDS Res Hum Retroviruses. 2017 Jan;33(1):1-10. doi: 10・・・

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