Human immunodeficiency virus-associated multicentric Castleman disease refractory to antiretroviral therapy: clinical features, treatment and outcome

2014 ◽  
Vol 56 (5) ◽  
pp. 1246-1251 ◽  
Author(s):  
Musa Alzahrani ◽  
Mark C. Hull ◽  
Christopher Sherlock ◽  
Deborah Griswold ◽  
Chantal S. Leger ◽  
...  
2019 ◽  
Vol 220 (5) ◽  
pp. 841-851 ◽  
Author(s):  
Melissa J Blumenthal ◽  
Charlotte Schutz ◽  
David Barr ◽  
Michael Locketz ◽  
Vickie Marshall ◽  
...  

AbstractBackgroundDespite increasing numbers of human immunodeficiency virus (HIV)–infected South Africans receiving antiretroviral therapy (ART), tuberculosis (TB) remains the leading cause of mortality. Approximately 25% of patients treated for TB have microbiologically unconfirmed diagnoses. We assessed whether elevated Kaposi’s sarcoma–associated herpesvirus (KSHV) viral load (VL) contributes to mortality in hospitalized HIV-infected patients investigated for TB.MethodsSix hundred eighty-two HIV-infected patients admitted to Khayelitsha Hospital, South Africa, were recruited, investigated for TB, and followed for 12 weeks. KSHV serostatus, peripheral blood KSHV-VL, and KSHV-associated clinical correlates were evaluated.ResultsMedian CD4 count was 62 (range, 0–526) cells/μL; KSHV seropositivity was 30.7% (95% confidence interval [CI], 27%–34%); 5.8% had detectable KSHV-VL (median, 199.1 [range, 13.4–2.2 × 106] copies/106 cells); 22% died. Elevated KSHV-VL was associated with mortality (adjusted odds ratio, 6.5 [95% CI, 1.3–32.4]) in patients without TB or other microbiologically confirmed coinfections (n = 159). Six patients had “possible KSHV-inflammatory cytokine syndrome” (KICS): 5 died, representing significantly worse survival (P < .0001), and 1 patient was diagnosed with KSHV-associated multicentric Castleman disease at autopsy.ConclusionsGiven the association of mortality with elevated KSHV-VL in critically ill HIV-infected patients with suspected but not microbiologically confirmed TB, KSHV-VL and KICS criteria may guide diagnostic and therapeutic evaluation.


2005 ◽  
Vol 79 (4) ◽  
pp. 337-339 ◽  
Author(s):  
Ségolène Neuville ◽  
Felix Agbalika ◽  
Claire Rabian ◽  
Josette Brière ◽  
Jean-Michel Molina

2019 ◽  
Vol 8 (1) ◽  
pp. 55 ◽  
Author(s):  
Monique Munro ◽  
Tejabhiram Yadavalli ◽  
Cheryl Fonteh ◽  
Safa Arfeen ◽  
Ann-Marie Lobo-Chan

Cytomegalovirus retinitis (CMVR) is a severe, vision-threatening disease that primarily affects immunosuppressed patients. CMVR is the most common ocular opportunistic infection in human immunodeficiency virus (HIV) infected patients and is the leading cause of blindness in this group; however, the incidence of CMVR in HIV patients has dramatically decreased with antiretroviral therapy. Other causes of immunosuppression, including organ transplantation, hematologic malignancies, and iatrogenic immunosuppression, can also lead to the development of CMVR. Herein, we describe the pathogenesis of CMVR and compare clinical features, epidemiology, and risk factors in HIV and non-HIV infected individuals with CMVR.


2013 ◽  
Vol 137 (3) ◽  
pp. 360-370 ◽  
Author(s):  
Amy Chadburn ◽  
Anmaar M. Abdul-Nabi ◽  
Bryan Scott Teruya ◽  
Amy A. Lo

Context.—Individuals who are immune deficient are at an increased risk for developing lymphoproliferative lesions and lymphomas. Human immunodeficiency virus (HIV) infection is 1 of 4 clinical settings associated with immunodeficiency recognized by the World Health Organization (WHO) in which there is an increased incidence of lymphoma and other lymphoproliferative disorders. Objectives.—To describe the major categories of benign lymphoid proliferations, including progressive HIV-related lymphadenopathy, benign lymphoepithelial cystic lesions, and multicentric Castleman disease, as well as the different types of HIV-related lymphomas as defined by the WHO. The characteristic morphologic, immunophenotypic, and genetic features of the different entities will be discussed in addition to some of the pathogenetic mechanisms. Data Sources.—The WHO classification of tumors of hematopoietic and lymphoid tissues (2001 and 2008), published literature from PubMed (National Library of Medicine), published textbooks, and primary material from the authors' current and previous institutions. Conclusions.—HIV infection represents one of the clinical settings recognized by the WHO in which immunodeficiency-related lymphoproliferative disorders may arise. Although most lymphomas that arise in patients with HIV infection are diffuse, aggressive B-cell lesions, other lesions, which are “benign” lymphoid proliferations, may also be associated with significant clinical consequences. These lymphoproliferations, like many other immunodeficiency-associated lymphoproliferative disorders, are often difficult to classify. Studies of HIV-associated lymphoid proliferations will continue to increase our understanding of both the immune system and lymphomagenesis.


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