Seronegative visceral leishmaniasis with relapsing and fatal course following rituximab treatment

Casabianca, Angelo; Marchetti, Monia; Zallio, Francesco; Feyles, Elda; Concialdi, Erika; Ferroglio, Ezio; Biglino, A

doi:10.1007/s15010-011-0109-5

Cited by 15 publications

(11 citation statements)

References 18 publications

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“…However, it is important to bear in mind that anti- Leishmania antibodies (a) are frequently undetectable in patients with a single LCL lesion123; (b) can be absent in immunocompetent or immunodeficient patients with asymptomatic or subclinical Leishmania infection90 124; (c) may be missing in patients with VL at the onset of disease125 or following immunosuppressive treatment (eg, rituximab)126; and (d) fail to indicate active disease or progression of asymptomatic patients to VL in endemic areas 91 120 124 127 128…”

Section: Diagnostic Proceduresmentioning

confidence: 99%

Leishmaniasis in rheumatology, haematology and oncology: epidemiological, immunological and clinical aspects and caveats: Figure 1

Bogdan

2012

Ann Rheum Dis

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Leishmaniasis is an intracellular protozoan infection that can lead to cutaneous, mucocutaneous, visceral or systemic manifestations depending on the parasite species and virulence and on the host immune response. It is endemic in countries of Europe (Mediterranean basin), Asia, Africa, Central and South America, but autochthonous cases begin to emerge outside classical disease areas. CD4+ T helper cells, interferon γ, dendritic cells and macrophages are the key components of antileishmanial defence. Leishmaniasis is an important differential diagnosis in patients with chronic lesions of the skin or mucous membranes or with fever, hepatosplenomegaly, lymphadenopathy, pancytopenia, histocytosis, haemophagocytic syndrome or glomerulonephritis. Organ transplant recipients and patients with autoimmune syndromes are at particular risk of developing visceral leishmaniasis following immunosuppressive therapy (eg, with steroids, methotrexate, ciclosporin or tumour necrosis factor-neutralising biological agents). Diagnosis and adequate treatment of leishmaniasis requires the combined use of culture, microscopic and nucleic acid amplication methods and species identification by sequencing and other molecular techniques. Standard regimens for the treatment of visceral leishmaniasis are intravenous liposomal amphotericin B (3 mg/kg body weight for 10 days) or oral miltefosine (150 mg/day for 28 days).

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Section: Diagnostic Proceduresmentioning

confidence: 99%

Leishmaniasis in rheumatology, haematology and oncology: epidemiological, immunological and clinical aspects and caveats: Figure 1

Bogdan

2012

Ann Rheum Dis

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“…Cellular immunity is a major defence mechanism against Leishmania, 17 and immunological function undergoes changes with ageing, including decreased T cell production, 7,18 changes in cytokine production (with higher levels of Th2 cytokines, such as IL-10 and TGF-B) and lower production of Th1 cytokines (IFN-G and IL12), contributing to protozoan survival. 17 In some cases, elderly patients are undergoing immunosuppressive drug therapy for underlying diseases such as rheumatoid arthritis 19 or lymphoma, 20 with an additional risk for VL development. In the present study, none of the 10 patients aged 80 years and over died.…”

Section: Discussionmentioning

confidence: 99%

Late diagnosis: a factor associated with death from visceral leishmaniasis in elderly patients

Driemeier

Oliveira

Druzian

et al. 2015

Pathogens and Global Health

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Introduction: Visceral leishmaniasis (VL) is among the seven global endemic diseases assigned a high priority by the World Health Organization. In Latin America, most cases occur in Brazil. Despite the availability of intensive treatment resources and protocols for specific treatment, lethality rates for VL have increased in several regions in the country over the past 10 years, particularly in patients under one and over 50 years of age. As the growth of the elderly population accelerates in Brazil, VL poses a greater challenge to public health. Given the scarcity of studies addressing the disease in this age group, the purpose of this study was to identify factors associated with VL lethality among the elderly. Methods/Key findings: This analytical, cross-sectional epidemiological study comprised 80 elderly patients who sought treatment at the teaching hospital of the Universidade Federal de Mato Grosso do Sul, Campo Grande, MS, Brazil, in the period 2000-2013.Clinical, laboratory and treatment variables were investigated from records of elderly patients with VL diagnosis confirmed by at least one laboratory test positive (culture for parasite or direct parasitological examination; reactive immunofluorescence; immunochromatographic test with recombinant antigens) or patients without laboratory confirmation who lived in endemic areas and responded favorably to therapeutic trial, as defined by the Brazilian Ministry of Health. Of the 80 patients included, 78 tested positive to at least one exam; in two cases, diagnosis was based on clinical and epidemiological criteria. The lethality rate was 20%. Multivariate analysis revealed an association between death and time elapsed from symptom onset.

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“…7 VL has been found in severely immunocompromised patients with T-cell defects, such as transplant recipients; people with leukemia, lymphoma, systemic lupus erythematous, and AIDS; and patients on corticosteroid or other immunosuppressive therapy. 3,[8][9][10][11][12][13][14] Although the clinical features of VL in the setting of HIV infection have been widely described, [4][5][6] there are only a few reports of VL in hematologic or solid organ transplant recipients, 3,8,9 and even fewer exploring the clinical profile of VL in immunocompromised individuals who are neither transplant recipients nor infected with HIV. [10][11][12][13][14] At the same time, there are very few reports comparing VL in immunosuppressed individuals versus VL in HIV-infected patients.…”

Section: Introductionmentioning

confidence: 99%

“…3,[8][9][10][11][12][13][14] Although the clinical features of VL in the setting of HIV infection have been widely described, [4][5][6] there are only a few reports of VL in hematologic or solid organ transplant recipients, 3,8,9 and even fewer exploring the clinical profile of VL in immunocompromised individuals who are neither transplant recipients nor infected with HIV. [10][11][12][13][14] At the same time, there are very few reports comparing VL in immunosuppressed individuals versus VL in HIV-infected patients. 15,16 The aim of this study is to begin to fill the gaps in knowledge about this population, defining the clinical and epidemiological differences of VL in three groups of immunocompromised patients: transplant recipients, HIV-infected patients, and people with other immunosuppressive conditions.…”

Section: Introductionmentioning

confidence: 99%

Is Visceral Leishmaniasis Different in Immunocompromised Patients Without Human Immunodeficiency Virus? A Comparative, Multicenter Retrospective Cohort Analysis

Ramos

León

Merino

et al. 2017

The American Journal of Tropical Medicine and Hygiene

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Although visceral leishmaniasis (VL) can affect immunocompromised patients, data from the human immunodeficiency virus (HIV) infection context are limited, and the characteristics of VL in other immunosuppression scenarios are not well defined. A retrospective review of all cases of VL in immunocompromised patients from January 1997 to December 2014 in two Spanish hospitals on the Mediterranean coast was performed. We included 18 transplant recipients (kidney: 7, liver: 4, lung: 3, heart: 2, and blood marrow: 2), 12 patients with other causes of immunosuppression (myasthenia gravis: 3 and rheumatoid arthritis: 2), and 73 VL HIV-positive patients. Fever was more common in transplant patients (94.4%) and patients with other types of immunosuppression (100%) than in HIV-positive individuals (73.3%). Hepatomegaly was less common in transplant recipients (27.8%) and patients with other types of immunosuppression (41.7%) compared with HIV-positive patients (69.9%) ( = 0.01; = 0.001, respectively). Patients with other types of immunosuppression had a median leukocyte count of 1.5 × 10/L, significantly lower than HIV-positive patients (2.5 × 10/L) ( = 0.04). Serology was more commonly positive in nontransplant immunosuppressed individuals (75%) and transplant recipients (78.6%) than in HIV-patients (13.8%) ( < 0.001). Antimonial therapy was rarely used in transplant recipients (1.9%) and never in patients with other immunosuppressive conditions, whereas 34.2% of HIV-positive patients received it ( = 0.05 and = 0.01, respectively). Mortality was 16.7% in both transplant recipients and patients with other immunosuppressive conditions and 15.1% in HIV-positive patients. The features of VL may be different in immunosuppressed patients, with more fever and less hepatomegaly and leukopenia than in HIV-infected patients.

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Seronegative visceral leishmaniasis with relapsing and fatal course following rituximab treatment

Cited by 15 publications

References 18 publications

Leishmaniasis in rheumatology, haematology and oncology: epidemiological, immunological and clinical aspects and caveats: Figure 1

Leishmaniasis in rheumatology, haematology and oncology: epidemiological, immunological and clinical aspects and caveats: Figure 1

Late diagnosis: a factor associated with death from visceral leishmaniasis in elderly patients

Is Visceral Leishmaniasis Different in Immunocompromised Patients Without Human Immunodeficiency Virus? A Comparative, Multicenter Retrospective Cohort Analysis

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