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Jeanjacques Lefrere - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of an elevated CD8 Lymphocyte Count in hiv infection results of a prospective study of 152 asymptomatic hiv positive individuals
AIDS, 1992Co-Authors: Sylvie Chevret, Helene Roquin, Pierre Ganne, Jeanjacques LefrereAbstract:OBJECTIVE: To evaluate the prognostic value of an elevated CD8 Lymphocyte Count in the early stages of HIV infection. DESIGN: A prospective study ongoing since January 1986. METHODS: One hundred and fifty-two asymptomatic HIV-positive individuals with a CD4 Lymphocyte Count > 400 x 10(6)/l at enrollment were included. Disease progression was defined as a CD4 Count 1500 x 10(6)/l in 38 individuals and doubled in 35. The risk of a decreasing CD4 Count was estimated to be 1.7-fold higher, although not significantly so, after the elevation of the CD8 Count to > 1500 x 10(6)/l than before or in the absence of such an increase. However, this predictive value disappeared when five baseline parameters found to predict the outcome (neopterin, beta 2-microglobulin, p24 antigen, anti-p18 antibody and immunoglobulin A) were adjusted. CONCLUSION: Elevated CD8 Count appears to be a weak marker for disease progression.
Diana N J Lockwood - One of the best experts on this subject based on the ideXlab platform.
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visceral leishmaniasis complicating idiopathic cd4 t cell lymphocytopenia 2 case reports
PLOS Neglected Tropical Diseases, 2017Co-Authors: Andrew Foxlewis, Diana N J LockwoodAbstract:HIV infection leads to worse treatment outcomes in visceral leishmaniasis (VL) and increases the risk of post-treatment relapse, suggesting that similar effects may be observed in other low CD4+ T cell states [1]. Idiopathic CD4+ T cell lymphocytopenia (ICL) was first described in 1992 in the setting of the emerging HIV pandemic [2]. It is a rare condition defined as a CD4+ T cell Count persistently <300 cells/μl in the absence of known secondary causes of lymphopenia, such as HIV infection [3]. VL infection in individuals with ICL is a little-reported clinical entity [4, 5, 6] and here we report in detail our experiences of 2 such patients from the Hospital for Tropical Diseases (HTD). The cases discussed here add an important clinical perspective to the immunological models. One patient has had complex refractory disease managed over the last 12 years, developing both ocular and dermal leishmaniasis and demonstrating how CD4 deficiency without HIV infection affects the clinical course of VL. Presentation of Case 1 A 53-year-old British male with known psoriasis and chronic kidney disease (CKD) presented to his general practitioner (GP) in August 2004 with fatigue, night sweats, weight loss, and exertional breathlessness. He lived in the United Kingdom and his lifetime travel history to Leishmania-endemic areas consisted of Spain in 2002, Cyprus annually from 1998–2003, and, in June 2004 (2 months prior to presentation), a 2-week holiday to the Greek island of Zakynthos, during which he reported insect bites. He was investigated and found to have pancytopenia, and in October 2004, Leishmania amastigotes were identified on a bone marrow biopsy, giving the patient a diagnosis of VL. Polymerase chain reaction (PCR) testing detected Leishmania donovani DNA. In November 2004, the patient had his first course of treatment with intravenous (IV) AmBisome (liposomal amphotericin B), leading to a resolution of his symptoms. In February 2005, the patient relapsed for the first time with recurrence of his presenting symptoms and was treated empirically with a further course of IV AmBisome. Following his second relapse in June 2005, the patient was referred to the HTD for management. Relapse was confirmed with a bone marrow biopsy showing Leishmania amastigotes, and in July 2005, the patient had his third treatment course, consisting of oral miltefosine and IV AmBisome. Between August 2005 and June 2008, the patient was managed with prophylactic IV pentamidine isethionate infusions once every 2 weeks and had a relapse-free period. In January 2006, the patient developed bilateral anterior uveitis and intraocular hypertension of unknown etiology. This was managed with systemic immunosuppression, intraocular steroid injections, and, in 2008, bilateral ocular surgical drainage. In June 2008, the patient presented with 6 months of new, small, tender, raised erythematous skin lesions over his abdomen and legs, distinct from the non-tender psoriatic patches on his elbows. Numerous Leishmania amastigotes were identified on skin biopsy of a lesion, giving the patient a diagnosis of Post-kala-azar dermal leishmaniasis (PKDL) and representing his third clinical relapse. In July 2008, Leishmania organisms or DNA were not identified on microscopy and PCR of a splenic aspirate, showing that the patient had not had a systemic recurrence of VL. The patient was not treated at this time. The patient's vision continued to deteriorate despite aggressive treatment of his anterior uveitis and intraocular hypertension, and he was registered as blind in April 2009. In May 2009, the patient underwent an ocular vitreous aspirate to determine if his visual deterioration could be related to his leishmaniasis. Leishmania species DNA was identified on PCR of the aspirate, confirming intraocular leishmaniasis and his fourth clinical relapse. In July 2009, the patient was admitted for treatment with 28 days of IV sodium stibogluconate. After 22 days, the course was halted due to drug toxicity. A repeat biopsy of a skin lesion at this time did not identify Leishmania on microscopy or PCR, and so stibogluconate treatment was not continued. Leishmania DNA was not identified on PCR of a further ocular vitreous aspirate in October 2009. Between October 2009 and May 2010, the patient remained off prophylactic pentamidine, which was stopped prior to admission and not restarted following discharge. In May 2010, the patient had a fifth clinical relapse. Leishmania amastigotes were visualized on microscopy of a bone marrow biopsy at this time, and Leishmania donovani complex DNA was identified on PCR of the sample. The patient was treated with a further course of IV AmBisome in June 2010. A splenic aspirate in July 2010 found no Leishmania amastigotes on microscopy, but Leishmania DNA continued to be isolated on PCR of the sample. At this time, the patient was re-commenced on prophylactic pentamidine infusions administered once every 3 weeks. In March 2011, Leishmania DNA was once again isolated from PCR of an ocular vitreous aspirate, but a splenic aspirate at this time did not identify Leishmania organisms or DNA, indicating that the pentamidine infusions were controlling his systemic infection but not the ocular disease. In August 2011, the patient presented to clinic with new erythematous papular lesions on his abdomen. Skin slit smear microscopy of these revealed amastigotes, confirming further dermal leishmaniasis and his sixth relapse. Leishmania DNA was identified on PCR of a splenic aspirate in April 2012, and the patient was managed with a further course of oral miltefosine and IV AmBisome. During this time, a cause was sought for the patient’s treatment refractory disease. HIV serology was negative and immunoglobulins were within normal range. Lymphocyte subset analysis, consisting of total Lymphocyte Count, CD3+ Lymphocyte Count (T cell Count), CD3+CD4+ Lymphocyte Count (helper or CD4+ T cell Count), and CD3+CD8+ Lymphocyte Count (cytotoxic or CD8+ T cell Count), was undertaken on multiple occasions during the course of the patient’s illness and revealed a persistently low CD4+ T cell Count of between 40–160 cells/μl along with a low CD8+ T cell Count of 180–220 cells/μl. Investigations for secondary causes of his persistent lymphopenia were non-diagnostic. There was no history of malnutrition, alcohol excess, radiotherapy, recent surgery, inflammatory bowel disease, or immunosuppressive medication other than intermittent systemic and local corticosteroid treatment for his anterior uveitis and intraocular hypertension. Multiple blood films, bone marrow biopsies, and splenic aspirates found no evidence of hematological malignancy, and cross-sectional imaging did not demonstrate any solid organ malignancies. Screening for autoimmune diseases and sarcoidosis was negative, and cardiac and renal function were grossly normal. When no known secondary cause of lymphopenia could be identified after extensive investigation, the patient was given a diagnosis of ICL. In August 2012, a post-treatment skin biopsy of a PKDL skin lesion showed mild chronic inflammation only, with no evidence of Leishmania on microscopy or PCR, suggesting the patient had cleared the Leishmania from his skin. Since this time, his leishmaniasis has been kept in remission by ongoing three-weekly pentamidine prophylaxis, and he has remained relapse-free.
Sylvie Chevret - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of an elevated CD8 Lymphocyte Count in hiv infection results of a prospective study of 152 asymptomatic hiv positive individuals
AIDS, 1992Co-Authors: Sylvie Chevret, Helene Roquin, Pierre Ganne, Jeanjacques LefrereAbstract:OBJECTIVE: To evaluate the prognostic value of an elevated CD8 Lymphocyte Count in the early stages of HIV infection. DESIGN: A prospective study ongoing since January 1986. METHODS: One hundred and fifty-two asymptomatic HIV-positive individuals with a CD4 Lymphocyte Count > 400 x 10(6)/l at enrollment were included. Disease progression was defined as a CD4 Count 1500 x 10(6)/l in 38 individuals and doubled in 35. The risk of a decreasing CD4 Count was estimated to be 1.7-fold higher, although not significantly so, after the elevation of the CD8 Count to > 1500 x 10(6)/l than before or in the absence of such an increase. However, this predictive value disappeared when five baseline parameters found to predict the outcome (neopterin, beta 2-microglobulin, p24 antigen, anti-p18 antibody and immunoglobulin A) were adjusted. CONCLUSION: Elevated CD8 Count appears to be a weak marker for disease progression.
Helene Roquin - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of an elevated CD8 Lymphocyte Count in hiv infection results of a prospective study of 152 asymptomatic hiv positive individuals
AIDS, 1992Co-Authors: Sylvie Chevret, Helene Roquin, Pierre Ganne, Jeanjacques LefrereAbstract:OBJECTIVE: To evaluate the prognostic value of an elevated CD8 Lymphocyte Count in the early stages of HIV infection. DESIGN: A prospective study ongoing since January 1986. METHODS: One hundred and fifty-two asymptomatic HIV-positive individuals with a CD4 Lymphocyte Count > 400 x 10(6)/l at enrollment were included. Disease progression was defined as a CD4 Count 1500 x 10(6)/l in 38 individuals and doubled in 35. The risk of a decreasing CD4 Count was estimated to be 1.7-fold higher, although not significantly so, after the elevation of the CD8 Count to > 1500 x 10(6)/l than before or in the absence of such an increase. However, this predictive value disappeared when five baseline parameters found to predict the outcome (neopterin, beta 2-microglobulin, p24 antigen, anti-p18 antibody and immunoglobulin A) were adjusted. CONCLUSION: Elevated CD8 Count appears to be a weak marker for disease progression.
Pierre Ganne - One of the best experts on this subject based on the ideXlab platform.
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prognostic value of an elevated CD8 Lymphocyte Count in hiv infection results of a prospective study of 152 asymptomatic hiv positive individuals
AIDS, 1992Co-Authors: Sylvie Chevret, Helene Roquin, Pierre Ganne, Jeanjacques LefrereAbstract:OBJECTIVE: To evaluate the prognostic value of an elevated CD8 Lymphocyte Count in the early stages of HIV infection. DESIGN: A prospective study ongoing since January 1986. METHODS: One hundred and fifty-two asymptomatic HIV-positive individuals with a CD4 Lymphocyte Count > 400 x 10(6)/l at enrollment were included. Disease progression was defined as a CD4 Count 1500 x 10(6)/l in 38 individuals and doubled in 35. The risk of a decreasing CD4 Count was estimated to be 1.7-fold higher, although not significantly so, after the elevation of the CD8 Count to > 1500 x 10(6)/l than before or in the absence of such an increase. However, this predictive value disappeared when five baseline parameters found to predict the outcome (neopterin, beta 2-microglobulin, p24 antigen, anti-p18 antibody and immunoglobulin A) were adjusted. CONCLUSION: Elevated CD8 Count appears to be a weak marker for disease progression.