Biomarkers of the early response to treatment of visceral leishmaniasis: A prospective cohort study

Abstract

Background Early biomarkers of the response to treatment are lacking and may help to reduce mortality by the vector‐borne disease visceral leishmaniasis (VL). Methods A prospective cohort study was conducted to investigate plasma cytokines and clinical laboratory data as biomarkers of the early response to specific treatment for VL in 36 patients. Results The mean interleukin 6 (IL‐6) concentration on the 7th day was 2.3% of the pre‐treatment concentration, interleukin 10 (IL‐10) was 8.0%, and interleukin 8 (IL‐8) was 8.2%. On the 7th day, IL‐10 was below half of the pre‐treatment concentration in 100.0%, IL‐8 in 95.5% and IL‐6 in 90.9%. The spleen and liver sizes, haemoglobin, interleukin 1 beta (IL‐1β) and tumour necrosis factor alpha (TNF‐α) showed a slower recovery. Fever disappeared in 91% on the 7th day, 69.4% had a normal white cell count, and 77.8% had a normal platelet value by this time. Conclusions The plasma cytokines IL‐6, IL‐10 and IL‐8 were demonstrated to be excellent markers of the early response to VL treatment and if tested before the 7th day, will likely prove to be better than fever measurement.

The spleen is the graveyard of CD4+ cells in patients with the immunological failure of visceral leishmaniasis and AIDS

“…On the opposite, these two last cellular elements had a fast regaining and increased above the normal levels, as previously seen. [11,12] The most critical question of this study is why L. infantum was not controlled in our patients with AIDS albeit the anti-Leishmania treatment and combined anti-retroviral therapy (cART). In immunocompetent humans, treatment failure of VL is unusual and can partially be explained by drug resistance.…”

From Infection to Death: An Overview of the Pathogenesis of Visceral Leishmaniasis

“…There is no evidence for a reduced production of platelets in VL patients, judging from their bone marrow megakaryocyte cellular integrity [ 77 , 154 ]. The recovery of platelet count is much faster than the spleen size reduction in convalescent patients, suggesting that the primary cause of thrombocytopenia is associated with inflammation leading to DIC, followed by consumption coagulopathy in VL [ 162 ].…”