Visceral leishmaniasis is associated with marked changes in serum lipid profile.

BACKGROUND: Infection is often accompanied by lipid profile alterations. The aim of this study was to evaluate the lipid profile changes in patients with visceral leishmaniasis (VL). MATERIALS AND METHODS: We included 15 patients [10 men, aged 50 (24-82) years old] with VL and 15 age- and sex-matched controls. The parameters estimated at diagnosis and 4 months after VL resolution were total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), apolipoproteins (apo) A-Ι, B, E, C-II, C-III, lipoprotein (a) [Lp(a)], activities of lipoprotein-associated phospholipase A2 (Lp-PLA2), HDL-Lp-PLA2, PON1 (paraoxonase 1) and cholesterol ester transfer protein (CETP), cytokines (interleukins 1ß and 6 and tumour necrosis factor α), as well as LDL subfraction profile. RESULTS: Patients with VL at diagnosis had lower levels of TC, LDL-C, apoΒ and Lp(a), and higher TG and apoE concentrations compared with 4 months after VL resolution. The activities of Lp-PLA2, HDL-Lp-PLA2 and ΡΟΝ1 were reduced at diagnosis compared with post-treatment values. VL patients had decreased levels of both large and sdLDL-C at diagnosis; no effect on mean LDL particle size was observed. Patients with VL at diagnosis had decreased HDL-C and apoA-I concentrations; these increased 4 months after VL resolution, but remained lower compared with controls. The activities of HDL-Lp-PLA2 and PON1 remained lower in patients after VL resolution compared with controls. CONCLUSIONS: Patients with VL exhibit increased TG levels and decreased cholesterol subclasses at diagnosis. HDL-C, apoA-I and associated enzymes remain lower 4 months after VL resolution compared with controls.

Diagnostic lipid changes in patients with visceral leishmaniasis.

BACKGROUND: Visceral leishmaniasis (VL) has been associated with the increase in triglyceride (TG) levels and the decrease in high-density lipoprotein cholesterol (HDL-C) concentration. The aim of the study was to evaluate whether there is a diagnostic cut-off point in these lipid profile changes. MATERIALS AND METHODS: We included 100 patients with febrile infections. Analytically, 22 patients with VL, 18 patients with leptospirosis, 20 patients with Brucella melitensis, and 40 age- and sex-matched patients with fever and proven bacteremia (endocarditis and pyelonephritis). The lipid parameters were assessed for their diagnostic accuracy using logistic regression and receiver operating characteristic statistics. RESULTS: It was observed that coexistence of HDL-C < 15 mg/dL and ΤG > 180 mg/dL had 100% sensitivity and 67.5% specificity for the confirmation of VL. The corresponding positive and negative predictive values were 59.4% and 100%, respectively. CONCLUSION: Coexistence of high TGs and low HDL-C values may suggest VL infection in a febrile patient.

Autoimmune manifestations in patients with visceral leishmaniasis.

Visceral leishmaniasis (VL) is a vector-borne protozoal infection caused by replication of Leishmania species in macrophages. VL is characterized by fever, hepatosplenomegaly and cytopenia. Apart from those classic clinical characteristics, VL has been associated with autoimmune clinical and laboratory features. Reported herein are 16 consecutive patients with VL who were checked for laboratory autoimmune manifestations. A variety of autoimmune antibodies including elevated titers of antinuclear antibodies and rheumatoid factor were detected in all patients. Of note, no laboratory autoimmune manifestations were detected in the seven patients who were re-evaluated 3 months after therapy. It is concluded that autoimmune laboratory manifestations during VL infection are common. These may mistakenly lead to diagnosis of an autoimmune disorder.

Leptospirosis is associated with markedly increased triglycerides and small dense low-density lipoprotein and decreased high-density lipoprotein.

The objective of the present study was to evaluate the effects of acute infection with Leptospira interrogans on lipids, lipoproteins and associated enzymes. Fasting serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), apolipoproteins (apo) A-Ι, B, E, C-II, C-III and lipoprotein (a) [Lp(a)] were determined in patients with Leptospirosis on diagnosis and 4 months after recovery as well as in age- and sex-matched controls. Activities of cholesteryl-ester transfer protein (CETP) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) as well as paraoxonase 1 (PON1) hydrolysing activity and levels of cytokines were determined. LDL subclass analysis was performed with Lipoprint LDL System. Eleven patients (10 men, mean age 49.5 ± 8.4 years) and 11 controls were included. TC, HDL-C, LDL-C, apoA-I, apoB and Lp(a) levels were lower at baseline, whereas TG and apoE levels were elevated compared with 4 months later. At baseline, higher levels of cytokines and cholesterol concentration of small dense LDL particles (sdLDL-C) were noticed, whereas LDL particle size was lower compared with follow-up. Activities of plasma Lp-PLA(2) and HDL-associated Lp-PLA(2) were lower at baseline compared with post treatment values, whereas PON1 activity was similar at baseline and 4 months later. 4 months after recovery, the levels of all lipid parameters evaluated did not differ compared with controls, except for HDL-C which remained lower. PON1 activity both at baseline and 4 months later was lower in patients compared with controls. Leptospirosis is associated with atherogenic changes of lipids, lipoproteins and associated enzymes.