Relapsing cutaneous leishmaniasis in a patient requiring TNF-α-inhibitor Infliximab for Takayasu-arteritis: Case report and review of the literature.

Leishmaniasis is a protozoan parasitic infection that can manifest as visceral or cutaneous disease. Immunosuppression, mainly through TNF-α) inhibition, is a risk factor for complicated leishmaniasis that is becoming increasingly known. Here, we present a case of cutaneous leishmaniasis (CL) in a patient who suffers from advanced Takayasu-Arteritis, requiring TNF-α inhibition with infliximab. The primary CL lesions in this 47-year-old, female patient were caused by Leishmaniapanamensis and occurred after a touristic trip to Panama on her right foot. The lesions first resolved under treatment with liposomal amphotericin B. However, ten months later, the patient returned with relapsing lesions requiring further treatment. We discuss the challenges and risks of leishmaniasis in patients with TNF-α inhibition and the rare phenomenon of relapsing CL and the management hereof. We review published cases of CL associated with TNF-α inhibition. A growing body of evidence now suggests that especially CL (and visceral leishmaniasis (VL)) can be associated with TNF-α inhibition. The host response to leishmaniasis is of the Th1-type and TNF-α and interferon-gamma expression are crucial for disease control. Inversely, TNF-α inhibition can lead to complicated and relapsing progression of leishmanial infection. Therefore, we propose that CL and VL should be considered in at-risk patients receiving immunosuppressants.

Impact of lipid apheresis on Egr-1, c-Jun, c-Fos, and Hsp70 gene expression in white blood cells.

Lipid apheresis treatment has been suggested to cause oxidative stress. Cells respond to oxidative stress in many ways, including, among others, altered gene expressions. In the present investigation we investigated whether the gene expression of known stress genes was affected in the WBCs of patients undergoing lipid apheresis. For this purpose cellular early-growth-response gene-1 (Egr-1), c-Jun, c-Fos, and heat shock protein 70 (Hsp70) mRNA expression was followed before and immediately after lipid apheresis treatments (N=24). Gene expression was determined by quantitative reverse transcription-polymerase chain reaction. With the exception of c-Fos, the expression of Egr-1, c-Jun, and Hsp70 mRNA was not affected in WBCs by a single lipid apheresis treatment (median [16th percentile; 84 th percentile]): Egr-1, before 0.30 (0.13; 0.53), after 0.31 (0.14; 1.33); c-Jun, before 0.03 (0.03; 0.16), after 0.05 (0.03; 0.18); Hsp70, before 0.49 (0.23; 1.07), after 0.53 (0.20; 1.61)). Expression of c-Fos was significantly decreased (P<0.01) after lipid apheresis treatment (before 2.18 [1.06; 5.27], after 1.65 [0.74; 4.12]). Hsp70 and c-Fos expression in lipid apheresis patients was not different from that in 35 healthy blood donors, whereas Egr-1 and c-Jun were significantly decreased (P<0.05) in lipid apheresis patients when compared to controls (Egr-1 0.96 [0.42; 1.83], c-Jun 0.64 [0.40; 0.98], c-Fos 2.77 [1.32; 4,02], Hsp70 0.43 [0.28; 0.61]). These results show that lipid apheresis procedures do not induce stress gene expression in WBCs. Therefore, all the lipid apheresis systems used seem to be safe with respect to oxidative stress and other injuries induced in WBCs due to contact with extracorporeal tubing and membranes.