Chronic steroid administration does not suppress Plasmodium development and maturation

The present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.

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Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

Moreira

Uberti

Gomes

et al. 2021

Sci Rep

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Complication of Corticosteroid Treatment by Acute Plasmodium malariae Infection Confirmed by Small-Subunit rRNA Sequencing

Teng

Wong

et al. 2010

J Clin Microbiol

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We report a case of acute Plasmodium malariae infection complicating corticosteroid treatment for membranoproliferative glomerulonephritis in a patient from an area where P. malariae infection is not endemic. A peripheral blood smear showed typical band-form trophozoites compatible with P. malariae or Plasmodium knowlesi. SSU rRNA sequencing confirmed the identity to be P. malariae. CASE REPORTA 72-year-old man with membranoproliferative glomerulonephritis, hypertension, and ␣-thalassemia trait was admitted to our hospital because of chills and rigor for 2 days and a fever on the day of admission. He had been diagnosed with membranoproliferative glomerulonephritis 3 years prior to admission, when he presented with nephrotic syndrome. Autoimmune marker testing showed a raised level of antinuclear antibody (Ͼ1/720), with a normal level of anti-double-stranded-DNA antibody (Ͻ5 IU/ml) and a negative result for antineutrophil cytoplasmic antibody (ANCA). Testing for hepatitis B virus surface antigen showed a negative result. His initial renal biopsy specimen at diagnosis showed immune deposits of IgA, IgG, IgM, C3, and C1q. He was treated with high-dose corticosteroid with partial response. Two months prior to admission, he had recurrent lower limb edema and was confirmed to have a relapse of the nephrotic syndrome, with urine protein excretion of 2.78 g/day. Prednisolone at 50 mg once daily was started 50 days before admission, with a gradual tailing dose. On the day of admission, his prednisolone dosage was 35 mg once daily. The patient was a resident of Hong Kong. He occasionally traveled to southern China, but he has never traveled outside this area in his lifetime. He has never received a blood transfusion.On admission, he had a temperature of 39.3°C and a heart rate of 138 beats per minute. His blood pressure was 144/68 mm Hg. Physical examination revealed bilateral lower limb edema. The spleen was not palpable. A blood test showed thrombocytopenia with a platelet count of 69 ϫ 10 9 /liter. The platelet count 6 weeks before admission was within the normal range (253 ϫ 10 9 /liter). The total white cell count was 4.4 ϫ 10 9 /liter, with a neutrophil count of 4.09 ϫ 10 9 /liter and a lymphocyte count of 0.26 ϫ 10 9 /liter. The hemoglobin level was 7.4 g/dl. Biochemical tests revealed a creatinine level of 2.68 mg/dl and an albumin level of 31 g/liter. The levels for bilirubin and liver parenchymal enzymes were within the normal range. A peripheral blood smear showed normalsized erythrocytes, thick rings (Fig. 1a), band-form trophozoites (Fig. 1b), and schizonts containing dark brown pigments (Fig. 1c), compatible with Plasmodium malariae or P. knowlesi.

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Chronic steroid administration does not suppress Plasmodium development and maturation

Cited by 2 publications

References 14 publications

Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

Complication of Corticosteroid Treatment by Acute Plasmodium malariae Infection Confirmed by Small-Subunit rRNA Sequencing

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