Vitamin D in malaria: more hypotheses than clues

Abstract

Vitamin D is a secosteroid hormone regulating calcium and phosphate metabolism, immune response and brain development. Low blood 25(OH)D levels have been reported in patients affected by infectious diseases caused by parasites, including malaria. Despite the high effectiveness of antimalarials, malaria is burdened with high morbidity and mortality, and the search for additional therapies is rapidly growing. Furthermore, available preventive measures have proved to be barely effective so far. Finding new prevention and therapy tools is a matter of urgency. Studies on animal models and humans have hypothesized some mechanisms by which the hormone can influence malaria pathogenesis, and the role of Vitamin D supplementation in preventing and treating this disease has been suggested. Few studies on the association between Vitamin D and malaria are available and disagreeing results have been reported. Studies in humans reporting an association between low 25(OH)D circulating levels and Malaria have a small sample size and observational study-set. Randomized controlled trials are needed in order to understand if Vitamin D administration might play a role in preventing and treating malaria.

Micronutrient levels and their effect on the prognosis of visceral leishmaniasis treatment; a prospective cohort study.

“…Malaria co-infection decreases the serum iron level of visceral leishmaniasis patients by 12.69 mcg/dl, the iodine level by 3.78 mcg/l, the serum vitamin A level by 4.8 mcg/dl and the serum vitamin D level by 0.61 ng/ml. This nding was in line with previously published works [54][55][56]. This is due to the ingestion of the nutrients by the parasites, decreases the intake from the host (anorexia), and increases the execration of the nutrients [57][58][59].…”

Micronutrient levels and their effect on the prognosis of visceral leishmaniasis treatment; a prospective cohort study.

“…Malaria co-infection decreases the serum iron level of visceral leishmaniasis patients by 12.69 mcg/dl, the iodine level by 3.78 mcg/l, the serum vitamin A level by 4.8 mcg/dl and the serum vitamin D level by 0.61 ng/ml. This nding was supported by other research results [53][54][55]. This is due to the multiple effects of malaria on serum micronutrient levels like ingestion of the nutrients by the parasites, decreases the intake from the host, increases the execration of the nutrients through vomiting, perspiration, etc [56][57][58].…”

The importance of vitamin d metabolism as a potential prophylactic, immunoregulatory and neuroprotective treatment for COVID-19

“…There are ongoing clinical trials of vitamin D in the prevention and treatment of pulmonary infection by utilizing its anti-microbial function and immunomodulatory role (Studies 5-9, Table 1). Our hypothesis is that vitamin D and its analogs might be considered as promising Vitamin D has antimalarial and anti-SLE function Previous in vitro studies have shown that vitamin D has antiplasmodial activity through VDR dependent and independent pathways [67]. The onset and progression of malaria has been shown to involve excessive Th1 cell responses, reduction of Th2 response, and dysfunction of Treg cells, all of which can be limited by the action of vitamin D. Furthermore, vitamin D is known to inhibit the synthesis of key pro-inflammatory cytokines involved in the development of fatal cerebral malaria such as IFN-γ and TNF-α [67].…”

“…Previous in vitro studies have shown that vitamin D has antiplasmodial activity through VDR dependent and independent pathways [ 67 ]. The onset and progression of malaria has been shown to involve excessive Th1 cell responses, reduction of Th2 response, and dysfunction of Treg cells, all of which can be limited by the action of vitamin D. Furthermore, vitamin D is known to inhibit the synthesis of key pro-inflammatory cytokines involved in the development of fatal cerebral malaria such as IFN-γ and TNF-α [ 67 ]. Vitamin D administered after an acute malarial infection increased the survival of diseased mice by at least 15 days compared to non-treated mice through inhibition of IFN-γ and TNF-α synthesis [ 68 ].…”