Findings in rodents, in which similar quantitative and qualitative immune responses changes were detected, are convergent. Higher parasite loads were reported in helminth-infected animals [20], increased severity of malaria infections (a non lethal P. yoelii strain becomes lethal), alteration of innate responses, and a profound decrease in Th1 responses [22]. Helminthic infections have also been found associated with a major increase in T-regulatory cells activity, and a modulation of inflammatory responses [42], [43]. Of note, one study did not illustrate a detectable impact of worm carriage on a rodent model of cerebral malaria, suggesting that various experimental host parasite combinations can yield different results [23]. A recent immuno-epidemiological study brings support to our findings [44]. Though it did not adress the susceptibility to disease, nor that of antibody responses, it indicated deep modifications of cellular responses to a P.falciparum extract in wormy individuals, leading to a contra-inflammatory profile of responses.
http://plosone.org/article/info:doi/10.1371/journal.pone.0009309#article1.body1.sec4.p7

Whereas the references from animal models are summoned to support the view that worms make malaria more severe, no references from human studies are cited (Briand, Brutus, Murray, Nacher). This selective omission does not make the claim more convincing. Again, the authors could have supported their view by comparing parasitemia between patients with and without helminths. as the saying goes "mice lie and monkeys don't always tell the truth". finding from the lab may not apply in humans in the tropics