ArticleParasitology research2011
Outcomes in mice with abdominal angiostrongyliasis treated with enoxaparin.
Article in Parasitology research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- A practical guide for the diagnosis of abdominal angiostrongyliasis caused by the nematode Angiostrongylus costaricensis.Parasites & vectors · 2023Review
- Abdominal angiostrongyliasis in the Americas: fifty years since the discovery of a new metastrongylid species, Angiostrongylus costaricensis.Parasites & vectors · 2021Review
- Activity profiling of peptidases in Angiostrongylus costaricensis first-stage larvae and adult worms.PLoS neglected tropical diseases · 2018Article
- Angiostrongylus costaricensis infection in Martinique, Lesser Antilles, from 2000 to 2017.Parasite (Paris, France) · 2018Observational
- PCR for the diagnosis of abdominal angiostrongyliasis in formalin-fixed paraffin-embedded human tissue.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abdominal angiostrongyliasis (AA) is caused by the nematode Angiostrongylus costaricensis. Parasite-associated thrombosis of mesenteric vessels may lead to intestinal infarction, which might be prevented with anti-thrombotic agents. This study assessed the effect of enoxaparin on survival and pathological findings in Swiss mice with AA. In this experiment, 24 mice were infected with A. costaricensis (10 L3 per animal) followed by treatment with subcutaneous enoxaparin (40 mg/kg/day) or water (sham), starting from 15 days post-infection (dpi) and continued until animal death. Animals were monitored until death or sacrifice at the 50th dpi. Ten mice (42%) were dead after 36 ± 8 dpi. Of these, five (50%) were treated with enoxaparin. Animals treated with enoxaparin and sham did not differ in terms of weight loss (median, 1.3 vs. 4.2 g; P = 0.303) and macroscopical findings. Microscopically, no difference was found in regard to vascular granuloma (median grade, 2 vs. 3; P = 0.293) and presence of either vasculitis (75% vs. 100%; P = 0.217), mesenteric thrombosis (33% vs. 50%; P = 0.680), or bowel necrosis (25% vs. 50%; P = 0.400). Mice dead before the 50th dpi showed more pneumonia (90% vs. 21%; P = 0.002), bowel infarction (40% vs. 0%; P = 0.02), and purulent peritonitis (60% vs. 7%; P = 0.008) compared to survivors. Prophylactic enoxaparin in mice did not prevent tissue damage and mortality related with AA. The lower prevalence of mesenteric thrombosis and bowel infarction regardless of treatment were notorious. Frequent septic complications suggest the need of studies addressing the effect of antibiotics in AA.
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