Sarcopenia, body composition and factors associated with variceal gastrointestinal bleeding and splenectomy in hepatosplenic schistosomiasis mansoni.

BACKGROUND: Sarcopenia is a common complication of cirrhosis and an important predictor of morbimortality. We aimed to determine the prevalence of sarcopenia and its associated factors in hepatosplenic schistosomiasis (HSS) as well as to evaluate whether muscle mass and function are associated with variceal upper gastrointestinal bleeding (VUGIB) and previous splenectomy in subjects without other liver diseases. METHODS: We conducted a cross-sectional study including adults with HSS who underwent clinical, biochemical, anthropometric, muscle strength and physical performance evaluations and were submitted to bioelectrical impedance analysis and abdominal ultrasound. Sarcopenia was diagnosed according to the 2019 European consensus criteria. RESULTS: A total of 66 patients with HSS (62.1% male; mean age 48.8±8.6 y) were included. Overall, six subjects (9.1%) were diagnosed with probable sarcopenia and none had confirmed sarcopenia. Fat-free body mass index (BMI) was independently associated with VUGIB (odds ratio 0.701 [95% confidence interval 0.51 to 0.96]; p=0.025). Compared with patients who did not undergo surgery, individuals who underwent esophagogastric devascularization combined with splenectomy (EGDS) had higher serum lipid levels, fat percentage and frequency of metabolic syndrome, with lower skeletal muscle mass index and hand grip strength. CONCLUSIONS: HSS mansoni seems not to cause sarcopenia. However, a lower fat-free BMI was associated with previous VUGIB and the subgroup of patients who underwent EGDS presented higher lipid levels, fat percentage and frequency of metabolic syndrome and lower muscle mass and function.

Portal vein thrombosis in patients with hepatosplenic schistosomiasis who underwent oesophagogastric devascularization combined with splenectomy.

BACKGROUND: Portal vein thrombosis (PVT) has been described in nearly 50% of patients who underwent oesophagogastric devascularization combined with splenectomy (EGDS), but no previous study has compared its occurrence in surgical and non-surgical groups. This study aimed to investigate PVT in hepatosplenic schistosomiasis (HSS) and its association with EGDS and upper variceal bleeding (UVB). METHODS: Retrospectively, 104 HSS individuals were enrolled. Following EGDS, the occurrence of PVT, mesenteric vein thrombosis (MVT), hospital admissions and UVB were recorded. RESULTS: EGDS was performed in 27 (26%) patients. PVT and MVT were detected in 30 (33%) and 8 (9.8%) patients, respectively. Patients who underwent EGDS were at greater risk of PVT (63% vs 19.7%; odds ratio [OR] 6.12 [95% confidence interval {CI} 2.3 to 16.1], p<0.001) when compared with a non-surgical approach. There was no significant difference in UVB occurrence and ß-blocker usage. PVT was associated with more hospital admissions (p=0.030) and higher alkaline phosphatase levels (p=0.008). UVB occurrence in patients with and without thrombosis was similar. In multivariate analysis, after adjustment, PVT was associated with the surgical approach (OR 4.56 [95% CI 1.55 to 13.38], p=0.006) and age at HSS diagnosis (OR 0.94 [95% CI 0.90 to 0.99], p=0.021). CONCLUSIONS: EGDS was not associated with a decreased frequency of UVB when compared with the non-surgical approach but was an independent risk factor for PVT.

Necator americanus infection: a possible cause of altered dendritic cell differentiation and eosinophil profile in chronically infected individuals.

BACKGROUND: Hookworms survive for several years (5 to 7 years) in the host lumen, inducing a robust but largely ineffective immune response. Among the most striking aspects of the immune response to hookworm (as with many other helminths) is the ablation of parasite-specific T cell proliferative response (hyporesponsiveness). While the role of the adaptive immune response in human helminth infection has been well investigated, the role of the innate immune responses (e.g., dendritic cells and eosinophils) has received less attention and remains to be clearly elucidated. METHODOLOGY/PRINCIPAL FINDINGS: We report on the differentiation/maturation of host dendritic cells in vitro and the eosinophil activation/function associated with human hookworm infection. Mature DCs (mDCs) from Necator americanus (Necator)-infected individuals showed an impaired differentiation process compared to the mDCs of non-infected individuals, as evidenced by the differential expression of CD11c and CD14. These same hookworm-infected individuals also presented significantly down-regulated expression of CD86, CD1a, HLA-ABC, and HLA-DR. The lower expression of co-stimulatory and antigen presentation molecules by hookworm-infected-derived mDCs was further evidenced by their reduced ability to induce cell proliferation. We also showed that this alternative DC differentiation is partially induced by excreted-secreted hookworm products. Conversely, eosinophils from the same individuals showed a highly activated status, with an upregulation of major cell surface markers. Antigen-pulsed eosinophils from N. americanus-infected individuals induced significant cell proliferation of autologous PBMCs, when compared to non-infected individuals. CONCLUSION: Chronic N. americanus infection alters the host's innate immune response, resulting in a possible modulation of the maturation process of DCs, a functional change that may diminish their ability for antigen presentation and thus contribute to the ablation of the parasite-specific T cell proliferative response. Interestingly, a concomitant upregulation of the major cell surface markers of eosinophils was observed in hookworm-infected individuals, indicative of antigen-specific immune responses, especially antigen presentation. We showed that in addition to the postulated role of the eosinophils as effector cells against helminth infection, activated cells may also be recruited to sites of inflammation and contribute to the immune response acting as antigen presenting cells.