2010
DOI: 10.1016/j.jhep.2009.11.017
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Hepatitis C virus viremia and low platelet count: A study in a hepatitis B & C endemic area in Taiwan

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Cited by 49 publications
(40 citation statements)
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References 43 publications
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“…A similar rate of 28–42% has been reported in hemophilia and thalassemia patients [16,17]. We noted a spontaneous clearance rate of 25.4% in this cohort, which is not far from that of the general population [45]and uremic patients in Taiwan [19]. Several factors have been associated with self-limited HCV infection.…”
Section: Discussionsupporting
confidence: 85%
“…A similar rate of 28–42% has been reported in hemophilia and thalassemia patients [16,17]. We noted a spontaneous clearance rate of 25.4% in this cohort, which is not far from that of the general population [45]and uremic patients in Taiwan [19]. Several factors have been associated with self-limited HCV infection.…”
Section: Discussionsupporting
confidence: 85%
“…Our findings agreed previous literature [33,35] in showing that the traditional model of increased platelets pooling by an enlarged spleen, is still relevant in many patients and represent a considerable factor contributing to thrombocytopenia in our patients with chronic hepatitis C. It had been suggested that high hepatitis C viral load in peripheral blood corresponds to elevated viral level in hepatocytes which are the major site of TPO synthesis [30] . A significant correlation was found between the level of viral load and the degree of thrombocytopenia in prior reports [30,33,36] . On the contrary, log viral load was not significantly different between thrombocytopenic and nonthrombocytopenic patients in the current study, and there was no correlation between the log viral load and the platelet count, however significant direct correlations were found between log viral load and each of serum ALT levels (r = 0.514; P < 0.001), serum AST levels (r = 0.432; P = 0.003) and INR values (r = 0.326; P = 0.031) which provide an evidence that direct inhibition of protein synthesis by the host that occur in the presence of an infection results in increased quantities of HCV inside hepatocytes.…”
Section: Discussionmentioning
confidence: 58%
“…Előrehaladott fi brosisban a betegek thrombocytaszáma jelentősen csökken, ami a csökkent hepaticus trombopoetinszintézisnek, a fokozott lebontásnak, a portalis hypertensiónak és a HCV myelosuppressiv hatásának a következménye [26]. Fouad és mtsai vizsgálata alapján az APRI érzékenysége 46,7%, fajlagossága 87,1%, pozitív prediktív értéke 46,7%, negatív prediktív értéke 87,1% [24].…”
Section: Apriunclassified