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1 ent specifically in injecting drug users and hemophiliacs.
2  the major cause of chronic liver disease in hemophiliacs.
3 els over time in a cohort of multitransfused hemophiliacs.
4 IV-infected blood transfusion recipients and hemophiliacs.
5 wo patients were classified as mild/moderate hemophiliacs.
6 o develop KS than AIDS-afflicted children or hemophiliacs.
7  the annualized bleeding rates in congenital hemophiliacs.
8 ong sibling pairs than among randomly paired hemophiliacs (31.3% vs 13.3%, respectively, P = ns).
9 luated end-stage liver disease (ESLD) in 157 hemophiliacs (85 HIV positive and 72 HIV negative) with
10 nto the fetal circulation of immunocompetent hemophiliac and normal outbred mice.
11 t in each, the HCV genotype distributions in hemophiliacs and blood donors were similar.
12 ster and trends in incidence in HIV-infected hemophiliacs and homosexual men (n=1218) were examined.
13 irus type 1 (HIV-1) coinfection is common in hemophiliacs and injection drug users.
14                                        Among hemophiliacs, children and adolescents had the highest z
15                           Among HIV-positive hemophiliacs, crude RR for ESLD was lower, but not signi
16 of FVIII pharmaceutical products, the use of hemophiliac dogs for gene therapy studies has several li
17 al recombinant protein in the bloodstream of hemophiliac, factor IX-deficient mice.
18 ting recombinant activated factor VII in non-hemophiliacs have been published as abstracts, supportin
19                                 Furthermore, hemophiliacs have the same degree of atherosclerosis as
20  CVC-related deep venous thrombosis (DVT) in hemophiliacs is not well defined.
21                                 Treatment of hemophiliac mice of both genotypes with potent, human FV
22 al vector encoding hFVIII, and transplant to hemophiliac mouse recipients, results in the induction o
23  plasma levels achieved were similar in both hemophiliac mouse strains.
24 ly different from that seen in a FVIII-naive hemophiliac mouse.
25 treatment and prophylaxis of bleeding in non-hemophiliac patients.
26 to human immunodeficiency virus infection in hemophiliacs rather than a susceptibility to hepatitis C
27 r among HIV-positive than among HIV-negative hemophiliacs (relative risk [RR], 3.72; 95% confidence i
28 munodeficiency virus type 1 (HIV-1)-infected hemophiliacs to define the relationship between the SDF1
29                              A comparison of hemophiliacs treated only with plasma fVIII or recombina
30 of the blood-borne TT virus (TTV) in Italian hemophiliacs treated with different preparations of fact
31 st, the major inhibitors in 35% (8 of 23) of hemophiliacs treated with plasma fVIII were directed aga
32 indicate that TTV frequently infects Italian hemophiliacs treated with plasma-derived factor VIII con
33 f neovessels during angiogenesis but renders hemophiliacs vulnerable to hemorrhage during healing.
34  demonstrated that the inhibitor response in hemophiliacs was more complex and the epitope specificit
35                                 About 23% of hemophiliacs who receive therapeutic fVIII infusions dev
36 sts over a lifetime for a typical 5-year-old hemophiliac with high inhibitor levels.
37 conclude that genotype changes are common in hemophiliacs with chronic HCV, particularly in those who
38 y of factor VIIa in the medical treatment of hemophiliacs with inhibitors is, in part, based on overc