Children's Prattle孩子话
时间: 来源: 编辑:tianxiaoy
Children's Prattle
by Hans Christian Andersen（1859）
At a rich merchant's house there was a children's party， and the children of rich and GREat people were there. The merchant was a learned man， for his father had sent him to college， and he had passed his examination. His father had been at first only a cattle dealer， but always honest and industrious， so that he had made money， and his son， the merchant， had managed to increase his store. Clever as he was， he had also a heart； but there was less said of his heart than of his money. All descriptions of people visited at the merchant's house， well born， as well as intellectual， and some who possessed neither of these recommendations.
Now it was a children's party， and there was children's prattle， which always is spoken freely from the heart. Among them was a beautiful little girl， who was terribly proud； but this had been taught her by the servants， and not by her parents， who were far too sensible people.
Her father was groom of the Chambers， which is a high office at court， and she knew it. &I am a child of the court，& she said； now she might just as well have been a child of the cellar， for no one can help his birth； and then she told the other children that she was well-born， and said that no one who was not well-born could rise in the world. It was no use to read and be industrious， for if a person was not well-born， he could never achieve anything. &And those whose names end with 'sen，'& said she， &can never be anything at all. We must put our arms akimbo， and make the elbow quite pointed， so as to keep these 'sen' people at a GREat distance.& And then she stuck out her pretty little arms， and made the elbows quite pointed， to show how it was to be done； and her little arms were very pretty， for she was a sweet-looking child.
But the little daughter of the merchant became very angry at this speech， for her father's name was Petersen， and she knew that the name ended in &sen，& and therefore she said as proudly as she could， &But my papa can buy a hundred dollars' worth of bonbons， and give them away to children. Can your papa do that？&
&Yes； and my papa，& said the little daughter of the editor of a paper， &my papa can put your papa and everybody's papa into the newspaper. All sorts of people are afraid of him， my mamma says， for he can do as he likes with the paper.& And the little maiden looked exceedingly proud， as if she had been a real princess， who may be expected to look proud.
But outside the door， which stood ajar， was a poor boy， peeping through the crack of the door. He was of such a lowly station that he had not been allowed even to enter the room. He had been turning the spit for the cook， and she had given him permission to stand behind the door and peep in at the well-dressed children， who were having such a merry time within； and for him that was a GREat deal. &Oh， if I could be one of them，& thought he， and then he heard what was said about names， which was quite enough to make him more unhappy. His parents at home had not even a penny to spare to buy a newspaper， much less could they write in one； and worse than all， his father's name， and of course his own， ended in &sen，& and therefore he could never turn out well， which was a very sad thought. But after all， he had been born into the world， and the station of life had been chosen for him， therefore he must be content.
And this is what happened on that evening.
Many years passed， and most of the children became grown-up persons.
there stood a splendid house in the town， filled with all kinds of beautiful and valuable objects. Everybody wished to see it， and people even came in from the country round to be permitted to view the treasures it contained.
Which of the children whose prattle we have described， could call this house his own？ One would suppose it very easy to guess. No， no； it is not so very easy. The house belonged to the poor little boy who had stood on that night behind the door. He had really become something GREat， although his name ended in &sen，&&for it was Thorwaldsen.
And the three other children&the children of good birth， of money， and of intellectual pride，&well， they were respected and honored in the world， for they had been well provided for by birth and position， and they had no cause to reproach themselves with what they had thought and spoken on that evening long ago， for， after all， it was mere &children's prattle.&
搜E搜推荐节目主题：SEN | 医源世界
≡ 收起全部文章
Aug. 26, 2009 -- Massachusetts Sen. Edward Kennedy died late last night at
his home in Hyannis Port, Mass., of brain cancer at age 77.
Kennedy had a malignant glioma, a type of brain cancer. A glioma is a brain
tumor that begins in glial cells, which are cells that surround and support
nerve cells.
In a statement posted on Kennedy's senate web site, the Kennedy family says,
"We've lost the irreplaceable center of our family and joyous light in our
lives, but the inspiration of his faith, optimism, and perseverance will live
on in our hearts forever. We thank everyone who gave him care and support over
this last year, and everyone who stood with him for so many years in his
tireless march for progress toward justice, fairness, and opportunity for all.
He loved this country and devoted his life to serving it. He always believed
that our best days were still ahead, but it's hard to imagine any of them
without him."
Remembering the Longtime Senator
your thoughts on Sen. Ted Kennedy on WebMD's Politics & Health message
Kennedy Remembered
Condolences and remembrances have been posted by officials from both sides
of the political aisle.
In a statement posted on the White House's web site, President Barack Obama
says, "Michelle and I were heartbroken to learn this morning of the death of
our dear friend, Senator Ted Kennedy."
"For five decades, virtually every piece of major legislation to advance the
civil rights, health and economic well-being of the American people bore his
name and resulted from his efforts," Obama says.
Sen. Orrin Hatch, a Republican Senator from Utah, issued a statement saying
that America had "lost a great elder statesman ... and I lost a treasured
friend." Hatch called Kennedy "larger than life" and said that "many had come
before, and many will come after, but Ted Kennedy's name will always be
remembered as someone who lived and breathed the United States Senate and the
work completed in its chamber."
Nancy Reagan, widow of former President Ronald Reagan, issued a statement
saying she was "terribly saddened" to hear of Kennedy's death. "Given our
political differences, people are sometimes surprised by how close Ronnie and I
have been to the Kennedy family. But Ronnie and Ted could always find common
ground, and they had great respect for one another. In recent years, Ted and I
found our common ground in stem cell research, and I considered him an ally and
dear friend. I will miss him."
Gov. Arnold Schwarzenegger, the Republican Senator of California and husband
of Kennedy's niece, Maria Shriver, is quoted by the Associated Press as saying
that he had "personally benefited and grown from his experience and advice, and
I know countless others have as well. Teddy taught us all that public service
isn't a hobby or even an occupation, but a way of life and his legacy will live
日期：日 - 来自[]栏目
June 2, 2008 -- Sen. Edward
Kennedy's brain surgery, done?this morning at Duke University Medical
Center in Durham, N.C. to treat Kennedy's brain cancer, was
"successful," Kennedy's doctor says.
Here is the statement from Duke neurosurgeon Allan Friedman, MD: "I am
pleased to report that Senator Kennedy's surgery was successful and
accomplished our goals. Senator Kennedy was awake during the resection, and
should therefore experience no permanent neurological affects from the surgery.
The surgery lasted roughly three and a half hours and is just the first step in
Senator Kennedy's treatment plan. After a brief recuperation, he will begin
targeted radiation at Massachusetts General Hospital and chemotherapy
treatment. I hope that everyone will join us in praying for Senator Kennedy to
have an uneventful and robust recovery."
A resection?removes the
tumor, but experts say the type of tumor Kennedy has likely can't be totally
removed by surgery.
Before the operation, Kennedy's
office released a statement noting that Kennedy will spend about a?week
recovering at Duke University Medical Center.
Kennedy will return to Massachusetts
General Hospital, where his tumor was diagnosed, for radiation treatments and
chemotherapy.
Kennedy, 76, has a type of brain
tumor called a malignant glioma. Doctors at Massachusetts General Hospital
announced Kennedy's brain cancer diagnosis on
The next day, Kennedy was discharged from Massachusetts General
Since then,
brain cancer survivors who have dealt with similar types of brain cancer
have encouraged Kennedy to remain hopeful.
In his presurgery
statement,?Kennedy said he
is "deeply grateful" to everyone
who has expressed support "as I tackle this new and unexpected health
challenge." Kennedy also says he looks forward to returning to the U.S.
Senate and "doing everything I can to help elect Barack Obama as our next
president."
Kennedy's Brain Surgery
WebMD spoke with two experts about Kennedy's brain surgery while the
operation was still under way.
Deborah Heros, MD, associate professor of clinical neurology and
neuro-oncology at the University of Miami Leonard M. Miller School of
Eugene S. Flamm, MD, professor and chairman, department of neurosurgery,
Montefiore Medical Center at Albert Einstein College of Medicine in New
Heros and Flamm aren't treating Kennedy.
What does "targeted surgery" involve?
Targeted surgery is kind of a nonspecific
term. If the purpose of the surgery is to achieve a maximum resection [removing
as much of the tumor as possible]; oftentimes the surgery is performed while
the patient is awake, so they can monitor the speech and avoid impairing his
ability to understand speech and speak. ... Also, they can examine him during
the procedure to make sure they do not cause motor weakness.
We know that we cannot totally
resect these tumors because of the rootlets of tumors invading or infiltrating
the brain tissue. ... There is evidence that if the tumor can be maximally
resected [removed as much as possible], that may increase the chance of longer
survival and better result from treatment.
日期：日 - 来自[]栏目
May 21, 2008 -- Sen. Edward Kennedy, diagnosed yesterday with brain cancer, headed to his Cape Cod, Mass., home today after being discharged from Massachusetts General Hospital.
"Senator Kennedy has recovered remarkably quickly from his Monday procedure" and was therefore released a day ahead of schedule, say Kennedy's doctors, who include Lee Schwamm, MD, vice chairman of the neurology department at Massachusetts General Hospital, and Larry Ronan, MD, a primary care physician at the same hospital.
Kennedy will stay at his Cape Cod home "while we await further test results and determine treatment plans. He's feeling well and eager to get started," say Schwamm and Ronan.
Kennedy's brain tumor is a malignant glioma in his left parietal lobe, an area of the brain involved in speech. WebMD spoke with Deborah Heros, MD, associate professor of clinical neurology and neuro-oncology at the University of Miami Leonard M. Miller School of Medicine, about cutting-edge treatments for malignant gliomas.
Heros is not involved in Kennedy's treatment or diagnosis. She notes that the location of Sen. Kennedy's glioma would likely rule out surgery to remove the tumor.
What are the latest or experimental treatments for malignant gliomas, and would Sen. Kennedy be a candidate for them?
The foundation for treatment of a glioma, through the years, has been radiation therapy. Most treatment plans or protocols start with radiation. The oral chemotherapy drug temozolomide (Temodar) has also become part of that initial plan that has been shown to be the most promising treatment. Most treatment begins with that combination of the radiation and the temozolomide.
There are many centers that are looking into newer treatments. Many of them are treatments that either could be added or perhaps used following the radiation and the temozolomide. ...
Some of the newer therapies include more specific chemotherapy agents that we call targeted therapies. We call them targeted therapies because the medication or chemotherapy has been developed to target a specific protein or function of the tumor cell to interfere with the tumor cell growth.
Many people will recognize the name Avastin as being one of the most popular and promising targeted therapies for many kinds of tumors and also gliomas. This targets the tumor's ability to produce new blood vessels, and the tumor needs new blood vessels to grow. The targeted therapy Avastin prevents the tumor from being able to produce new blood vessels. And so, in a sense, the tumor starves itself or cannot continue to grow because it's run out of its blood supply. Some physicians are using Avastin in a clinical protocol with other chemotherapeutic agents and some are using it along with the temozolomide during different phases of the treatment. That could be one add-on that maybe some of the physicians involved in Sen. Kennedy's care are considering.
日期：日 - 来自[]栏目
May 20, 2008 -- Sen. Edward M.
Kennedy, 76, has been diagnosed with a malignant glioma, a type of brain
A glioma is a brain tumor that begins in glial
cells, which are cells that surround and support nerve cells.
Kennedy remains at Massachusetts
General Hospital, where he has been since he suffered a seizure on
His doctors -- who include Lee
Schwamm, MD, vice chairman of the neurology department at Massachusetts General
Hospital, and Larry Ronan, MD, a primary care physician at Massachusetts
General Hospital -- today released the following statement about Kennedy's
condition:
"Over the course of the last
several days, we've done a series of tests on Senator Kennedy to determine the
cause of his seizure. He has had no further seizures, remains in good overall
condition, and is up and walking around the hospital. Some of the tests we had
performed were inconclusive, particularly in light of the fact that the senator
had severe narrowing of the left carotid artery [which supplies blood from the
heart to the brain] and underwent surgery just 6 months ago. However,
preliminary results from a biopsy of the brain identified the cause of the
seizure as a malignant glioma in the left parietal lobe. The usual course of
treatment includes combinations of various forms of radiation and chemotherapy.
Decisions regarding the best course of treatment for Senator Kennedy will be
determined after further testing and analysis. Senator Kennedy will remain at
Massachusetts General Hospital for the next couple of days, according to
routine protocol. He remains in good spirits and full of
WebMD spoke about Kennedy's
diagnosis with Deborah Heros, MD, associate professor of clinical neurology and
neuro-oncology at the University of Miami Leonard M. Miller School of Medicine.
Heros is not involved in Kennedy's treatment or diagnosis.
What do you make of the
doctors' statement?
I think that he had a biopsy and
it showed that he had what's called a malignant glioma, and seizures can be a
presenting symptom for a brain tumor. As they had mentioned, usually we use
radiation therapy and chemotherapy for treatment of this tumor after surgery.
It appears as though Massachusetts General Hospital will be discussing that
further and that we would expect him to begin treatment.
The newer treatments available
include oral chemotherapy. Oftentimes, the oral chemotherapy is combined with
the radiation treatments over six weeks and people tolerate it well. Hopefully,
he'll be released from the hospital soon and be able to begin his treatment as
an outpatient.
You mentioned surgery. What
kind of surgery would that be?
Typically surgery can be a biopsy
alone to identify and document the specific type of tumor and prove that it is
a tumor. A biopsy alone is done if the tumor is located either deep in the
brain or in an area where removing tissue could cause neurological impairment
[brain damage]. Apparently, this may have been on the left side of his brain,
where speech function is located. So that may have been the reason why they
chose to do a biopsy rather than what we call a craniotomy, with tumor removal.
If the tumor is in an area that can be operated on, sometimes a larger surgical
procedure is done to remove as much tumor as possible. The limiting factor is
the location in the brain.
日期：日 - 来自[]栏目
May 20, 2008 -- Sen. Edward M. Kennedy, 76, has been diagnosed with a
malignant glioma, a type of brain
A glioma is a brain tumor that begins in glial
cells, which are cells that surround and support nerve cells.
Kennedy remains at Massachusetts General Hospital, where he has been since
he suffered a seizure last Saturday.
His doctors -- who include Lee Schwamm, MD, vice chairman of the neurology
department at Massachusetts General Hospital, and Larry Ronan, MD, a primary
care physician at Massachusetts General Hospital -- today released the
following statement about Kennedy's condition:
"Over the course of the last several days, we've done a series of tests
on Senator Kennedy to determine the cause of his seizure. He has had no further
seizures, remains in good overall condition, and is up and walking around the
hospital. Some of the tests we had performed were inconclusive, particularly in
light of the fact that the senator had severe narrowing of the left carotid
artery [which supplies blood from the heart to the brain] and underwent surgery
just 6 months ago. However, preliminary results from a biopsy of the brain
identified the cause of the seizure as a malignant glioma in the left parietal
lobe. The usual course of treatment includes combinations of various forms of
radiation and chemotherapy. Decisions regarding the best course of treatment
for Senator Kennedy will be determined after further testing and analysis.
Senator Kennedy will remain at Massachusetts General Hospital for the next
couple of days, according to routine protocol. He remains in good spirits and
full of energy."
日期：日 - 来自[]栏目
April 16, 2008 -- Sen. Arlen Specter's
Hodgkin's disease, first diagnosed in 2005, has returned, the senator has
announced.
Hodgkin's is a type of lymphoma (cancer of the lymphatic
Specter (R-Pa.), who is 78 years old, says he will not disrupt Senate
activities because of the relapse, which will require 12 weeks of chemotherapy.
Specter also says he plans to run for re-election when his term expires in
The recurrence of his Hodgkin's disease was diagnosed after a routine
follow-up PET scan. The scan led to a biopsy, which showed evidence of disease
recurrence, according to a news release from Specter's Senate office. The
examination showed no cancer in Specter's bone marrow.
"I was surprised by the PET scan findings because I have been feeling so
good.?I consider this just another bump on the road to a successful
recovery from Hodgkin's, from which I've been symptom-free for three
years," Specter says in the news release.
Specter has an "excellent chance" of complete remission of his
Hodgkin's disease, says John H. Glick, MD, the senator's oncologist, in the
news release.
"He is in superb physical condition, with a normal physical examination
and blood work, no symptoms of disease, plays squash regularly, and follows a
careful diet," says Glick, a professor of medicine at the Abramson Cancer
Center at the University of Pennsylvania.
Specter underwent treatment after his first diagnosis of Hodgkin's disease
in 2005. He has had a series of serious health concerns throughout his career,
including surgery for a brain tumor in 1993 and a
recurrence of that tumor in 1996.
Specter also underwent cardiac bypass surgery during his re-election
campaign in 1998, which he won.
"I've beaten some tough medical problems and tough political opponents
and I expect to beat this too," Specter says in the statement.
日期：日 - 来自[]栏目
1Graduate Institute of Clinical Medicine, 2Department of Internal Medicine, and 3Hepatitis Research Center, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei
Received 29 July 2002; revised 4 October 2002; electronically published 19 December 2002.
To clarify the influence that a recently identified SEN virus (SENV) has on hepatitis C virus (HCV) response to therapy with interferon plus ribavirin, 2 SENV variants, SENV-D and SENV-H, were studied in 100 patients with chronic hepatitis C; 57 of these patients were positive for SENV-D/H DNA, and there were no differences, in clinicopathological features, between patients with and without SENV coinfection. However, patients with SENV coinfection had a higher prevalence of HCV genotype 2a than did those without it. The sustained HCV response rate after combination therapy was comparable between patients with and without SENV coinfection. Of the 57 patients with SENV coinfection, 18 (32%) had a sustained SENV response to combination therapy, and SENV-D had a higher sustained response rate than did SENV-H. These results suggest that SENV has a specific link to HCV genotype 2a and that SENV infection has no apparent effect on coexisting chronic hepatitis C.
&&&&&Informed consent was obtained from the patients or their parents or guardians, and human-experimentation guidelines of National Taiwan University Hospital were followed in the conduct of this research.&&&&&Financial support: Liver Disease Prevention & Treatment Research F Department of Health and National Science Council, Executive Yuan, Taiwan.&&&&&Reprints or correspondence: Dr. Jia-Horng Kao, Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, 7 Chung-Shan South Rd., Taipei 100, Taiwan .
&&&&&Chronic liver diseases are endemic in Taiwan, and most of them can be attributed to infection with hepatitis B virus (HBV) or hepatitis C virus (HCV). Although GB virus C and TT virus (TTV) have been claimed to be associated with chronic non-Anon-E hepatitis [, ], most studies have indicated that neither virus causes liver disease [, ]. Recently, a new family of single-stranded DNA viruses has been isolated and designated "SEN virus" (SENV) []. By phylogenetic analysis, 8 different isolates (AH) have been identified, with varying prevalence in different populations []. Among these isolates, SENV-D and SENV-H have been extensively studied []. However, the association of SENV infection with liver cell damage remains controversial. Furthermore, one of our recent studies has shown that persons with SENV-D/H infection alone or coinfected with SENV-D/H and either HBV or HCV did not have increased evidence of liver disease []. These results therefore argued against the causative role of SENV-D/H in liver disease. Rigas et al. [] recently have suggested that coinfection with SENV-D/H might adversely affect the outcome of treatment with interferon and ribavirin in patients with chronic hepatitis C; however, their findings have been challenged.
&&&&&Taking advantage of the frequency of SENV-D/H coinfection in cases of chronic hepatitis C in Taiwan [], we investigated (1) the influence that SENV-D/H infection has on the clinical, virologic, and histologic characteristics of chronic hepatitis C, (2) the effect that SENV-D/H coinfection has on HCV response to combination therapy with interferon plus ribavirin, and (3) the effect that combination therapy has on the clearance of SENV-D/H.
&&&&&Patients, materials, and methods.&&&&&We studied serum samples from 100 patients (64 men and 36 women [mean age ± SD, 46 ± 11 years]) with histologically verified chronic hepatitis C, at the gastroenterological clinics of the National Taiwan University Hospital. These patients had persistent elevation of serum alanine aminotransferase (ALT) levels and were positive for anti-HCV and HCV RNA for 6 months. All the enrolled patients were negative for hepatitis B surface antigen (HBsAg) and had no markers suggestive of autoimmune hepatitis. None had a history of alcoholism or hepatotoxic drug intake. Metabolic liver disease was excluded on the basis of clinical and laboratory data. The diagnosis of chronic hepatitis was based on clinical and pathological grounds, including chronic persistent hepatitis and chronic active hepatitis []. No case was at the cirrhosis stage. Serum samples were stored at -70°C until used.
&&&&&The patients had received 3 MU of interferon -2b (Intron A; Schering-Plough) thrice weekly, plus
mg of orally administered ribavirin (ICN Pharmaceuticals) daily for 24 weeks. The presence of HCV RNA and SENV DNA in the serum was determined (1) before initiation of combination therapy, (2) at the end of therapy, and (3) 24 weeks after the therapy had been completed. The response to combination therapy was classified into 2 patterns, according to the positivity of serum viral genomes. Patients with a sustained HCV response were defined as those whose HCV RNA in serum was undetectable both at the end of therapy and 24 weeks after combination therapy had been completed. Unsustained HCV response was defined as serum HCV RNA that remained detectable either at the end of therapy or 24 weeks after combination therapy had been completed. Similarly, patients with a sustained SENV response were defined as those whose SENV DNA was undetectable both at the end of therapy and 24 weeks after combination therapy had been completed.
&&&&&HBsAg and anti-HCV were tested with commercially available kits (Abbott Laboratories).
&&&&&Serum HCV RNA was tested by reverse transcriptionpolymerase chain reaction with primers from the most conserved 5 untranslated region of the viral genome, and HCV genotypes were identified by type-specific primers []. Serum HCV RNA level was determined by a second-generation branched-DNA signal-amplification assay (Quantiplex HCV RNA; Bayer Diagnostics) with a detection limit of 0.2 mEq/mL.
&&&&&SENV-D DNA and SENV-H DNA were amplified by polymerase chain reaction using strain-specific primers, as described elsewhere []. The amplified products (231 bp for SENV-D and 230 bp for SENV-H) were separated by 3% agarose gel electrophoresis and were stained with ethidium bromide. The presence of TTV DNA was assayed by nested polymerase chain reaction with primer pairs from open reading frame 1 of the viral genome [].
&&&&&Data were analyzed by Fisher's exact test, 2 test with Yates's correction, or Student's t test, and variables that achieved statistical significance in univariate analysis were subjected to multivariate Cox regression analysis, to determine the significantly independent factors. A P value of &.05 was considered to be statistically significant.
&&&&&Results.&&&&&Of the 100 patients with chronic hepatitis C, 57 (57%) were positive for serum SENV DNA. Of the 57 patients with SENV coinfection, 41 (72%) were infected with SENV-H alone, 8 (14%) with SENV-D alone, and 8 (14%) with both SENV-D and SENV-H. In addition, of the 57 patients with SENV coinfection, 27 (47%) also were positive for serum TTV DNA.
&&&&&Of the 100 patients receiving combination therapy, 40 (40%) were sustained responders, and the remaining 60 (60%) were nonresponders. There was no significant difference, in terms of sex, age, or mean serum ALT level at onset of therapy, between responders and nonresponders. Although the baseline mean ± SD serum HCV RNA level in the responders was lower than that in the nonresponders (1.3 ± 3.1 vs. 2.0 ± 4.3 mEq/mL), the difference was not statistically significant. However, sustained HCV response rate in patients with either genotype 2a or genotype 2b was higher than that in patients with genotype 1b (57% vs. 22% [P & .001]).
&&&&&There was no significant difference, in the clinicopathological features, between patients with chronic hepatitis C with and without SENV coinfection . However, by univariate analysis, the prevalence of HCV genotype 2a in patients with SENV coinfection was significantly higher than that in those without it (37% vs. 16% [P = .03]); by multivariate analysis, HCV genotype 2a was independently associated with SENV coinfection (P & .05). In contrast, the sustained HCV response rate after combination therapy was comparable in patients with and without SENV coinfection (44% vs. 35%; see ). Further analysis indicated that the sustained HCV response rate in patients with genotype 1b with and without SENV coinfection was 26% and 15%, respectively, whereas the sustained HCV response rate in patients with genotype 2a with and without SENV coinfection was 50% and 38%, respectively. These differences too were not statistically significant.
fig.ommitted
Table&1.&&&&&&&&&&Demographic and clinical data on 100 patients with chronic hepatitis C, with and without SEN virus (SENV) DNA.
&&&&&Of the 57 patients with SENV coinfection before initiation of combination therapy, 21 (37%) lost serum SENV DNA at the end of therapy, and 20 (35%) remained negative for serum SENV DNA 6 months after therapy had been completed . Accordingly, the sustained response rate of SENV was comparable to that of HCV (35% vs. 40%), whereas no correlation between sustained HCV response and sustained SENV response was seen. However, both the end-of-therapy and the sustained viral response rates of SENV-D were significantly higher than those of SENV-H (88% vs. 34% [P = .02] and 88% vs. 27% [P = .004], respectively).
fig.ommitted
Table&2.&&&&&&&&&&Response of SEN virus (SENV) variants to combination therapy with interferon plus ribavirin, in 57 patients with chronic hepatitis C with SENV coinfection.
&&&&&Discussion.&&&&&Of the 8 SENV isolates, only SENV-D and SENV-H have higher prevalence ratios. In Taiwan, our recent study had indicated that SENV-D/H infections occur more often in high-risk groups (54%90%), patients with chronic hepatitis B (41%), HBV-related hepatocellular carcinoma (HCC) (54%), chronic hepatitis C (67%), and HCV-related HCC (76%) than in healthy adults (15%) []. However, the prevalence of SENV-D/H DNA in patients with non-Anon-E fulminant hepatitis (30%) was comparable to that in healthy adults (15%). In addition, most subjects with SENV-D/H infection alone had either no hepatitis or mild hepatitis. Thus, although an association of SENV-D/H with transfusion-associated hepatitis has been reported [], whether SENV-D/H serve as causative agents of non-Anon-E hepatitis remains controversial [].
&&&&&The geographic distribution of different SENV variants remains unclear. Previous studies have shown that SENV-D is the predominant strain in Japan [, ], whereas SENV-H is predominant in the United States and Taiwan [, ]. The findings of the present study consistently indicate that 72% of Taiwanese patients with chronic hepatitis C with SENV coinfection were infected with SENV-H, 14% with SENV-D. Whether differences in SENV variants affect the heterogeneity in clinical outcome and response to antiviral therapy in patients with chronic SENV infection in different parts of the world awaits further studies.
&&&&&Coinfection with SENV has been frequently observed in 20%76% of patients with chronic hepatitis C [, ]. The results of the present study showed that the prevalence of SENV-D/H infection in patients with chronic hepatitis C was 57%, implying that HCV and SENV may share common modes of transmission. Nonetheless, the mean serum HCV RNA level did not differ significantly between patients with HCV and SENV coinfection and those with HCV infection alone (). Accordingly, our data consistently showed that SENV might not interfere with the replication of HCV [].
&&&&&The clinical relevance of SENV infection in combination with HCV infection remains controversial [, , , ]. Our data showed no significant difference, in terms of demographic features, peak serum ALT level, histological severity, and serum HCV RNA level, between patients with HCV and SENV coinfection and those with HCV infection alone (). This fact confirms that coinfection with SENV-D/H in patients with chronic hepatitis C is not associated with increased biochemical or histological evidence of liver disease. However, HCV genotype 2a was more often found among patients with HCV and SENV coinfection than among those with HCV infection alone (37% vs. 16% [P = .03]), suggesting a specific link between SENV and HCV genotype 2a.
&&&&&Combination therapy with interferon and ribavirin is the standard of therapy for na&ve patients with chronic hepatitis C and has an overall sustained viral response rate of 40%50% []. Both HCV genotype and pretreatment serum HCV RNA level are known predictors of sustained viral response to combination therapy [, ]. The present study consistently showed that 40% of the patients receiving therapy with interferon plus ribavirin had a sustained viral response and that patients infected with either genotype 2a or genotype 2b were more likely to have a sustained response than were those infected with genotype 1b (57% vs. 22% [P & .001]). In addition, there was no significant difference, in sustained HCV response, between those with HCV and SENV coinfection and those with HCV infection alone (44% vs. 35%; see ). Although patients with either genotype 1b or genotype 2a and SENV coinfection had a higher sustained HCV response rate than did those without it, the difference was not statistically significant. Our results contrast with those of a recent report indicating that HCV with SENV coinfection adversely affect sustained HCV response to combination therapy with interferon plus ribavirin []. Differences in patient selection, sample size, and/or distribution of HCV and SENV genotypes may explain this discrepancy. Thus, further studies are needed to address this important and interesting issue.
&&&&&Umemura et al. [] have recently reported that the sustained response rate of SENV to interferon therapy is significantly higher than that of HCV (69% vs. 37% [P = .035]) and that the sustained response rate of SENV-D was higher than that of SENV-H (73% vs. 33%), suggesting that SENV-D is highly susceptible to interferon. In our study, 21 (37%) of 57 patients with chronic hepatitis C with SENV coinfection lost serum SENV DNA at the end of therapy, and 20 (35%) remained negative for serum SENV DNA 6 months after therapy had been completed (). Particularly noteworthy is that the end-of-therapy and sustained viral response of SENV-D were significantly higher than those of SENV-H (88% vs. 34% [P = .02] and 88% vs. 27% [P = .004], respectively), confirming that SENV-D is more sensitive to antiviral treatment than is SENV-H. Thus, the lower sustained SENV response rate in our study, compared with that in a Japanese report [], may reflect merely the more prevalent SENV-H strain in Taiwan.
&&&&&In summary, we found that coinfection with SENV is frequent in chronic hepatitis C in Taiwan and that it has a specific link to HCV genotype 2a. However, coinfection with SENV does not affect the clinicopathological features of chronic hepatitis C and the response to combination therapy. In addition, SENV-D is more susceptible to combination therapy than is SENV-H.
References
日期：日 - 来自[]栏目共 1 页，当前第 1 页
Copyright & 2008
All rights reserved. 医源世界 版权所有
医源世界所刊载之内容一般仅用于教育目的。您从医源世界获取的信息不得直接用于诊断、治疗疾病或应对您的健康问题。如果您怀疑自己有健康问题，请直接咨询您的保健医生。医源世界、作者、编辑都将不负任何责任和义务。
本站内容来源于网络，转载仅为传播信息促进医药行业发展，如果我们的行为侵犯了您的权益，请及时与我们联系我们将在收到通知后妥善处理该部分内容联系Email: