Aa
platelets
after 5 weeks on double dose peg and riba,my platelets went down to 56 from pre treatment of 70,and this past friday week 6 was a single dose due to drop in count.my rbc and wbc are down as well.all this is to be expected on treatment,but im praying as i go tommorrow to give blood my virus is und. and platelets are up so i can continue treatment without any hitches.someone on forum mentioned a drug named oprelvekin used for cancer patients finished on chemo with low platelets.i read up on it,and the possible side effects are scary.i dont even know if this drug can be taken while on hep c meds.has anyone gone thru a similar situation with their platelet count,even if you were on single dose peg and had to either stop treatment or reduce your dose.thanks and god bless you all who are fighting the good fight
Good news! Keep those platelets up and you will be fine. The values for platelets, WBC, and RBC will change over time within a range. Going up sometimes and going down at others. As long as you can keep them from a constant free fall you should be good to continue treatment.
Can't wait to see viral load results to see how the meds are working on your HCV!
Keep up the good work! Hang in there!
Hector
Can't wait to see viral load results to see how the meds are working on your HCV!
Keep up the good work! Hang in there!
Hector
thanks for your response and concern.my labs just came back except for the viral load.platelets up to 77,wbc up a little,everything else the same,alt at 27,which is down from 55 pre tx.,nice.will tell you the vl. when it comes in,hope you are doing well and hang in there bro.god bless you and may the lord give you the desires of your heart as you delight in him
I believe coinfection does lower your odds. I have HCV and HBV and believe that sped up cirrhosis and lessened my chance of SVR also. I don't have any experience in this area. But I agree with you that to go two stages in 2-3 seems unrealistic. Because how can anyone even survive for 10 years at that rate of progression?
Here is some info that may shed some light on the subject...
"Retreatment Strategies for Patients Failing First-Line Therapy"
Source: Advanced Topics in Hepatitis C Management: Tools for Nurse Practitioners and Physician Assistants
By: HoChong Gilles, RN, MS, FNP
"Coinfection With HIV"
"The treatment of patients with HCV and HIV coinfection is complicated by a number of conditions that can lead to nonresponse or relapse to HCV therapy. Some studies show that patients harboring both HCV and HIV experience faster fibrosis progression compared with patients infected only with HCV.[45] Coinfection with both HCV and HIV is also associated with a high incidence of end-stage liver disease and can be associated with an increased risk of hepatotoxicity during anti-HIV therapy.[46,47] Coinfection with HIV has likewise been shown to reduce the survival rate and increase the recurrence of HCV infection among individuals who have undergone liver transplantation (Capsule Summary).[48] These findings stress the importance of controlling both HCV and HIV infections in coinfected individuals through the use of therapy.Three randomized, controlled trials by Carat and colleagues,[49] by Torriani and colleagues,[50] and by Chung and colleagues[51] have demonstrated that 48 weeks of treatment with peginterferon/ribavirin is safe and effective in HCV/HIV-coinfected individuals (Table 3) (Capsule Summaries 1, 2, and 3). In summary, the SVR rates achieved with therapy were lower in coinfected patients (27% to 40%) when compared with the rates typically observed in HCV-monoinfected patients (40% to 76%), particularly for individuals with genotype 1 HCV. However, given that peginterferon/ribavirin produced superior outcomes compared with standard interferon/ribavirin, these trials helped to garner US Food and Drug Administration (FDA) approval for peginterferon alfa-2a 180 µg/week plus ribavirin 800 mg/day as treatment for HCV-infected patients with stable HIV disease. Coinfected patients with HCV genotype 1 may benefit from higher ribavirin dosing (1000-1200 mg/day) given that insufficient ribavirin levels likely contribute to a lower SVR rate among this population, although this is currently being studied prospectively.Although a sizeable proportion of HCV/HIV-coinfected patients will not achieve an undetectable HCV RNA on treatment, they may still attain improvements in liver histology.[51] In 1 study, 32% to 43% of patients who did not achieve an SVR on treatment still showed histologic improvement, leading the researchers to suggest that improvement in biopsies might be an alternative goal of therapy.[52]The optimal time to start HCV therapy in relation to starting antiretrovirals is not well defined. Patients with high CD4+ cell counts appear to have the best response to HCV therapy, suggesting that good immune status may facilitate sustained clearance of HCV. Highly active antiretroviral therapy for HIV can slow fibrosis progression even though it does not improve the virologic response to HCV treatment.[53,54] Therapy initiation should involve weighing the risks of an expected, transient CD4+ count decline while on interferon with the benefits of improving tolerance to HIV medications if HCV is treated first."
Can't wait to hear your VL results. I hoping it is very low or undetectable!!!
Best of luck!
Hector
Here is some info that may shed some light on the subject...
"Retreatment Strategies for Patients Failing First-Line Therapy"
Source: Advanced Topics in Hepatitis C Management: Tools for Nurse Practitioners and Physician Assistants
By: HoChong Gilles, RN, MS, FNP
"Coinfection With HIV"
"The treatment of patients with HCV and HIV coinfection is complicated by a number of conditions that can lead to nonresponse or relapse to HCV therapy. Some studies show that patients harboring both HCV and HIV experience faster fibrosis progression compared with patients infected only with HCV.[45] Coinfection with both HCV and HIV is also associated with a high incidence of end-stage liver disease and can be associated with an increased risk of hepatotoxicity during anti-HIV therapy.[46,47] Coinfection with HIV has likewise been shown to reduce the survival rate and increase the recurrence of HCV infection among individuals who have undergone liver transplantation (Capsule Summary).[48] These findings stress the importance of controlling both HCV and HIV infections in coinfected individuals through the use of therapy.Three randomized, controlled trials by Carat and colleagues,[49] by Torriani and colleagues,[50] and by Chung and colleagues[51] have demonstrated that 48 weeks of treatment with peginterferon/ribavirin is safe and effective in HCV/HIV-coinfected individuals (Table 3) (Capsule Summaries 1, 2, and 3). In summary, the SVR rates achieved with therapy were lower in coinfected patients (27% to 40%) when compared with the rates typically observed in HCV-monoinfected patients (40% to 76%), particularly for individuals with genotype 1 HCV. However, given that peginterferon/ribavirin produced superior outcomes compared with standard interferon/ribavirin, these trials helped to garner US Food and Drug Administration (FDA) approval for peginterferon alfa-2a 180 µg/week plus ribavirin 800 mg/day as treatment for HCV-infected patients with stable HIV disease. Coinfected patients with HCV genotype 1 may benefit from higher ribavirin dosing (1000-1200 mg/day) given that insufficient ribavirin levels likely contribute to a lower SVR rate among this population, although this is currently being studied prospectively.Although a sizeable proportion of HCV/HIV-coinfected patients will not achieve an undetectable HCV RNA on treatment, they may still attain improvements in liver histology.[51] In 1 study, 32% to 43% of patients who did not achieve an SVR on treatment still showed histologic improvement, leading the researchers to suggest that improvement in biopsies might be an alternative goal of therapy.[52]The optimal time to start HCV therapy in relation to starting antiretrovirals is not well defined. Patients with high CD4+ cell counts appear to have the best response to HCV therapy, suggesting that good immune status may facilitate sustained clearance of HCV. Highly active antiretroviral therapy for HIV can slow fibrosis progression even though it does not improve the virologic response to HCV treatment.[53,54] Therapy initiation should involve weighing the risks of an expected, transient CD4+ count decline while on interferon with the benefits of improving tolerance to HIV medications if HCV is treated first."
Can't wait to hear your VL results. I hoping it is very low or undetectable!!!
Best of luck!
Hector
had to redo hep viral load today,should have results soon.trying to understand everything you sais.does it mean that since im coinfected,my odds of svr is not good?do you think i could have gone from stage 2 to cirrhosis in 2-3 years,even being on treatment for 48 weeks of that time?looking forward to your response,god bless
Hi! How are you?
Any viral load results as yet? (or did I miss it?)
You had all the indications of Stage 2, Grade 2 at the end of 2005. Necrosis (cell death) and inflammation at the edge of the portal areas, so-called “piecemeal necrosis”. All sounds consistant with Stage 2 which is good.
I found this acticle. I'm not sure how representative it is of other studies? But I thought it worth mentioning.....
"Liver fibrosis often progresses rapidly in HIV/HCV co-infected; elevated AST levels best predictor"
Derek Thaczuk, Friday, October 19, 2007
A prospective study of patients co-infected with HIV and hepatitis C has found significant progression of liver fibrosis in a quarter of the cohort over a span of three years, despite little or no evidence of fibrosis at the beginning of the study.
HIV disease state, HIV treatment, and hepatitis C virus (HCV) treatment were found to play little or no role in the risk of progression of fibrosis: analysis identified only elevations of serum aspartate aminotransferase (AST) as a significant predictor of progression.
The findings, from a research team at Baltimore's Johns Hopkins University School of Medicine, headed by Mark Sulkowski, were published in the October 2007 issue of AIDS.
The short-term goal of hepatitis C treatment is sustained virologic response (SVR): prolonged undetectable HCV viral load after the course of treatment is concluded. However, SVR rates are often low, especially in HIV/HCV co-infection. Studies have reported conflicting results as to the effect of virologically unsuccessful HCV treatment on the progression of liver disease, and on the impact of HAART on hepatitis C disease.
Sulkowski's research team has been following a prospective cohort of HIV/HCV co-infected adults, using repeat liver biopsies to measure the progression of fibrosis, to determine the impacts of HAART and HCV treatment, and assess the risk factors for progression. Data on 61 people from this cohort were presented previously at the Twelfth Conference on Retroviruses and Opportunistic Infections (CROI) in 2005 and again at the Thirteenth CROI in February 2006.
The published cohort consisted of 184 adults with HIV and HCV infection, who had had at least two liver biopsies between January 1998 and July 2006, and who did not have cirrhosis of the liver at the first biopsy. The cohort was largely African-American (86%) and people with a history of injection drug use (80%); most were men (74%) with a median age of 44 years.
HIV disease was well-controlled in most: the median CD4 cell count was 379 cells/mm3, 60% had a viral load of less than 400 copies/ml, 83% had received antiretroviral therapy, and 62% were on HAART at the time of the first biopsy.
Nearly all (95%) had HCV genotype 1; the median HCV RNA level was 573,000 at first biopsy and very few (1.7%) had received HCV treatment at or before this time.
This study used the Ishak modified scale to measure fibrosis: biopsy findings were graded as stage F0 to F6. At the time of first biopsy, 136 patients (77%) had minimal or no fibrosis (F0 or F1), 9% had stage F2, and 11% had "bridging" (stage F3 or F4) fibrosis. (Ten patients were excluded due to cirrhosis - stage F5 or higher.)
"Significant progression" between biopsies was defined as an increase of at least two stages. By this definition, 41 (24%) of the patients were "progressors", who experienced a significant increase in fibrosis between their first and second biopsy – a median interval of 2.9 years. (The greatest number (48%) had no change in fibrosis score over that time; 22% had a one-stage (less than significant) increase.)
Of the 136 who had no or minimal fibrosis at the first biopsy, 32% were progressors, including 14% who progressed to stage F3, F4, or even the cirrhotic stages F5 or F6. Among the progressors, the median rate of progression was 0.83 units per year.
The research team then compared the characteristics of the progressors with those of the non-progressors. Surprisingly, very few factors were found to differ between the two groups, especially after multivariate analysis. None of the following factors were found to be significant predictors: age, sex, race, CD4 cell count, HIV viral load, length of ART exposure, antiretroviral drug class used, or length of exposure to individual antiretroviral drugs, HCV genotype, or HCV RNA level.
Between biopsies, 37 (21%) of the patients received HCV treatment with interferon (standard or pegylated) plus ribavirin. SVR rates were extremely low: only three patients (2.7%) achieved sustained HCV suppression; all three were non-progressors.
Significant fibrosis progression was more common in those who received HCV treatment (35% vs. 20%), but those who were treated were more likely to already have had significant fibrosis at the first biopsy, and had higher ALT and AST levels between biopsies.
In multivariate analysis, the difference due to HCV treatment disappeared: the only risk factor associated with progression of fibrosis was elevated AST level between biopsies. ("Elevated" in this case was taken to be 2.5 or more times the upper limit of normal, 37 U/l.) Elevated ASTs were found in 25% of progressors vs. 12% of non-progressors (p = 0.03); by multivariate analysis the odds ratio was 3.4 (95% confidence interval, 1.4 – 7.9).
The researchers note several key conclusions. Firstly, their finding of significant fibrosis progression in a quarter of the cohort is significantly greater than that reported in many HCV-monoinfected cohorts, and "was unexpected in this cohort of [co-infected] patients with minimal liver disease on initial biopsy."
Secondly, they found little or no effect of either antiretroviral or HCV treatment on the progression of fibrosis. These data "suggest that the effect of ART on hepatic fibrogenesis is likely to be modest over a 3-year period".
Other studies have reported that HCV treatment is associated with stable or improved hepatic fibrosis (Rodriguez-Torres 2007). In contrast, the Johns Hopkins team "failed to detect a beneficial effect of HCV treatment on fibrosis progression in the absence of SVR," although they "can not exclude a modest effect of HIV and HCV treatment", and note that "the non-random selection of patients to receive HCV treatment may … introduce bias and randomized controlled trials are needed." Alcohol use (which was self-reported) may have been "incompletely assessed". As most patients were already on HAART at the time of first biopsy, the effects of HAART may have been underestimated, and the extremely low response rates to HCV treatment may have limited the observed treatment effect.
Reference
Sulkowski M et al. Rapid fibrosis progression among HIV/hepatitis C virus-co-infected adults. AIDS 21: 2209-2216, 2007.
Keep in touch. Let us know how things are progressing with your treatment.
Hector
Any viral load results as yet? (or did I miss it?)
You had all the indications of Stage 2, Grade 2 at the end of 2005. Necrosis (cell death) and inflammation at the edge of the portal areas, so-called “piecemeal necrosis”. All sounds consistant with Stage 2 which is good.
I found this acticle. I'm not sure how representative it is of other studies? But I thought it worth mentioning.....
"Liver fibrosis often progresses rapidly in HIV/HCV co-infected; elevated AST levels best predictor"
Derek Thaczuk, Friday, October 19, 2007
A prospective study of patients co-infected with HIV and hepatitis C has found significant progression of liver fibrosis in a quarter of the cohort over a span of three years, despite little or no evidence of fibrosis at the beginning of the study.
HIV disease state, HIV treatment, and hepatitis C virus (HCV) treatment were found to play little or no role in the risk of progression of fibrosis: analysis identified only elevations of serum aspartate aminotransferase (AST) as a significant predictor of progression.
The findings, from a research team at Baltimore's Johns Hopkins University School of Medicine, headed by Mark Sulkowski, were published in the October 2007 issue of AIDS.
The short-term goal of hepatitis C treatment is sustained virologic response (SVR): prolonged undetectable HCV viral load after the course of treatment is concluded. However, SVR rates are often low, especially in HIV/HCV co-infection. Studies have reported conflicting results as to the effect of virologically unsuccessful HCV treatment on the progression of liver disease, and on the impact of HAART on hepatitis C disease.
Sulkowski's research team has been following a prospective cohort of HIV/HCV co-infected adults, using repeat liver biopsies to measure the progression of fibrosis, to determine the impacts of HAART and HCV treatment, and assess the risk factors for progression. Data on 61 people from this cohort were presented previously at the Twelfth Conference on Retroviruses and Opportunistic Infections (CROI) in 2005 and again at the Thirteenth CROI in February 2006.
The published cohort consisted of 184 adults with HIV and HCV infection, who had had at least two liver biopsies between January 1998 and July 2006, and who did not have cirrhosis of the liver at the first biopsy. The cohort was largely African-American (86%) and people with a history of injection drug use (80%); most were men (74%) with a median age of 44 years.
HIV disease was well-controlled in most: the median CD4 cell count was 379 cells/mm3, 60% had a viral load of less than 400 copies/ml, 83% had received antiretroviral therapy, and 62% were on HAART at the time of the first biopsy.
Nearly all (95%) had HCV genotype 1; the median HCV RNA level was 573,000 at first biopsy and very few (1.7%) had received HCV treatment at or before this time.
This study used the Ishak modified scale to measure fibrosis: biopsy findings were graded as stage F0 to F6. At the time of first biopsy, 136 patients (77%) had minimal or no fibrosis (F0 or F1), 9% had stage F2, and 11% had "bridging" (stage F3 or F4) fibrosis. (Ten patients were excluded due to cirrhosis - stage F5 or higher.)
"Significant progression" between biopsies was defined as an increase of at least two stages. By this definition, 41 (24%) of the patients were "progressors", who experienced a significant increase in fibrosis between their first and second biopsy – a median interval of 2.9 years. (The greatest number (48%) had no change in fibrosis score over that time; 22% had a one-stage (less than significant) increase.)
Of the 136 who had no or minimal fibrosis at the first biopsy, 32% were progressors, including 14% who progressed to stage F3, F4, or even the cirrhotic stages F5 or F6. Among the progressors, the median rate of progression was 0.83 units per year.
The research team then compared the characteristics of the progressors with those of the non-progressors. Surprisingly, very few factors were found to differ between the two groups, especially after multivariate analysis. None of the following factors were found to be significant predictors: age, sex, race, CD4 cell count, HIV viral load, length of ART exposure, antiretroviral drug class used, or length of exposure to individual antiretroviral drugs, HCV genotype, or HCV RNA level.
Between biopsies, 37 (21%) of the patients received HCV treatment with interferon (standard or pegylated) plus ribavirin. SVR rates were extremely low: only three patients (2.7%) achieved sustained HCV suppression; all three were non-progressors.
Significant fibrosis progression was more common in those who received HCV treatment (35% vs. 20%), but those who were treated were more likely to already have had significant fibrosis at the first biopsy, and had higher ALT and AST levels between biopsies.
In multivariate analysis, the difference due to HCV treatment disappeared: the only risk factor associated with progression of fibrosis was elevated AST level between biopsies. ("Elevated" in this case was taken to be 2.5 or more times the upper limit of normal, 37 U/l.) Elevated ASTs were found in 25% of progressors vs. 12% of non-progressors (p = 0.03); by multivariate analysis the odds ratio was 3.4 (95% confidence interval, 1.4 – 7.9).
The researchers note several key conclusions. Firstly, their finding of significant fibrosis progression in a quarter of the cohort is significantly greater than that reported in many HCV-monoinfected cohorts, and "was unexpected in this cohort of [co-infected] patients with minimal liver disease on initial biopsy."
Secondly, they found little or no effect of either antiretroviral or HCV treatment on the progression of fibrosis. These data "suggest that the effect of ART on hepatic fibrogenesis is likely to be modest over a 3-year period".
Other studies have reported that HCV treatment is associated with stable or improved hepatic fibrosis (Rodriguez-Torres 2007). In contrast, the Johns Hopkins team "failed to detect a beneficial effect of HCV treatment on fibrosis progression in the absence of SVR," although they "can not exclude a modest effect of HIV and HCV treatment", and note that "the non-random selection of patients to receive HCV treatment may … introduce bias and randomized controlled trials are needed." Alcohol use (which was self-reported) may have been "incompletely assessed". As most patients were already on HAART at the time of first biopsy, the effects of HAART may have been underestimated, and the extremely low response rates to HCV treatment may have limited the observed treatment effect.
Reference
Sulkowski M et al. Rapid fibrosis progression among HIV/hepatitis C virus-co-infected adults. AIDS 21: 2209-2216, 2007.
Keep in touch. Let us know how things are progressing with your treatment.
Hector
this is my liver biopsy of 11/05 info,i started tx. 1/06, stage 2,grade 2 fibrosis,mild hepatic steatosis,mild peripheal fibrosis,rare hepatocytes,peace meal necrosis[peace meal must mean scattered],no evidence cirrhosis.i started tx from 1/06-11/06.und at about week 12-16,on single dose peg and riba,for 48 weeks,virus came back,now on 72 week tx.of double dose,although for the last 2 of 3 weeks i did single because of lo platelets,did double yesterday.i doubt stage 2 turned into cirrhosis between 11/05 and now,especially that i was on tx. for almost a year.whats your take on this .thanks in advance for your response and your food for thought that got me to get you this info on my liver biopsy.god bless
Maybe I can add something or at least food for thought...
That is great you are only at stage 2! Your liver damage won't affect your chance of SVR.
I see you went UND between week 12 and 24. You are a "slow responder". Very important information to know for retreatment. So according to the newest treatment duration protocols you realize you should have been treated for 72 weeks to have given yourself better odds of achieving SVR. Correct?
By: Mitchell L. Shiffman, MD
"Three recent studies have now demonstrated that relapse can be significantly reduced in slow-to-respond genotype 1 patients—those who achieve undetectable HCV RNA after Week 12—by extending the duration of treatment from 48 to 72 weeks. In each of these studies, the relapse rate was reduced from more than 50% to less than 20%. Two of these studies suggest that this benefit may be less or nonexistent in patients with higher HCV RNA levels at baseline and at Week 12. However, these observations will need to be confirmed in future studies before these patients are not considered for treatment extension. Therefore, for now it appears that prolonging the duration of therapy will increase SVR rates in patients who are slow to respond and should be routinely practiced. "
So does your doctor understand this now and agree that you should have been treated longer the first time? What has your doc changed to give you better odds of success this time? I see you are double dosing. I've never seen studies on that improving odds of SVR. What matters is how your VL responds to tx.
What was your viral load at week 4?
Where did your viral load start at?
As far as the biopsy… You don't need one. It isn't going to change within 2 years. By the way, what was the Grade of inflammation? That usually will tell you how quickly the disease will progress.
“prothrombin time [pt] test which is called the poor mans liver biopsy,and it came back normal,as the platelets went from 56-61.the pt test is usually a sign of cirrhosis.my pre tx labs showes my wbc and rbc as well as platelets to be low, what this means i or my dr. dont know.i am hiv+ as well.”
This is the part that is confusing to me...Let me take a stab at it. INR. Okay I am stage 4, compensated, with portal hypertension. My INR has alway been within normal range. So I wouldn't rely on that too much. My platelets count is about 70k off of treatment. Your doc doesn't know why platelets, WBC, RBC are low? That doesn't inspire confidence in me personally. Maybe it is due to the HCV/HIV co-infection?
Okay I Goggled HCV HIV platelets RBC WBC...It looks like it is not uncommon for these level to be low when infected by HCV/HIV.
http://www.cig.salk.edu/extra_html/etc_hiv_diagonstics.htm
Red Blood Cell (RBC) Count -
Many people with HIV may have values below the normal range, and slightly decreased values should not be cause for alarm. However, greatly reduced numbers, a sign of anemia, should be carefully examined and treated if necessary. Symptoms include fatigue, shortness of breath and a pale skin color. Anemia can be due to certain medications or illness. Low RBC counts are accompanied by lower hemoglobin and hematocrit levels.
Platelet Count -
Platelets are a part of the blood that are needed for blood clotting. Platelets migrate to the site of an injury where they "stick" to the injured site and help to develop a clot or scab to stop the bleeding. A normal platelet count is between 150,000 and 440,000. Low platelet count (thrombocytopenia) can be caused by HIV infection itself or by certain drugs. Although a platelet count below 150,000 can be considered low, most people are not at risk of internal bleeding with counts of 50,000 or even lower. However, because platelets are necessary for blood clotting, the chance of major bleeding rises as the platelet count drops.
White Blood Cell (WBC) Count -
WBCs (leukocytes) help prevent and fight infections in the body. The normal white blood cell count ranges from 4,000 to 11,000 per cubic millimeter in an average healthy adult. High WBC count may indicate that the body is fighting an infection. Low counts may be a result of certain drugs (AZT or ganciclovir), minor viral infections, stress, or opportunistic infections (tuberculosis, histoplasmosis, and other fungal infections). Low counts are cause for concern as the body becomes more susceptible to infection.
I give you credit. Dealing with these two diseases must be a monster!!! So you must be really tough and you are retreating again. Wow! More power to you!!!
Best of luck on your retreatment!!!
Hector
That is great you are only at stage 2! Your liver damage won't affect your chance of SVR.
I see you went UND between week 12 and 24. You are a "slow responder". Very important information to know for retreatment. So according to the newest treatment duration protocols you realize you should have been treated for 72 weeks to have given yourself better odds of achieving SVR. Correct?
By: Mitchell L. Shiffman, MD
"Three recent studies have now demonstrated that relapse can be significantly reduced in slow-to-respond genotype 1 patients—those who achieve undetectable HCV RNA after Week 12—by extending the duration of treatment from 48 to 72 weeks. In each of these studies, the relapse rate was reduced from more than 50% to less than 20%. Two of these studies suggest that this benefit may be less or nonexistent in patients with higher HCV RNA levels at baseline and at Week 12. However, these observations will need to be confirmed in future studies before these patients are not considered for treatment extension. Therefore, for now it appears that prolonging the duration of therapy will increase SVR rates in patients who are slow to respond and should be routinely practiced. "
So does your doctor understand this now and agree that you should have been treated longer the first time? What has your doc changed to give you better odds of success this time? I see you are double dosing. I've never seen studies on that improving odds of SVR. What matters is how your VL responds to tx.
What was your viral load at week 4?
Where did your viral load start at?
As far as the biopsy… You don't need one. It isn't going to change within 2 years. By the way, what was the Grade of inflammation? That usually will tell you how quickly the disease will progress.
“prothrombin time [pt] test which is called the poor mans liver biopsy,and it came back normal,as the platelets went from 56-61.the pt test is usually a sign of cirrhosis.my pre tx labs showes my wbc and rbc as well as platelets to be low, what this means i or my dr. dont know.i am hiv+ as well.”
This is the part that is confusing to me...Let me take a stab at it. INR. Okay I am stage 4, compensated, with portal hypertension. My INR has alway been within normal range. So I wouldn't rely on that too much. My platelets count is about 70k off of treatment. Your doc doesn't know why platelets, WBC, RBC are low? That doesn't inspire confidence in me personally. Maybe it is due to the HCV/HIV co-infection?
Okay I Goggled HCV HIV platelets RBC WBC...It looks like it is not uncommon for these level to be low when infected by HCV/HIV.
http://www.cig.salk.edu/extra_html/etc_hiv_diagonstics.htm
Red Blood Cell (RBC) Count -
Many people with HIV may have values below the normal range, and slightly decreased values should not be cause for alarm. However, greatly reduced numbers, a sign of anemia, should be carefully examined and treated if necessary. Symptoms include fatigue, shortness of breath and a pale skin color. Anemia can be due to certain medications or illness. Low RBC counts are accompanied by lower hemoglobin and hematocrit levels.
Platelet Count -
Platelets are a part of the blood that are needed for blood clotting. Platelets migrate to the site of an injury where they "stick" to the injured site and help to develop a clot or scab to stop the bleeding. A normal platelet count is between 150,000 and 440,000. Low platelet count (thrombocytopenia) can be caused by HIV infection itself or by certain drugs. Although a platelet count below 150,000 can be considered low, most people are not at risk of internal bleeding with counts of 50,000 or even lower. However, because platelets are necessary for blood clotting, the chance of major bleeding rises as the platelet count drops.
White Blood Cell (WBC) Count -
WBCs (leukocytes) help prevent and fight infections in the body. The normal white blood cell count ranges from 4,000 to 11,000 per cubic millimeter in an average healthy adult. High WBC count may indicate that the body is fighting an infection. Low counts may be a result of certain drugs (AZT or ganciclovir), minor viral infections, stress, or opportunistic infections (tuberculosis, histoplasmosis, and other fungal infections). Low counts are cause for concern as the body becomes more susceptible to infection.
I give you credit. Dealing with these two diseases must be a monster!!! So you must be really tough and you are retreating again. Wow! More power to you!!!
Best of luck on your retreatment!!!
Hector
the last 2 weeks i did single shot on the peg due to caution by my dr. over lo platelets.i under stand what you are saying about pre treatment low platelets as a case i have cirrhosis,but during my first treatment in 1/2006 i was stage 2,1a hep c,went und at approximately week 16,tx. was 48 wk. on single dose peg and riba,virus came back.my recent results of a prothrombin time [pt] test which is called the poor mans liver biopsy,and it came back normal,as the platelets went from 56-61.the pt test is usually a sign of cirrhosis.my pre tx labs showes my wbc and rbc as well as platelets to be low,what this means i or my dr. dont know.i am hiv+ as well.i dont know if i should get a liver biopsy now while on tx to see whats going on,as my dr. hasnt mentioned this.any input would be appreciated,or advice as well as i think you are knowledgeable.god bless and enjoy the holiday
I am assuming you have cirrhosis because you had such a low platelet count before treatment?
Actually you have not dropped your platelet count very much. The problem is, you don't have much room to drop. Normally a person platelet count will be at least 150k.
Interferon knocks platelets down. Double dose Peg even more. If you get in the 20ks you will probaly have to stop treatment. There are no "helper drugs" that work for platelets that I know of. Although there may be one coming to market in the next year or so. That will be good news for many of us!!!
If you have cirrhosis your doc should be expecting this. What is his plan? How low will he let you go before cutting peg or stopping treatment all together? Stepping down Peg after reaching UND will not effect your chances of SVR if you can hang on until then. What is your VL now?
Hang in there!
Hector
Actually you have not dropped your platelet count very much. The problem is, you don't have much room to drop. Normally a person platelet count will be at least 150k.
Interferon knocks platelets down. Double dose Peg even more. If you get in the 20ks you will probaly have to stop treatment. There are no "helper drugs" that work for platelets that I know of. Although there may be one coming to market in the next year or so. That will be good news for many of us!!!
If you have cirrhosis your doc should be expecting this. What is his plan? How low will he let you go before cutting peg or stopping treatment all together? Stepping down Peg after reaching UND will not effect your chances of SVR if you can hang on until then. What is your VL now?
Hang in there!
Hector
im taking shot # 7,waiting for dr. to call me as i just took labs includind vl,waiting to see if platelets went up since i did single shot last week.if im und i will stay with single for remainder of 72 weeks,and if platelets still go down,i will have to take less than a full dose which is 180 ug.usually it takes at least 6 weeks to go und. even on double dose.my 1st time tx back in 2006 on single dose peg. and 1200 mg riba,i was at 1000 vl at week 8,and und at around 16.i will let you know my labs and tx. course of action.thanks for the response and god bless
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A list of national and international resources and hotlines to help connect you to needed health and medical services.
Herpes sores blister, then burst, scab and heal.
Herpes spreads by oral, vaginal and anal sex.
STIs are the most common cause of genital sores.
Condoms are the most effective way to prevent HIV and STDs.
PrEP is used by people with high risk to prevent HIV infection.
