Aa
purpose of procrit?
ok, after 3 weeks off tx due to low blood counts, am restarting today at week 1. have weekly neupogen and will take riba 800 instead of 1000. today he was explaining the procrit and i didn't understand it. low H+H can be due to either hemolysis or bone marrow suppression. the procrit will help the bone marrow, but if due to hemolysis, procrit will not help. now hemolytic anemia is listed as a major side effect of the riba, and procrit is pretty standard tx, but if the procrit doesn't work for it.........guess i missed something somewhere. i also don't know how they tell the difference between hemolysis and bone marrow suppression. all this came about after talking about the ins co, they have parameters i must meet before they give me procrit- one of those was that i do a trial period off the meds. maybe this doc wasn't the cause of all my problems after all :))))
any insight into this would be appreciated
and the march continues......
any insight into this would be appreciated
and the march continues......
what is your hgb now? I spaced my Procrit further because it went higher than before tx and I read that high hgb is not good for the body, either. Are you on any other meds,like NSAIDS?
I keep thinking someone may come along with some experience here, but the thread may have gotten stale.
I am not on Procrit, but have had a hemoglobin drop -- I am taking #7 tonight. I have personally been noticing more bruising (of course, I bump into a lot of things going to the bathroom at night too) and wonder if it is not from the anemia or hemoglobin drop.
I know Procrit takes about 4 weeks to take effect. You said you have been on it for 3 weeks. What was your HGB before you started? Perhaps it is the anemia doing this before the Procrit has become effective. I have got to believe it is related somehow, but do not see bruising listed as a sx of Procrit. Here is a link to some PRocrit sx.
http://www.rxlist.com/cgi/generic/epoetin_ad.htm
Kathy
I am not on Procrit, but have had a hemoglobin drop -- I am taking #7 tonight. I have personally been noticing more bruising (of course, I bump into a lot of things going to the bathroom at night too) and wonder if it is not from the anemia or hemoglobin drop.
I know Procrit takes about 4 weeks to take effect. You said you have been on it for 3 weeks. What was your HGB before you started? Perhaps it is the anemia doing this before the Procrit has become effective. I have got to believe it is related somehow, but do not see bruising listed as a sx of Procrit. Here is a link to some PRocrit sx.
http://www.rxlist.com/cgi/generic/epoetin_ad.htm
Kathy
I found the most intersting information that shed a little light on your problem getting Procrit. It seems that most insurance companies will not cover Procrit for Riba anemia...
"You see....if your doctor uses an anemia code.....for a diagnosis of "Hemolytic anemia caused by the Ribavirin", it won't be covered. You need to use an oncology code....remember that interferon is chemo."
So it sounds like this is what your doc needs to do to get the Procrit covered. If he can't do it, perhaps you need to have your bloodwork monitored by a hemotologist, not a Gastro doc.
Kathy
"You see....if your doctor uses an anemia code.....for a diagnosis of "Hemolytic anemia caused by the Ribavirin", it won't be covered. You need to use an oncology code....remember that interferon is chemo."
So it sounds like this is what your doc needs to do to get the Procrit covered. If he can't do it, perhaps you need to have your bloodwork monitored by a hemotologist, not a Gastro doc.
Kathy
Hello all, has anyone had any bruising or discoloration on your body since beginning procrit. I am week 23 and 3 weeks ago, my doctor started me on procrit. Yesterday I noticed what looks like a bruise(purplish/red in color) in the palms of both of my hands. Much more prevalent in my right than my left.
May not be procrit, but didn't have these symptoms until I began taking it.
May not be procrit, but didn't have these symptoms until I began taking it.
I checked with my Dr. today about the Procrit. It can make the muscle aches worse. I noticed it more on the few days after the Procrit and after I've gone through the week as I'm due for another shot, the bone/muscle pain appears to start easing up again and then, it comes back after the Procrit shot. He said that my red blood cells/hemoglobin, etc. is really getting high on the Procrit and that we may have to cut it back a little bit because of the possibility of the pain and blood clots. However, he also increased my Riba this time, so that may balance out the high hemoglobin. I might have to start on Neupogen next visit because my white cells have dropped so much, which will then, make the bone pain worse. It's all a **** shot. We're just a bunch of guinea pigs! I'm not complaining mind you, it's just the way it is. Why do you think that they call it 'practicing medicine?' Because they still haven't gotten it right, which is why that still have to 'practice'. LOL! Tee-Hee Susan
That is crazy. Your doctor is way too conservative and uninformed about hepatitis c treatment. I am glad you are changing doctors. I mean we know the hep c riba anemia is not from bone marrow suppression. It is from the D.... Riba shooting down all the red blood cells. But you MUST stimulate the bone marrow with the Procrit to make more. At this point, the new doc appears to be your only hope. Good luck. Too bad it is still a month away.
Kathy
Kathy
lauren, i have appt with your doc on 10/3. until then, will muddle thru with the old doc.
kathy, NOT on procrit, only riba 800 instead of 1000. doc says he has to determine if low H+H is because of hemolysis or bone marrow suppression. don't know how he tells the difference. once that is determined, he will prescribe procrit if bone marrow suppression only. i do know that once he took me off the meds ,it took 3 weeks for counts to come back up to an acceptable level, and that was nowhere near where they started from.
i was pretty smug about all this in the beginning...having a medical background and all. figured everything would make sense, tx would go smoothly, i'd understand everything that was happening. how quickly we can be humbled!! :)
kathy, NOT on procrit, only riba 800 instead of 1000. doc says he has to determine if low H+H is because of hemolysis or bone marrow suppression. don't know how he tells the difference. once that is determined, he will prescribe procrit if bone marrow suppression only. i do know that once he took me off the meds ,it took 3 weeks for counts to come back up to an acceptable level, and that was nowhere near where they started from.
i was pretty smug about all this in the beginning...having a medical background and all. figured everything would make sense, tx would go smoothly, i'd understand everything that was happening. how quickly we can be humbled!! :)
I tried my best to reproduce the text, but I couldn't do the registered trademark symbol or superscript or subscript text; I "spelled out" Greek letters and so on.
There is bracketed information [like this] that was part of the text and those occurrances are not my comments. What is in the text is my best effort to reproduce accurately a hard-copy report I have (thanks again Helen!).
The hard-copy has "Dated Material - Revised 8/2000" on each page.
So, after finishing all this cover-my-butt stuff, here is the information:
===================================================
PROCRIT(r) (epoetin alfa)
Use in Patients with Hepatitis C
Several studies discussed the use of PROCRIT(r) (epoetin alfa) or recombinant human erythropoietin (r-HuEPO) in patients with hepatitis C (HCV) infection. The majority of these reports were conducted in HCV-infected patients with anemia due to interferon alfa/ribavirin therapy (Bizollon et al. 1997; Brinkley-Laughton et al. 1999; Dieterich et al. 1999a; Weisz et al. 1998a). The other settings included HCV-infected patients with iron overload (de la Serna et
al. 1999; Kohan et al. 1996), orthotopic liver transplantation (OLT) (Detry et al. 1999), nephrotic syndrome (Bayes et al. 1998), and paroxysmal nocturnal hemoglobinuria (Ikeda et al. 1993).
Use with Interferon Alfa/Ribavirin
Dietrich et al. (1999a) evaluated the efficacy of interferon alfa with ribavirin for patients coinfected with HIV and HCV. Of the 21 patients studied, 11 received combination therapy with interferon alfa (3 x 10^6 U thrice weekly
[TIW]) and ribavirin (1,000-1,200 mg/day), whereas ten started therapy with interferon alfa for three months, followed by combination therapy. Nineteen of the 21 patients were receiving highly-active antiretroviral therapy (HAART) with either zidovudine or stavudine. During the six-month evaluation, both groups experienced decreases in HCV RNA, CD4+ count, and HIV RNA values. In terms of adverse events, 23.8% (n = 5) experienced anemia; treatment with
r-HuEPO (40,000 U once weekly [QW] increased hemoglobin (Hb) values (from 10 g/dL at baseline to 12.7 g/dL) after a median of four weeks. A total of five patients discontinued therapy (one for anemia; four for constitutional symptoms). In conclusion, the authors found that interferon alfa/ribavirin therapy successfully treated HIV/HCV-coinfected patients. Further, ribavirin-induced anemia was successfully treated with r-HuEPO. In addition to this abstract, a post of this information was presented at the 39th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) (Weisz et al. 1999a).
At the 50th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD), Dieterich et al. (1999b) presented 12-month follow-up data on the previous study. At that point, three more patients were available for evaluation; all three of these subjects received initial combination therapy with interferon alfa/ribavirin. While the overall incidence of anemia decreased to 20.8%, the total number of patients experiencing anemia did not change (n = 5/24). In addition, a poster of these data was also presented at AASLD (Weisz et al. 1999b).
Weisz et al. (1998a) evaluated the efficacy of r-HuEPO for treatment of anemia associated with interferon alfa/ribairin therapy in HCV-infected, HIV-negative patients. During a one-year period, 16 of 46 (35%) patients receiving interferon alfa (3 x 10^6 U subcutaneously [SC] TIW) with ribavirin (1,000-1,200 mg/day) experienced new onset anemia. Of the 16 anemic patients, 12 (75%) had a decrease in Hb of 1-3 g/dL (median 10.9 g/dL) and two (12.5%) had a Hb decrease of > 3 g/dL (median 8.5 g/dL). At baseline, the mean Hb was 14.1 g/dL compared with the mean nadir of 10.0 g/dL at week 8. Dyspnea occurred in 19% (n = 3) of patients, fatigue in 25% (n = 4), and both dyspnea and fatigue in 56% (n = 9). Initially, 10 of the 16 (63%) anemic patients experienced increased Hb levels (mean 11.6 g/dL) when ribavirin was decreased to 800 mg/day, but symptoms did not resolve until r-HuEPO 30,000-40,000 U SC QW was started. at week 12, 14 patients (88%) reported symptom relief within a median of ten days after starting r-HuEPO. The authors concluded that r-HuEPO may be effective for treatment of anemia associated with interferon alfa/ribavirin therapy in HCV-infected, HIV-negative patients. In addition, a poster of these data was also presented at the 38th ICAAC (Weisz et al. 1998b).
Bizollon et al. (1997) conducted an open-label, pilot study to determine the efficacy of interferon alfa-2b/ribavirin therapy in patients with recurring HCV after OLT. For six months, patients received interferon alfa-2b (3 x 10^6 SC TIW) with ribavirin (400 mg TID). Subsequently, patients received an additional six months of ribavirin monotherapy (1,200 mg/day). If patients experienced significant anemia (Hb < 10 g/dL) with hemolysis (reticulocytosis and reduced haptoglobins), the ribavirin dose was decreased to 200 mg/day until the Hb value was greater that 10 g/dL. For those who were unable to tolerate ribavirin due to anemia, treatement with r-HuEPO 3,000 U SC TIW was initiated. After six months of therapy, 48% (n = 10) of the 21 evaluable patients had undetectable HCV RNA levels. After 12 months of therapy, there was a statistically significant improvement in alanine aminotransferase (ALT) levels (p = 0.003) and histology activity index score (p = 0.0013). Shortly after initiation of therapy, hemolysis occurred in all patients as evidenced by a statistically significant (p < 0.05) decrease in Hb values (10.4 +/- 0.4 g/dL at 12 months compared with 12.4 +/- 1.2 g/dL at baseline). While none of the 21 patients required a reduction in dose, three patients with impaired renal function (S sub Cr > 1.6 mg/dL/150 microL/L) experienced symptomatic anemia, which subsequently resolved upon cessation of ribavirin therapy. Treatment with r-HuEPO in these three patients permitted successful retreatment with ribavirin for 12 months. Based on this pilot study, the authors concluded that concomitant use of interferon alfa and ribavirin was safe and effective for recurrent HCV infection in OLT patients.
Brinkley-Laughton et al. (1999) prospectively compared the safety and antiviral efficacy of interferon monotherapy (n = 11) with interferon/ribavirin combination therapy (n = 16) in HIV/HCV co-infected patients. Patients who received interferon/ribavirin combination therapy had significant improvement in early virologic response (p = 0.04) and mean HCV viral load (p = 0.02) compared with the interferon monotherapy group. In terms of side effects, six patients on interferon/ribavirin therapy required r-HuEPO therapy (dose not provided) for anemia. The authors concluded that interferon/ribavirin therapy had enhanced activity against HCV compared to interferon alone for HIV-infected patients.
Iron Overload
In a case report, de la Serna et al. (1999) described the use of iron depletion techniques to prevent veno-occlusive disease prior to hematopoietic stem cell transplantation (HSCT). The patient was a 26-year-old woman with a history of acute promyelocytic leukemia (APL), multiple blood transfusions, and chronic liver disease (secondary to HCV and severe iron overload). Upon the patient's third remission of APL, HSCT was delayed due to liver dysfunction and iron overload. Regular phlebotomies (450 mL) were enhanced with r-HuEPO (2,000 U [25 U/kg] SC TIW) to maintain Hb > 10.5 g/dL. After nine months of r-HuEPO treatment, the patient successfully completed 34 phlebotomies. One month later, the patient underwent HSCT without any liver toxicity during post-transplant follow up. The authors felt this case demonstrated that the use of r-HuEPO with phlebotomies could deplete iron stores to minimize organ dysfunction.
Kohan et al. (1996) evaluated the efficacy and tolerance of large volume erythropheresis (LVE) plus r-HuEPO for patients with iron overload. Of the 15 patients studied, six had chronic hepatitis C, while the others had hereditary esferocytosis or thalassemia. All patients underwent LVE while receiving r-HuEPO (100 U/kg/wk SC) and folic acid (10 mg/day). For patients with hepatitis C, LVE procedures were needed 3.6 times (range 2-5) per 30-day perod (range 25-45 days) resulting in significant decreases in iron (from 170 g/dL to 56 g/dL; p < 0.0104), transferrin saturation (from 60% to 17%; p < 0.02), and ferritin levels (from 559 micrograms/mL to 27.8 micrograms/mL; p < 0.0033). The authors concluded that LVE with r-HuEPO was an efficient way to normalize lab values (< 3 months) in 80% of all patients with iron overload.
Orthotopic Liver Transplantation
Detry et al. (1999) reported on a male Jehovah's witness (JW), with a history of cirrhosis due to HCV, who required an OLT secondary to hepatic cancer. Since the patient's religious beliefs prohibited the use of blood products, preoperative packed-cell volume was enhanced with r-HuEPO and oral iron (doses not provided). Prior to surgery, the patient experienced thrombocytopenia (platelets - 15 x 10^9/L) from hypersplenism due to portal hypertension. The use of gelfoam pledgets and microcoils helped to achieve subtotal arterial splenic embolization. Upon correction of thrombocytopenia, the patient underwent OLT with the use of continuous cell saver an aprotinin; intraoperative blood loss was approximately < 500 mL. Postoperatively, initial immunosuppression included tacrolimus and steroids; however, biopsy-proven acute rejection on day 14 required treatment with intravenous steroid boluses. Eleven days later, the patient was discharged. The authors found that appropriate preoperative preparation and surgical techniques may permit successful OLT in JW patients.
Nephrotic Syndrome
Bayes et al. (1998) described two case reports of patients with severe anemia due to nephrotic syndrome who were successfully treated with r-HuEPO; one of these patients had a history of hepatitis C. This 67-year-old woman presented with anemia (Hb < 7.8 g/dL), mildly decreased renal function (S sub Cr = 148 micromol/L), and proteinuria (24-h collection = 10.5 g). After four weeks of treatment with r-HuEPO (4,000 U TIW), both anemia (Hb - 10.9 g/dL) and proteinuria (24-h collection = 8.3 g) improved. The authors concluded that anemia due to nephrotic syndrome may respond to treatment with r-HuEPO.
Paroxysmal Nocturnal Hemoglobinuria
In a Japanese article with an English abstract, Ikeda et al. (1993) discussed the use of r-HuEPO to treat anemia in a patient with paroxysmal nocturnal hemoglobinuria. Initially, the patient's hemolytic anemia with hemosiderinuria was unsuccessfully treated with oral iron and oxymetholone. However, after treatment with r-HuEPO (3,000 U/day SC), Hb values increased from 7.5 g/dL to 12.0 g/dL in four weeks and general fatigue subsided. Since the patient also had chronic hepatitis C, interferon alfa was given concomitantly and Hb values between 10-11 g/dL were maintained. The authors suggested that r-HuEPO may be useful for hemolytic anemia.
References
Bayes B, Serra A, Junca J, Lauzurica R. Successful treatment of anaemia of nephrotic syndrome with recombinant human erythropoietin [letter]. Nephrol Dial Transplant 1998;13:1894-5.
Bizollon T, Pallazzo U, Ducerf C, et al. Pilot study of the combination of interferon alfa and ribavirin as therapy of recurrent hepatitis C after liver transplantation. Hepatology 1997;26:500-4.
Brinkley-Laughton SC, Dieterich DT, Weisz KB, et al. Interferon (IFN) or interferon plus ribavirin (RBV) for the treatment of hepatitis C virus (HCV) infection among HIV-infected persons [abstract]. Proceedings of the 37th Annual Meeting of the Infectious Disease Society of America; 1999 Nov 18-21; Philadelphia, Pennsylvania.
de La Serna J, Bornstein R, Garcia-Bueno MJ, Lahuerta-Palacios JJ. Iron depletion by phlebotomy with recombinant erythropoietin prior to allogeneic transplantation to prevent liver toxicity. Bone Marrow Transplant 1999;23:95-7.
Detry O, Honore P, Delwaide J, et al. Liver transplantation in a Jehovah's Witness [letter]. Lancet 1999;353(9165):1680.
Dieterich D, Weisz K, Goldman D, et al. Interferon (IFN) and ribavirin (RBV) therapy for hepatitis C (HCV) in HIV-coinfected patients [abstract]. Proceedings of the 39th Interscience Conference on Antimicrobial Agents and Chemotherapy; 1999a Sep 26-29; San Francisco, California.
Dieterich DT, Weisz KB, Goldman DJ, Malicdem ML. Combination treatment with Interferon (IFN) and ribavirin (RBV) for hepatitis C (HCV) in HIV co-infection patients [abstract]. Hepatology 1999b;30(4 Pt 2):266A.
Ikeda Y, Yoshinaga K, Iki S, et al. Improvement of anemia by recombinant human erythropoietin in paroxysmal nocturnal hemoglobinuria [in Japanese]. Rinsho Ketsueki 1993;34(9):1022-6.
Kohan A, Niborski R, Daruich J, et al. Large volume erythropheresis (LVE) with recombinant erythropoyetin [sic] (Epo) as alternative treatment for iron overload [abstract]. Blood 1996;88(10 Suppl 1 Pt 2):12b.
Weisz KB, Braun JF, Dieterich DT, et al. Erythropoietin use for ribavirin/interferon-induced anemia in hepatitis C patients [abstract]. Proceedings of the 38th Interscience Conference on Antimicrobial Agents and Chemotherapy; 1998a Sep 24-27;San Diego, California.
Weisz K, Hau T, Kreiswirth S, et al. Erythropoietin use for ribavirin/interferon induced anemia in patients with hepatitis C. Poster presented at: Interscience Conference on Antimicrobial Agents and Chemotherapy; September 24-27 1998b; San Diego, California.
Weisz K, Goldman D, Talal A, et al. Interferon-alpha (IFN-alpha) and ribavirin (RBV) therapy for hepatitis C (HCV) in HIV co-infected patients. Poster presented at: Interscience Conference on Antimicrobial Agents and Chemotherapy; September 26, 1999a; San Francisco, California.
Weisz K, Goldman D, Talal A, et al. Combination treatment with interferon-alpha and ribavirin for hepatitis C in HIV co-infected patients: 12-month follow-up. Poster presented at: American Association for the Study of Liver Diseases; November 5-9, 1999b; Dallas, Texas.
There is bracketed information [like this] that was part of the text and those occurrances are not my comments. What is in the text is my best effort to reproduce accurately a hard-copy report I have (thanks again Helen!).
The hard-copy has "Dated Material - Revised 8/2000" on each page.
So, after finishing all this cover-my-butt stuff, here is the information:
===================================================
PROCRIT(r) (epoetin alfa)
Use in Patients with Hepatitis C
Several studies discussed the use of PROCRIT(r) (epoetin alfa) or recombinant human erythropoietin (r-HuEPO) in patients with hepatitis C (HCV) infection. The majority of these reports were conducted in HCV-infected patients with anemia due to interferon alfa/ribavirin therapy (Bizollon et al. 1997; Brinkley-Laughton et al. 1999; Dieterich et al. 1999a; Weisz et al. 1998a). The other settings included HCV-infected patients with iron overload (de la Serna et
al. 1999; Kohan et al. 1996), orthotopic liver transplantation (OLT) (Detry et al. 1999), nephrotic syndrome (Bayes et al. 1998), and paroxysmal nocturnal hemoglobinuria (Ikeda et al. 1993).
Use with Interferon Alfa/Ribavirin
Dietrich et al. (1999a) evaluated the efficacy of interferon alfa with ribavirin for patients coinfected with HIV and HCV. Of the 21 patients studied, 11 received combination therapy with interferon alfa (3 x 10^6 U thrice weekly
[TIW]) and ribavirin (1,000-1,200 mg/day), whereas ten started therapy with interferon alfa for three months, followed by combination therapy. Nineteen of the 21 patients were receiving highly-active antiretroviral therapy (HAART) with either zidovudine or stavudine. During the six-month evaluation, both groups experienced decreases in HCV RNA, CD4+ count, and HIV RNA values. In terms of adverse events, 23.8% (n = 5) experienced anemia; treatment with
r-HuEPO (40,000 U once weekly [QW] increased hemoglobin (Hb) values (from 10 g/dL at baseline to 12.7 g/dL) after a median of four weeks. A total of five patients discontinued therapy (one for anemia; four for constitutional symptoms). In conclusion, the authors found that interferon alfa/ribavirin therapy successfully treated HIV/HCV-coinfected patients. Further, ribavirin-induced anemia was successfully treated with r-HuEPO. In addition to this abstract, a post of this information was presented at the 39th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) (Weisz et al. 1999a).
At the 50th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD), Dieterich et al. (1999b) presented 12-month follow-up data on the previous study. At that point, three more patients were available for evaluation; all three of these subjects received initial combination therapy with interferon alfa/ribavirin. While the overall incidence of anemia decreased to 20.8%, the total number of patients experiencing anemia did not change (n = 5/24). In addition, a poster of these data was also presented at AASLD (Weisz et al. 1999b).
Weisz et al. (1998a) evaluated the efficacy of r-HuEPO for treatment of anemia associated with interferon alfa/ribairin therapy in HCV-infected, HIV-negative patients. During a one-year period, 16 of 46 (35%) patients receiving interferon alfa (3 x 10^6 U subcutaneously [SC] TIW) with ribavirin (1,000-1,200 mg/day) experienced new onset anemia. Of the 16 anemic patients, 12 (75%) had a decrease in Hb of 1-3 g/dL (median 10.9 g/dL) and two (12.5%) had a Hb decrease of > 3 g/dL (median 8.5 g/dL). At baseline, the mean Hb was 14.1 g/dL compared with the mean nadir of 10.0 g/dL at week 8. Dyspnea occurred in 19% (n = 3) of patients, fatigue in 25% (n = 4), and both dyspnea and fatigue in 56% (n = 9). Initially, 10 of the 16 (63%) anemic patients experienced increased Hb levels (mean 11.6 g/dL) when ribavirin was decreased to 800 mg/day, but symptoms did not resolve until r-HuEPO 30,000-40,000 U SC QW was started. at week 12, 14 patients (88%) reported symptom relief within a median of ten days after starting r-HuEPO. The authors concluded that r-HuEPO may be effective for treatment of anemia associated with interferon alfa/ribavirin therapy in HCV-infected, HIV-negative patients. In addition, a poster of these data was also presented at the 38th ICAAC (Weisz et al. 1998b).
Bizollon et al. (1997) conducted an open-label, pilot study to determine the efficacy of interferon alfa-2b/ribavirin therapy in patients with recurring HCV after OLT. For six months, patients received interferon alfa-2b (3 x 10^6 SC TIW) with ribavirin (400 mg TID). Subsequently, patients received an additional six months of ribavirin monotherapy (1,200 mg/day). If patients experienced significant anemia (Hb < 10 g/dL) with hemolysis (reticulocytosis and reduced haptoglobins), the ribavirin dose was decreased to 200 mg/day until the Hb value was greater that 10 g/dL. For those who were unable to tolerate ribavirin due to anemia, treatement with r-HuEPO 3,000 U SC TIW was initiated. After six months of therapy, 48% (n = 10) of the 21 evaluable patients had undetectable HCV RNA levels. After 12 months of therapy, there was a statistically significant improvement in alanine aminotransferase (ALT) levels (p = 0.003) and histology activity index score (p = 0.0013). Shortly after initiation of therapy, hemolysis occurred in all patients as evidenced by a statistically significant (p < 0.05) decrease in Hb values (10.4 +/- 0.4 g/dL at 12 months compared with 12.4 +/- 1.2 g/dL at baseline). While none of the 21 patients required a reduction in dose, three patients with impaired renal function (S sub Cr > 1.6 mg/dL/150 microL/L) experienced symptomatic anemia, which subsequently resolved upon cessation of ribavirin therapy. Treatment with r-HuEPO in these three patients permitted successful retreatment with ribavirin for 12 months. Based on this pilot study, the authors concluded that concomitant use of interferon alfa and ribavirin was safe and effective for recurrent HCV infection in OLT patients.
Brinkley-Laughton et al. (1999) prospectively compared the safety and antiviral efficacy of interferon monotherapy (n = 11) with interferon/ribavirin combination therapy (n = 16) in HIV/HCV co-infected patients. Patients who received interferon/ribavirin combination therapy had significant improvement in early virologic response (p = 0.04) and mean HCV viral load (p = 0.02) compared with the interferon monotherapy group. In terms of side effects, six patients on interferon/ribavirin therapy required r-HuEPO therapy (dose not provided) for anemia. The authors concluded that interferon/ribavirin therapy had enhanced activity against HCV compared to interferon alone for HIV-infected patients.
Iron Overload
In a case report, de la Serna et al. (1999) described the use of iron depletion techniques to prevent veno-occlusive disease prior to hematopoietic stem cell transplantation (HSCT). The patient was a 26-year-old woman with a history of acute promyelocytic leukemia (APL), multiple blood transfusions, and chronic liver disease (secondary to HCV and severe iron overload). Upon the patient's third remission of APL, HSCT was delayed due to liver dysfunction and iron overload. Regular phlebotomies (450 mL) were enhanced with r-HuEPO (2,000 U [25 U/kg] SC TIW) to maintain Hb > 10.5 g/dL. After nine months of r-HuEPO treatment, the patient successfully completed 34 phlebotomies. One month later, the patient underwent HSCT without any liver toxicity during post-transplant follow up. The authors felt this case demonstrated that the use of r-HuEPO with phlebotomies could deplete iron stores to minimize organ dysfunction.
Kohan et al. (1996) evaluated the efficacy and tolerance of large volume erythropheresis (LVE) plus r-HuEPO for patients with iron overload. Of the 15 patients studied, six had chronic hepatitis C, while the others had hereditary esferocytosis or thalassemia. All patients underwent LVE while receiving r-HuEPO (100 U/kg/wk SC) and folic acid (10 mg/day). For patients with hepatitis C, LVE procedures were needed 3.6 times (range 2-5) per 30-day perod (range 25-45 days) resulting in significant decreases in iron (from 170 g/dL to 56 g/dL; p < 0.0104), transferrin saturation (from 60% to 17%; p < 0.02), and ferritin levels (from 559 micrograms/mL to 27.8 micrograms/mL; p < 0.0033). The authors concluded that LVE with r-HuEPO was an efficient way to normalize lab values (< 3 months) in 80% of all patients with iron overload.
Orthotopic Liver Transplantation
Detry et al. (1999) reported on a male Jehovah's witness (JW), with a history of cirrhosis due to HCV, who required an OLT secondary to hepatic cancer. Since the patient's religious beliefs prohibited the use of blood products, preoperative packed-cell volume was enhanced with r-HuEPO and oral iron (doses not provided). Prior to surgery, the patient experienced thrombocytopenia (platelets - 15 x 10^9/L) from hypersplenism due to portal hypertension. The use of gelfoam pledgets and microcoils helped to achieve subtotal arterial splenic embolization. Upon correction of thrombocytopenia, the patient underwent OLT with the use of continuous cell saver an aprotinin; intraoperative blood loss was approximately < 500 mL. Postoperatively, initial immunosuppression included tacrolimus and steroids; however, biopsy-proven acute rejection on day 14 required treatment with intravenous steroid boluses. Eleven days later, the patient was discharged. The authors found that appropriate preoperative preparation and surgical techniques may permit successful OLT in JW patients.
Nephrotic Syndrome
Bayes et al. (1998) described two case reports of patients with severe anemia due to nephrotic syndrome who were successfully treated with r-HuEPO; one of these patients had a history of hepatitis C. This 67-year-old woman presented with anemia (Hb < 7.8 g/dL), mildly decreased renal function (S sub Cr = 148 micromol/L), and proteinuria (24-h collection = 10.5 g). After four weeks of treatment with r-HuEPO (4,000 U TIW), both anemia (Hb - 10.9 g/dL) and proteinuria (24-h collection = 8.3 g) improved. The authors concluded that anemia due to nephrotic syndrome may respond to treatment with r-HuEPO.
Paroxysmal Nocturnal Hemoglobinuria
In a Japanese article with an English abstract, Ikeda et al. (1993) discussed the use of r-HuEPO to treat anemia in a patient with paroxysmal nocturnal hemoglobinuria. Initially, the patient's hemolytic anemia with hemosiderinuria was unsuccessfully treated with oral iron and oxymetholone. However, after treatment with r-HuEPO (3,000 U/day SC), Hb values increased from 7.5 g/dL to 12.0 g/dL in four weeks and general fatigue subsided. Since the patient also had chronic hepatitis C, interferon alfa was given concomitantly and Hb values between 10-11 g/dL were maintained. The authors suggested that r-HuEPO may be useful for hemolytic anemia.
References
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Bizollon T, Pallazzo U, Ducerf C, et al. Pilot study of the combination of interferon alfa and ribavirin as therapy of recurrent hepatitis C after liver transplantation. Hepatology 1997;26:500-4.
Brinkley-Laughton SC, Dieterich DT, Weisz KB, et al. Interferon (IFN) or interferon plus ribavirin (RBV) for the treatment of hepatitis C virus (HCV) infection among HIV-infected persons [abstract]. Proceedings of the 37th Annual Meeting of the Infectious Disease Society of America; 1999 Nov 18-21; Philadelphia, Pennsylvania.
de La Serna J, Bornstein R, Garcia-Bueno MJ, Lahuerta-Palacios JJ. Iron depletion by phlebotomy with recombinant erythropoietin prior to allogeneic transplantation to prevent liver toxicity. Bone Marrow Transplant 1999;23:95-7.
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Dieterich D, Weisz K, Goldman D, et al. Interferon (IFN) and ribavirin (RBV) therapy for hepatitis C (HCV) in HIV-coinfected patients [abstract]. Proceedings of the 39th Interscience Conference on Antimicrobial Agents and Chemotherapy; 1999a Sep 26-29; San Francisco, California.
Dieterich DT, Weisz KB, Goldman DJ, Malicdem ML. Combination treatment with Interferon (IFN) and ribavirin (RBV) for hepatitis C (HCV) in HIV co-infection patients [abstract]. Hepatology 1999b;30(4 Pt 2):266A.
Ikeda Y, Yoshinaga K, Iki S, et al. Improvement of anemia by recombinant human erythropoietin in paroxysmal nocturnal hemoglobinuria [in Japanese]. Rinsho Ketsueki 1993;34(9):1022-6.
Kohan A, Niborski R, Daruich J, et al. Large volume erythropheresis (LVE) with recombinant erythropoyetin [sic] (Epo) as alternative treatment for iron overload [abstract]. Blood 1996;88(10 Suppl 1 Pt 2):12b.
Weisz KB, Braun JF, Dieterich DT, et al. Erythropoietin use for ribavirin/interferon-induced anemia in hepatitis C patients [abstract]. Proceedings of the 38th Interscience Conference on Antimicrobial Agents and Chemotherapy; 1998a Sep 24-27;San Diego, California.
Weisz K, Hau T, Kreiswirth S, et al. Erythropoietin use for ribavirin/interferon induced anemia in patients with hepatitis C. Poster presented at: Interscience Conference on Antimicrobial Agents and Chemotherapy; September 24-27 1998b; San Diego, California.
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Weisz K, Goldman D, Talal A, et al. Combination treatment with interferon-alpha and ribavirin for hepatitis C in HIV co-infected patients: 12-month follow-up. Poster presented at: American Association for the Study of Liver Diseases; November 5-9, 1999b; Dallas, Texas.
NY - I think the definition of hemolysis is the destruction of RBCs. From the ribivirin we have "extrinsic" hemolytic anemia. So, I don't think that it matters that we don't have "bone marrow suppression." All that matters is that we give that bone marrow something to stimulate the grown of RBC so that it can make them faster than the ribivirin can kill them.. (what a battle)
This is coped from a website on hemolytic anemia --
"Hemolytic Anemia
What is hemolytic anemia?
Hemolytic anemia is a disorder in which the red blood cells are destroyed faster than the bone marrow can produce them. The term for destruction of red blood cells is hemolysis. There are two types of hemolytic anemia, including the following:
This is coped from a website on hemolytic anemia --
"Hemolytic Anemia
What is hemolytic anemia?
Hemolytic anemia is a disorder in which the red blood cells are destroyed faster than the bone marrow can produce them. The term for destruction of red blood cells is hemolysis. There are two types of hemolytic anemia, including the following:
my point exactly....procrit stimulates the bone marrow to produce more red blood cells. so even if H+H is low because of hemolysis, procrit should be beneficial. will take that thought with me to next dr visit :)
Hi Lorrie,
I was just thinking about you last night, wondering how you are doing. I'm glad you are able to make another go of it. Maybe if the docs are on top of the anemia thing from the get-go, it will be easier on you. Have you stayed with your first dr or did you switch?
Lauren
I was just thinking about you last night, wondering how you are doing. I'm glad you are able to make another go of it. Maybe if the docs are on top of the anemia thing from the get-go, it will be easier on you. Have you stayed with your first dr or did you switch?
Lauren
ny - you set me into research mode. All I can find on the internet indicates that Procrit does help for hepatitis c riba induced hemolytic anemia. Normally the life span of the red blood cell is about 120 days. In hemolytic anemia, red blood cells are destroyed faster that new ones can be made. One interesting note is that ribavirin-induced hemolytic anemia cannot be treated by eating iron rich foods or taking iron supplements.
susan400 -- I thought it was the Neupogen that could make your bones ache--that's what my hemotologist said. Are you taking that too? Still, if you are very sensitive I would think the Procrit might make your bones ache. It does, after all, encourage the bone marrow to make new RBC.
Kathy
susan400 -- I thought it was the Neupogen that could make your bones ache--that's what my hemotologist said. Are you taking that too? Still, if you are very sensitive I would think the Procrit might make your bones ache. It does, after all, encourage the bone marrow to make new RBC.
Kathy
I've been taking Procrit for 34 yrs now and have never noticed anything like your symtoms. For me it has been real lifesaver. Good Luck Linda
My NP told me "bone pain" is a common sympton of Procrit but I never had it. Not sure if that matches your symptons.
-- Jim
-- Jim
Sorry to cut in here, but all the threads are used up.
This is the first time that I've ever done treatment with the Procrit. For some reason, this time around, I'm having a lot more pain in my legs. It's really annoying. I don't know if it's the Procrit causing it or not. I exercise and where TED stocking at night, so I don't think it's blood clotting issues. I'm definitely going to bring it up with my doctor when I see him on Wed. I don't want to have to stop the Procrit because I want to stay on the higher dosing of Riba. I basically just want some reassurance that this is normal.
Well, that's the question.
Susan
This is the first time that I've ever done treatment with the Procrit. For some reason, this time around, I'm having a lot more pain in my legs. It's really annoying. I don't know if it's the Procrit causing it or not. I exercise and where TED stocking at night, so I don't think it's blood clotting issues. I'm definitely going to bring it up with my doctor when I see him on Wed. I don't want to have to stop the Procrit because I want to stay on the higher dosing of Riba. I basically just want some reassurance that this is normal.
Well, that's the question.
Susan
Yes, Procrit works for hemolytic anemia, which is a common side effect of riba. What your doctor says may be technically correct but not very relevant to hep c treatment. There's "hemolysis" and there's ribavirin induced hemolytic anemica. Big difference. Procrit has made a big difference in my treatment. Take it, you'll like it. :)
Sunspot, mine fell to 9.7 which made me feel pretty run down but it was a severe rash problem which prompted my doctor to switch me from 1000 mg of riba to 800. She was prepared to let my hemoglobin fall more. My hemoglobin climbed though after that switch and I felt better. Fortunately, I was a geno 2 and the 800 was good enough for that anyways.
Sorry I don't have a comment for you on your post but I want to thank you for that term "hemolytic anemia". I'm setting up a visit to a blood doc due to my Hgb being at 9.6, my baseline was 16.0
Procrit definitely works, and there is some evidence that it improves SVR significantly especially for type 1's
See this link
http://www.hivandhepatitis.com/2005icr/ddw2005/docs/hcv_052305_c.html
This site, along with Janis' site is one of the best sources of info, research findings and reviews:
http://www.hivandhepatitis.com/hep_c.html
Here's a review about Milk Thistle which I know many people are interested in:
http://www.hivandhepatitis.com/hep_c/news/2005/ad/062905_b.html
Tim
See this link
http://www.hivandhepatitis.com/2005icr/ddw2005/docs/hcv_052305_c.html
This site, along with Janis' site is one of the best sources of info, research findings and reviews:
http://www.hivandhepatitis.com/hep_c.html
Here's a review about Milk Thistle which I know many people are interested in:
http://www.hivandhepatitis.com/hep_c/news/2005/ad/062905_b.html
Tim
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