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Haptoglobin High-Apolipoprotein low
Just got new results from yet another Fibrosure Test:F3-F4 for fibrosis and cirrhosis and two new scores I never heard of; Haptaglobin 600 H and Apoloprotein 24 low-Of course it is friday and my Hepatologist is not available.
Does anyone know what this means. I searched web MD and couldn't find much. Thanks Frank
Does anyone know what this means. I searched web MD and couldn't find much. Thanks Frank
From; Quantitative Tests of Liver Function (QTFT) Measure Hepatic Improvement After Sustained Virological Response: Results from the HALT-C Trial
See: http://www.medscape.com/viewarticle/707042
"...Impaired hepatic function and portal hypertension account for the
major manifestations and clinical complications of liver disease.
Because our battery of QLFTs measured both hepatic metabolism and the
portal circulation, we reasoned that these QLFTs could be useful
surrogates to identify clinically relevant beneficial effects of SVR.
Indeed, we found that SVR was associated with improvements in hepatic
metabolism, portal blood flow and portal-systemic shunt. These
physiological improvements after SVR would, at least theoretically,
reduce risk for clinical decompensation or complications. Absence of
clinical complications in the long-term follow-up of patients with
advanced fibrosis or cirrhosis after SVR supports this interpretation.
[23]
Sustained virological response improved the clearance or metabolism of
caffeine, antipyrine and lidocaine-MEGX by 9-38% without affecting
liver volume. Caffeine is metabolized by an array of hepatic
microsomal cytochrome P450 (CYP) enzymes (1A1, 1A2, 2A6, 2E1, 3A),[32]
antipyrine by CYP 1A2, 2B6, 2C8, 3C9 and 2C18[33] and lidocaine-MEGX
primarily by CYP 3A4.[33,34] Ocker et al.[35] used a different battery
of QLFTs (aminopyrine breath test, galactose elimination capacity,
sorbitol clearance and indocyanine green clearance) to study 50
patients with chronic hepatitis C at baseline and 3 months after
initiation of interferon-based therapy. They observed improvement in
hepatic metabolism in the patients who were HCV RNA negative. We
interpret these results to indicate that HCV or inflammation and
fibrosis related to HCV interfere with the hepatic metabolism of a
wide range of drugs, medications and xenobiotics and that these
effects are reversible with effective therapy.
Sustained virological response improves portal blood flow and perfused
hepatic mass, as measured by cholate Cl oral and SPECT-LSS and reduces
portal-systemic shunting, as measured by cholate shunt. Reduction in
hepatic inflammation and fibrosis after SVR may lower hepatic
resistance to portal inflow, reduce portal pressure and diminish
portal-systemic shunt. This interpretation is further supported by our
observation of a 12% increase in platelet count and the study by
Rincon et al.,[36] which demonstrated a 26% reduction in hepatic
venous pressure gradient in a subset of patients who achieved SVR. We
observed 32% increase in cholate Cl oral and 25% decrease in cholate
shunt. Globally, these results suggest that SVR reverses portal
hypertension, improves portal inflow and diminishes portal-systemic
shunting. ..."
Regarding Haptoglobin: I had this test along with a reticulocyte test to assess hemolytic anemia. I am not sure this is related but I know that an order for a haptoglobin test is frequently ordered with a reticulocyte count. I believe that as haptoglobin decreases the reticulocyte increases.
I found this at Wikipedia. http://en.wikipedia.org/wiki/Haptoglobin
"...A decrease in haptoglobin can support a diagnosis of hemolytic anemia, especially when correlated with a decreased RBC count, Hemoglobin, and Hematocrit, and also an increased reticulocyte count.
If the reticulocyte count is increased, but the haptoglobin level is normal, this may indicate that cellular destruction is occurring in the spleen and liver, which may indicate a drug-induced hemolysis, or a red cell dysplasia. The spleen and liver recognize an error in the red cells (either Drug coating the red cell membrane or a dysfunctional red cell membrane), and destroy the cell. This type of destruction does not release hemoglobin into the peripheral blood, so the haptoglobin cannot bind to it. Thus, the haptoglobin will stay normal.
If there are symptoms of anemia but both the reticulocyte count and the haptoglobin level are normal, the anemia is most likely not due to hemolysis, but instead some other error in cellular production, such as aplastic anemia
Haptoglobin levels that are decreased but do not accompany signs of anemia may indicate liver damage, as the liver is not producing enough haptoglobin to begin with.
As haptoglobin is indeed an acute-phase protein, any inflammatory process (infection, extreme stress, burns, major crush injury, allergy, etc.) may increase the levels of plasma haptoglobin..."
See: http://www.medscape.com/viewarticle/707042
"...Impaired hepatic function and portal hypertension account for the
major manifestations and clinical complications of liver disease.
Because our battery of QLFTs measured both hepatic metabolism and the
portal circulation, we reasoned that these QLFTs could be useful
surrogates to identify clinically relevant beneficial effects of SVR.
Indeed, we found that SVR was associated with improvements in hepatic
metabolism, portal blood flow and portal-systemic shunt. These
physiological improvements after SVR would, at least theoretically,
reduce risk for clinical decompensation or complications. Absence of
clinical complications in the long-term follow-up of patients with
advanced fibrosis or cirrhosis after SVR supports this interpretation.
[23]
Sustained virological response improved the clearance or metabolism of
caffeine, antipyrine and lidocaine-MEGX by 9-38% without affecting
liver volume. Caffeine is metabolized by an array of hepatic
microsomal cytochrome P450 (CYP) enzymes (1A1, 1A2, 2A6, 2E1, 3A),[32]
antipyrine by CYP 1A2, 2B6, 2C8, 3C9 and 2C18[33] and lidocaine-MEGX
primarily by CYP 3A4.[33,34] Ocker et al.[35] used a different battery
of QLFTs (aminopyrine breath test, galactose elimination capacity,
sorbitol clearance and indocyanine green clearance) to study 50
patients with chronic hepatitis C at baseline and 3 months after
initiation of interferon-based therapy. They observed improvement in
hepatic metabolism in the patients who were HCV RNA negative. We
interpret these results to indicate that HCV or inflammation and
fibrosis related to HCV interfere with the hepatic metabolism of a
wide range of drugs, medications and xenobiotics and that these
effects are reversible with effective therapy.
Sustained virological response improves portal blood flow and perfused
hepatic mass, as measured by cholate Cl oral and SPECT-LSS and reduces
portal-systemic shunting, as measured by cholate shunt. Reduction in
hepatic inflammation and fibrosis after SVR may lower hepatic
resistance to portal inflow, reduce portal pressure and diminish
portal-systemic shunt. This interpretation is further supported by our
observation of a 12% increase in platelet count and the study by
Rincon et al.,[36] which demonstrated a 26% reduction in hepatic
venous pressure gradient in a subset of patients who achieved SVR. We
observed 32% increase in cholate Cl oral and 25% decrease in cholate
shunt. Globally, these results suggest that SVR reverses portal
hypertension, improves portal inflow and diminishes portal-systemic
shunting. ..."
Regarding Haptoglobin: I had this test along with a reticulocyte test to assess hemolytic anemia. I am not sure this is related but I know that an order for a haptoglobin test is frequently ordered with a reticulocyte count. I believe that as haptoglobin decreases the reticulocyte increases.
I found this at Wikipedia. http://en.wikipedia.org/wiki/Haptoglobin
"...A decrease in haptoglobin can support a diagnosis of hemolytic anemia, especially when correlated with a decreased RBC count, Hemoglobin, and Hematocrit, and also an increased reticulocyte count.
If the reticulocyte count is increased, but the haptoglobin level is normal, this may indicate that cellular destruction is occurring in the spleen and liver, which may indicate a drug-induced hemolysis, or a red cell dysplasia. The spleen and liver recognize an error in the red cells (either Drug coating the red cell membrane or a dysfunctional red cell membrane), and destroy the cell. This type of destruction does not release hemoglobin into the peripheral blood, so the haptoglobin cannot bind to it. Thus, the haptoglobin will stay normal.
If there are symptoms of anemia but both the reticulocyte count and the haptoglobin level are normal, the anemia is most likely not due to hemolysis, but instead some other error in cellular production, such as aplastic anemia
Haptoglobin levels that are decreased but do not accompany signs of anemia may indicate liver damage, as the liver is not producing enough haptoglobin to begin with.
As haptoglobin is indeed an acute-phase protein, any inflammatory process (infection, extreme stress, burns, major crush injury, allergy, etc.) may increase the levels of plasma haptoglobin..."
Yes I have had bleeds, pitting edema, ascites, jaundice-been banded for varicies. Taking prednisone, lactulose and a food supplement called Hepatic Aid, High Echogenecity of the liver-Portal Hypertension between the Liver and Spleen-spider veins back and chest
what SX's are you still experiencing after treatment? did you ever have a biopsy and what were the results?
I'm somewhat puzzled here, A doctor, especially a Hepatologist should not make a diagnosis of "end stage" based on a Fibrospect & U/S. And besides that F3/4 is not "end stage". Unless of course you have other markers like edema, bloodtest abnormalities, etc.
Something is just not right and I suggest you may want to get another opinion if this doctor don't give you specific answers.
best of luck
I'm somewhat puzzled here, A doctor, especially a Hepatologist should not make a diagnosis of "end stage" based on a Fibrospect & U/S. And besides that F3/4 is not "end stage". Unless of course you have other markers like edema, bloodtest abnormalities, etc.
Something is just not right and I suggest you may want to get another opinion if this doctor don't give you specific answers.
best of luck
Thank you for your help. I had what was called a fibrospect which put me at F3F4 for cirrhosis and bridging fibrosis after I was declared SVR. My Sxs never went away and after 4 years I found this forum and was encouraged to seek a different Hepatologist. He did all the blood work, an ultrasound and a fibrosure test. Said I was clear of the Hep C but am in end stage liver disease and a biopsy was not necessary-also because of a heart condition and COPD not qualified for transplant. Didn't get the actual report until yesterday and the Hepatologist was gone for weekend. I am now wondering if the high Haptoglobin and low Apo are making me ill and not the Sxs from Tx. Mostly curious-I;m doomed anyway-LOL but I am grasping for some relief until that day comes. All I can find is it could be a biliary duct blockage or rheumatic disease on the Haptoglobin and the Apo 1 A could be what is causing me to rash and feel sunburned and light dementia. Thanks again
It sounds like you have had a fibrosure before. What were those results? Try not to stress to much because the Fibrosure is not that accurate for the middle stages. Hopefully your test is showing you higher when in fact you are not. At this point I would look at getting a biopsy because of the fibrosure results. Personally I would want to know what a biopsy shows. Good luck
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