Aa
How often/When is endoscopy necessary?
Hi folks, was wondering, is an endoscopy considered "routine maintenance" with active HCV?
Is it usually recommended to be done on a regular basis? I was under the impression that varices were a concern only in situations of portal hypertension. Would a doctor recommend endoscopy in the absence of portal hypertension? (My husband who has HCV is questioning how necessary this test is.)
Or, is it just routine course of "clearing to start treatment" kind of test? For those are starting/started/had treatment, was this part of pre-treatment work-up?
Thanks for any input.
Is it usually recommended to be done on a regular basis? I was under the impression that varices were a concern only in situations of portal hypertension. Would a doctor recommend endoscopy in the absence of portal hypertension? (My husband who has HCV is questioning how necessary this test is.)
Or, is it just routine course of "clearing to start treatment" kind of test? For those are starting/started/had treatment, was this part of pre-treatment work-up?
Thanks for any input.
Very thought provoking stuff, thanks! (If collagen indeed does double every 2 years, then the fact that we don't see similar increases at correlative rates in biochemical and serum markers further underlines the lack of a direct relationship between fibrosis/cirrhosis progression and 'liver function'.)
As far as the pathogenesis of liver disease and HCV... I'm of the mind that if we can't find a cure by eradicating the presence of the virus, and we're not effective at killing it, perhaps by unravelling the mystery of its molecular pathways (fibrosis, hcc, etc.), we can at least learn to neutralize it, predict its progress, and, that way, we might still be able to defeat it by manipulating and/or interrupting its intra-hepatic alterations.
As far as the pathogenesis of liver disease and HCV... I'm of the mind that if we can't find a cure by eradicating the presence of the virus, and we're not effective at killing it, perhaps by unravelling the mystery of its molecular pathways (fibrosis, hcc, etc.), we can at least learn to neutralize it, predict its progress, and, that way, we might still be able to defeat it by manipulating and/or interrupting its intra-hepatic alterations.
at the close of all that grim news there's a bit of light as well:
"Hepatic fibrosis is a dynamic process, characterized by a balance between fibrogenesis and fibrolysis. The current study shows the value of morphometric image analysis as well as the necessity of a placebo control group in testing new therapeutic agents designed to inhibit fibrogenesis or promote fibrolysis. If a new therapeutic agent is effective, significantly less increase in the amount of fibrous tissue compared with progression in a placebo group should be seen, and if it is truly effective in a clinically significant way, an actual decrease in the mean collagen of the treatment cohort should occur. This approach cannot be used to manage individual patients, but only to study cohorts with sufficient statistical power to show a eaningful change. Although liver biopsy is an invasive procedure, it is necessary for this type of study because standard laboratory tests do not appear to change enough to reflect changes in the quantity of fibrous tissue. Whether newer batteries of biochemical tests, serum fibrosis markers, imaging techniques, or measurement of iver stiffness by transient elastography will be able to detect changes in fibrous tissue with this degree of sensitivity remains to be determined."
so there's encouraging recognition that fibrolytic pathways exist - even if systematic detection of what works and what doesn't looks far away (all the more so for unpatentable compounds). I'm been trying to believe in to HR's anti-fibrotic regime but am still troubled by scarcity of the evidence. Some have an easier time being born again than others - still, given the advancing time, partial evidence will have to be good enough and I'm taking my pills. Hope you're doing well.
"Hepatic fibrosis is a dynamic process, characterized by a balance between fibrogenesis and fibrolysis. The current study shows the value of morphometric image analysis as well as the necessity of a placebo control group in testing new therapeutic agents designed to inhibit fibrogenesis or promote fibrolysis. If a new therapeutic agent is effective, significantly less increase in the amount of fibrous tissue compared with progression in a placebo group should be seen, and if it is truly effective in a clinically significant way, an actual decrease in the mean collagen of the treatment cohort should occur. This approach cannot be used to manage individual patients, but only to study cohorts with sufficient statistical power to show a eaningful change. Although liver biopsy is an invasive procedure, it is necessary for this type of study because standard laboratory tests do not appear to change enough to reflect changes in the quantity of fibrous tissue. Whether newer batteries of biochemical tests, serum fibrosis markers, imaging techniques, or measurement of iver stiffness by transient elastography will be able to detect changes in fibrous tissue with this degree of sensitivity remains to be determined."
so there's encouraging recognition that fibrolytic pathways exist - even if systematic detection of what works and what doesn't looks far away (all the more so for unpatentable compounds). I'm been trying to believe in to HR's anti-fibrotic regime but am still troubled by scarcity of the evidence. Some have an easier time being born again than others - still, given the advancing time, partial evidence will have to be good enough and I'm taking my pills. Hope you're doing well.
the numbers do seem a bit more informative than the adjectives - and I expect the hepatologist will be able to elaborate on the interpretation when you meet. I came across the following article, which includes Afdhal among its authors
Progression of fibrosis in advanced chronic hepatitis C: evaluation by morphometric image analysis.
Hepatology. 2007 Apr;45(4):886-94. PMID: 17393526
http://www.ncbi.nlm.nih.gov/pubmed/17393526
They had a large number of paired biopsies from an ifn-gamma trial ( drug didn't work) and in addition to the usual checks for fibrosis progression, they ran some computer-based image-analysis software to quantify the total amount of collagen visible from stains of the bx samples. Here's a couple of paragraphs from the conclusions. A bit long but very much on point to the "how sure can be one be" issue:
"In our study, we found that in 245 patients with paired biopsies adequate for morphometric analysis, the amount of fibrous tissue increased on average by 58% over the 48-week period of the study.....Even though our patients had been treated with potentially antifibrotic agents, the findings in this cohort are quite similar to those in the small groups of untreated patients reported by Manabe et al.[32] and Kage et al.[5] Extrapolating the reported data, Manabe et al.[32] found an average increase in fibrosis of approximately 52% per year in 16 patients, Kage et al.[5] found 55% per year in 25 patients, and we found 58% per year in 245 patients, despite the differences in patients and in the baseline levels of fibrosis.
This implies that in patients with chronic hepatitis C, the average amount of hepatic collagen doubles in approximately 2 years, and if this is true at all degrees of fibrosis, then the fibrous tissue may actually increase exponentially rather than linearly. Although there are clearly differences between individuals in the rate of progression of fibrosis, a doubling of the amount of collagen every 2 years could partly explain the apparent acceleration of fibrosis in older individuals who presumably have had the disease for longer time.[5][8][13][34] Only by direct measurement of fibrosis within a sufficiently large cohort does this become apparent, because histological stages are neither a continuous function nor a sensitive measure of this type of change. In the current study, we examined fibrosis progression in a cohort of patients who had already proved themselves rapid fibrosers. ....
Progression of fibrosis leads to cirrhosis with its complications. In patients with advanced liver disease, one might expect a relationship between increase in fibrous tissue and increase in portal pressure or decrease in synthetic capacity of liver, but this was not found in the current study. Only weak correlations of laboratory tests that reflect portal hypertension and hepatic synthetic function were seen (Table 6), no correlation with clinical decompensation, and no significant change in mean test values (Table 5), despite the fact that the mean collagen content of the cohort increased by 58%. This suggests that factors other than the absolute amount of fibrous tissue play an important role in the clinical and laboratory changes in advanced liver disease or that the pathophysiologic effects of increased fibrosis lag the increase in fibrous tissue. The architectural distortion that accompanies nodular parenchymal regeneration as well as shunting of blood through vascularized fibrotic septa may be of equal or greater importance than the amount of scar tissue. Similarly, the mass of functioning hepatic parenchyma may be more important than the proportion of parenchyma replaced with scar tissue. Therefore, in the evaluation of an individual patient, the histologic diagnosis, based on the combination of architectural changes and amount of fibrosis, may well be more important than the amount of fibrosis alone."
This is all still sinking in, but the impression I'm coming away with is that while all roads that ultimately lead to liver failure share a common destination it's not necessarily easy to tell which one you're traveling on. Extensive collagen buildup can precede other traditional indicators, like portal hypertension and out-of range wbc/platelet/clotting, and that doubling every two years rule is pretty impressive! My assumption is that a fibroscan, which basically measures overall stiffness, would correlate well with total sample collagen content as measured in this study.
Bottom line seems to be that one may not be able to count on getting two or more confirming indicators...
Progression of fibrosis in advanced chronic hepatitis C: evaluation by morphometric image analysis.
Hepatology. 2007 Apr;45(4):886-94. PMID: 17393526
http://www.ncbi.nlm.nih.gov/pubmed/17393526
They had a large number of paired biopsies from an ifn-gamma trial ( drug didn't work) and in addition to the usual checks for fibrosis progression, they ran some computer-based image-analysis software to quantify the total amount of collagen visible from stains of the bx samples. Here's a couple of paragraphs from the conclusions. A bit long but very much on point to the "how sure can be one be" issue:
"In our study, we found that in 245 patients with paired biopsies adequate for morphometric analysis, the amount of fibrous tissue increased on average by 58% over the 48-week period of the study.....Even though our patients had been treated with potentially antifibrotic agents, the findings in this cohort are quite similar to those in the small groups of untreated patients reported by Manabe et al.[32] and Kage et al.[5] Extrapolating the reported data, Manabe et al.[32] found an average increase in fibrosis of approximately 52% per year in 16 patients, Kage et al.[5] found 55% per year in 25 patients, and we found 58% per year in 245 patients, despite the differences in patients and in the baseline levels of fibrosis.
This implies that in patients with chronic hepatitis C, the average amount of hepatic collagen doubles in approximately 2 years, and if this is true at all degrees of fibrosis, then the fibrous tissue may actually increase exponentially rather than linearly. Although there are clearly differences between individuals in the rate of progression of fibrosis, a doubling of the amount of collagen every 2 years could partly explain the apparent acceleration of fibrosis in older individuals who presumably have had the disease for longer time.[5][8][13][34] Only by direct measurement of fibrosis within a sufficiently large cohort does this become apparent, because histological stages are neither a continuous function nor a sensitive measure of this type of change. In the current study, we examined fibrosis progression in a cohort of patients who had already proved themselves rapid fibrosers. ....
Progression of fibrosis leads to cirrhosis with its complications. In patients with advanced liver disease, one might expect a relationship between increase in fibrous tissue and increase in portal pressure or decrease in synthetic capacity of liver, but this was not found in the current study. Only weak correlations of laboratory tests that reflect portal hypertension and hepatic synthetic function were seen (Table 6), no correlation with clinical decompensation, and no significant change in mean test values (Table 5), despite the fact that the mean collagen content of the cohort increased by 58%. This suggests that factors other than the absolute amount of fibrous tissue play an important role in the clinical and laboratory changes in advanced liver disease or that the pathophysiologic effects of increased fibrosis lag the increase in fibrous tissue. The architectural distortion that accompanies nodular parenchymal regeneration as well as shunting of blood through vascularized fibrotic septa may be of equal or greater importance than the amount of scar tissue. Similarly, the mass of functioning hepatic parenchyma may be more important than the proportion of parenchyma replaced with scar tissue. Therefore, in the evaluation of an individual patient, the histologic diagnosis, based on the combination of architectural changes and amount of fibrosis, may well be more important than the amount of fibrosis alone."
This is all still sinking in, but the impression I'm coming away with is that while all roads that ultimately lead to liver failure share a common destination it's not necessarily easy to tell which one you're traveling on. Extensive collagen buildup can precede other traditional indicators, like portal hypertension and out-of range wbc/platelet/clotting, and that doubling every two years rule is pretty impressive! My assumption is that a fibroscan, which basically measures overall stiffness, would correlate well with total sample collagen content as measured in this study.
Bottom line seems to be that one may not be able to count on getting two or more confirming indicators...
Truth be told, I wasn't fully convinced of the bx sample dx until it was confirmed by the left lobe removal's surgical pathology. (Yeah, I'm hard to convince and usually demand overwhelming proof.)
To be completely accurate, the measurements I gave were free pressures; if I were to extrapolate according the the article (HVPG = wedged hepatic venous pressure minus free hepatic vein pressure), the calculations would be:
wedged hepatic 16 - 8 free right atrium free = 8 HVPG
wedged hepatic 16 - 11 free renal inferior vena cava = 5 HVPG
wedged hepatic 16 - 10 free hepatic IVC = 6 HVPG
wedged hepatic 16 - 9 free hepatic vein = 7 HVPG
... so, not "clinically significant"? (Sometimes I think 'not clinically significant' doesn't mean it isn't there, it means they can't figure it out or can't detect it by usual methods. :P)
"...it has been shown that varices do not develop ... if the HVPG is <12 mmHg [13]" could be disputed, here.
Thanks for the article above... got more out of the biopsy report from that!
(PS I believe in the 'squeaky well gets the oil' theory and upholding expectations that docs be 'very thorough'. I made the mistake ONCE of not demanding 'the best doc for the job', and it almost cost my husband his life during a 'routine cardiac procedure' -- the 'down' side of university hospitals is that there are many not-so-experienced fellows -- and, these days, I don't hesitate to remind the hospital and providers that they messed up once and I don't intend on letting them do it again if I can help it.)
To be completely accurate, the measurements I gave were free pressures; if I were to extrapolate according the the article (HVPG = wedged hepatic venous pressure minus free hepatic vein pressure), the calculations would be:
wedged hepatic 16 - 8 free right atrium free = 8 HVPG
wedged hepatic 16 - 11 free renal inferior vena cava = 5 HVPG
wedged hepatic 16 - 10 free hepatic IVC = 6 HVPG
wedged hepatic 16 - 9 free hepatic vein = 7 HVPG
... so, not "clinically significant"? (Sometimes I think 'not clinically significant' doesn't mean it isn't there, it means they can't figure it out or can't detect it by usual methods. :P)
"...it has been shown that varices do not develop ... if the HVPG is <12 mmHg [13]" could be disputed, here.
Thanks for the article above... got more out of the biopsy report from that!
(PS I believe in the 'squeaky well gets the oil' theory and upholding expectations that docs be 'very thorough'. I made the mistake ONCE of not demanding 'the best doc for the job', and it almost cost my husband his life during a 'routine cardiac procedure' -- the 'down' side of university hospitals is that there are many not-so-experienced fellows -- and, these days, I don't hesitate to remind the hospital and providers that they messed up once and I don't intend on letting them do it again if I can help it.)
Considering the bx sample and the HVPG, it seems your husband's Drs were *very* thorough in their diagnosis. Here's some additional text from that DeFranchis'04 review cited above
"Measuring the HVPG involves the catheterisation of the hepatic vein via a transfemoral or a transjugular route; the HVPG is calculated by subtracting the free hepatic vein pressure from the wedged hepatic venous pressure. The normal upper limit of the HVPG is 5 mmHg; values above this limit denote portal hypertension [12]. HVPG measurement can be used to evaluate the risk of developing oesophageal varices and of variceal bleeding, since it has been shown that varices do not develop and do not bleed if the HVPG is <12 mmHg [13]. In addition, HVPG measurement is useful to monitor the portal pressure response under pharmacological treatment [14], and to evaluate the prognosis of acute variceal bleeding [15]. The pros of HVPG are that it is a safe and reproducible procedure: when a correct technique is used, the coefficient of variation of the method is 2.6 ± 2.6% [13] However, at present, HVPG measurement is not applicable on a routine basis, because it is invasive, relatively expensive and requires highly trained personnel."
It seems that normal range is up to 5 , 5-10mm indicates portal hypertension, 10-12 is "clinically significant" and above 12 is "severe" with pronounced varices expected. A measurement between 5-12 along with observation of trace varices on the endoscopy would confirm that your husband's bx was reliable evidence. Thanks again - all helpful information.
"Measuring the HVPG involves the catheterisation of the hepatic vein via a transfemoral or a transjugular route; the HVPG is calculated by subtracting the free hepatic vein pressure from the wedged hepatic venous pressure. The normal upper limit of the HVPG is 5 mmHg; values above this limit denote portal hypertension [12]. HVPG measurement can be used to evaluate the risk of developing oesophageal varices and of variceal bleeding, since it has been shown that varices do not develop and do not bleed if the HVPG is <12 mmHg [13]. In addition, HVPG measurement is useful to monitor the portal pressure response under pharmacological treatment [14], and to evaluate the prognosis of acute variceal bleeding [15]. The pros of HVPG are that it is a safe and reproducible procedure: when a correct technique is used, the coefficient of variation of the method is 2.6 ± 2.6% [13] However, at present, HVPG measurement is not applicable on a routine basis, because it is invasive, relatively expensive and requires highly trained personnel."
It seems that normal range is up to 5 , 5-10mm indicates portal hypertension, 10-12 is "clinically significant" and above 12 is "severe" with pronounced varices expected. A measurement between 5-12 along with observation of trace varices on the endoscopy would confirm that your husband's bx was reliable evidence. Thanks again - all helpful information.
You're a veritable wealth of information! Thanks! I'm truly relieved that he finally did go thru with it -- and even though varices is not a current concern, it feels even more reassuring to know the ins and outs (no pun intended).
Have a great weekend :D!
Have a great weekend :D!
I'll be interested in hearing the results from the endoscopy. Hopefully it will be minimal indicating your husband liver fibrosis is still stable and compensated.
Thanks for all the info.
Thank care for now.
All the best!
Hector
Thanks for all the info.
Thank care for now.
All the best!
Hector
We're certainly thinking congruently -- the initial question on this thread was posed because I, too, had thought varices were "basically a response to the increased pressure." In reviewing my husband's last biopsy, docs actually DID do hepatic vein pressure measurements, and free pressure all measured less than 12 mm Hg. Again, no suspected portal hypertension. The more I learn, the more everything leads me to suspect that in the viral world of hepatitis 1+1 does not always equal 2 (and 2 does not necessarily follow 1, either.)
Hi again.
Here is some info on the relationship between cirrhosis, blood liver levels, varices, portal hypertension, and enlarged spleen.
The following findings are typical in cirrhosis:
* Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.
* Alkaline phosphatase - usually slightly elevated.
* GGT -- correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
* Bilirubin - may elevate as cirrhosis progresses.
* Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
* Prothrombin time - increases since the liver synthesizes clotting factors.
* Thrombocytopenia (low platelet count) - due to both congestive splenomegaly (enlarged spleen) as well as decreased thrombopoietin from the liver. However this rarely results in platete count < 50,000/mL.
SUBJECT Manifestations of Liver Disease
Portal hypertension is abnormally high blood pressure in branches of the portal vein, the large vein that brings blood from the intestine to the liver. The portal vein receives blood from the entire intestine and from the spleen, pancreas, and gallbladder. After entering the liver, the vein divides into right and left branches and then into tiny channels that run through the liver. When blood leaves the liver, it flows back into the general (systemic, or body-wide) circulation through the hepatic vein.Two factors can increase blood pressure in the portal blood vessels:
* Increased volume of blood flowing through the vessels
* Increased resistance to the blood flow through the liver
The most common cause of portal hypertension is increased resistance to blood flow caused by extensive scarring of the liver in cirrhosis.Portal hypertension leads to the development of new veins (called collateral vessels) that directly connect the portal blood vessels to the general circulation, bypassing the liver. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation. Collateral vessels develop at specific places. The most important are located at the lower end of the esophagus and at the upper part of the stomach. Here, the vessels become engorged and full of twists and turns—that is, they become varicose veins of the esophagus (esophageal varices) or stomach (gastric varices). These engorged vessels are fragile and prone to bleeding, sometimes seriously and occasionally with fatal results. Other collateral vessels may develop on the abdominal wall and at the rectum.Portal hypertension often causes the spleen to enlarge because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause protein-containing (ascitic) fluid from the surface of the liver and intestine to leak into the abdominal cavity. This condition is called ascites.
Symptoms and Diagnosis:
Portal hypertension itself does not cause symptoms, but some of its consequences do. If a large amount of ascitic fluid accumulates, the person's abdomen swells (distends), sometimes noticeably and sometimes enough to make the abdomen greatly enlarged and taut. This distention is painless. An enlarged spleen may cause a vague sense of discomfort in the upper left part of the abdomen. Esophageal and gastric varices bleed easily and sometimes massively. Much less commonly, varicose veins in the rectum bleed.When substances that are normally removed from the liver pass into the general circulation and reach the brain, they may cause confusion or drowsiness (hepatic encephalopathy). Collateral vessels may be visible on the skin over the abdominal wall or around the rectum. Because most people with portal hypertension also have severe liver dysfunction, they may have symptoms of liver failure, such as a tendency to bleed.Doctors can usually recognize hepatic encephalopathy based on symptoms and findings during the physical examination. Doctors can usually feel an enlarged spleen through the abdominal wall. They can detect fluid in the abdomen by noting abdominal swelling and by listening for a dull sound when tapping (percussing) the abdomen. An ultrasound scan may be used to examine blood flow in the portal vein and nearby blood vessels and to detect fluid in the abdomen. An ultrasound or computed tomography (CT) scan can be used to look for and examine collateral vessels. Rarely, a catheter is inserted through an incision in the neck and threaded through blood vessels into the liver or spleen to directly measure pressure in the portal blood vessels (manometry).
Treatment:
To reduce the risk of bleeding from esophageal varices, a doctor may try to reduce pressure in the portal vein. One way is to drugs such as propranolol or nadolol.Bleeding from esophageal varices is a medical emergency. Drugs such as vasopressin or octreotide may be given intravenously to constrict the bleeding veins, and blood transfusions are given to replace lost blood. An endoscopic examination is usually done to confirm that the bleeding is from varices. The veins can then be blocked off with rubber bands or with injections of a chemical given through the endoscope.If the bleeding continues or recurs repeatedly, a surgical procedure may be done to create a bypass (called a shunt) between the portal venous system and the general (systemic, or body-wide) venous system. This bypass lowers pressure in the portal vein because pressure is much lower in the general venous system.There are various types of portal-systemic shunt procedures. In one type, called transjugular intrahepatic portal-systemic shunting (TIPS), an x-ray-guided needle is passed through the liver to create a shunt connecting the portal vein directly with one of the hepatic veins. Shunt procedures are usually successful in stopping the bleeding but pose certain risks, such as hepatic encephalopathy.The TIPS procedure, although less dangerous than other portal-systemic shunt procedures, may need to be repeated periodically because the shunt narrows in some people.
Glad your husband got tested.
Hector
Here is some info on the relationship between cirrhosis, blood liver levels, varices, portal hypertension, and enlarged spleen.
The following findings are typical in cirrhosis:
* Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.
* Alkaline phosphatase - usually slightly elevated.
* GGT -- correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
* Bilirubin - may elevate as cirrhosis progresses.
* Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
* Prothrombin time - increases since the liver synthesizes clotting factors.
* Thrombocytopenia (low platelet count) - due to both congestive splenomegaly (enlarged spleen) as well as decreased thrombopoietin from the liver. However this rarely results in platete count < 50,000/mL.
SUBJECT Manifestations of Liver Disease
Portal hypertension is abnormally high blood pressure in branches of the portal vein, the large vein that brings blood from the intestine to the liver. The portal vein receives blood from the entire intestine and from the spleen, pancreas, and gallbladder. After entering the liver, the vein divides into right and left branches and then into tiny channels that run through the liver. When blood leaves the liver, it flows back into the general (systemic, or body-wide) circulation through the hepatic vein.Two factors can increase blood pressure in the portal blood vessels:
* Increased volume of blood flowing through the vessels
* Increased resistance to the blood flow through the liver
The most common cause of portal hypertension is increased resistance to blood flow caused by extensive scarring of the liver in cirrhosis.Portal hypertension leads to the development of new veins (called collateral vessels) that directly connect the portal blood vessels to the general circulation, bypassing the liver. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation. Collateral vessels develop at specific places. The most important are located at the lower end of the esophagus and at the upper part of the stomach. Here, the vessels become engorged and full of twists and turns—that is, they become varicose veins of the esophagus (esophageal varices) or stomach (gastric varices). These engorged vessels are fragile and prone to bleeding, sometimes seriously and occasionally with fatal results. Other collateral vessels may develop on the abdominal wall and at the rectum.Portal hypertension often causes the spleen to enlarge because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause protein-containing (ascitic) fluid from the surface of the liver and intestine to leak into the abdominal cavity. This condition is called ascites.
Symptoms and Diagnosis:
Portal hypertension itself does not cause symptoms, but some of its consequences do. If a large amount of ascitic fluid accumulates, the person's abdomen swells (distends), sometimes noticeably and sometimes enough to make the abdomen greatly enlarged and taut. This distention is painless. An enlarged spleen may cause a vague sense of discomfort in the upper left part of the abdomen. Esophageal and gastric varices bleed easily and sometimes massively. Much less commonly, varicose veins in the rectum bleed.When substances that are normally removed from the liver pass into the general circulation and reach the brain, they may cause confusion or drowsiness (hepatic encephalopathy). Collateral vessels may be visible on the skin over the abdominal wall or around the rectum. Because most people with portal hypertension also have severe liver dysfunction, they may have symptoms of liver failure, such as a tendency to bleed.Doctors can usually recognize hepatic encephalopathy based on symptoms and findings during the physical examination. Doctors can usually feel an enlarged spleen through the abdominal wall. They can detect fluid in the abdomen by noting abdominal swelling and by listening for a dull sound when tapping (percussing) the abdomen. An ultrasound scan may be used to examine blood flow in the portal vein and nearby blood vessels and to detect fluid in the abdomen. An ultrasound or computed tomography (CT) scan can be used to look for and examine collateral vessels. Rarely, a catheter is inserted through an incision in the neck and threaded through blood vessels into the liver or spleen to directly measure pressure in the portal blood vessels (manometry).
Treatment:
To reduce the risk of bleeding from esophageal varices, a doctor may try to reduce pressure in the portal vein. One way is to drugs such as propranolol or nadolol.Bleeding from esophageal varices is a medical emergency. Drugs such as vasopressin or octreotide may be given intravenously to constrict the bleeding veins, and blood transfusions are given to replace lost blood. An endoscopic examination is usually done to confirm that the bleeding is from varices. The veins can then be blocked off with rubber bands or with injections of a chemical given through the endoscope.If the bleeding continues or recurs repeatedly, a surgical procedure may be done to create a bypass (called a shunt) between the portal venous system and the general (systemic, or body-wide) venous system. This bypass lowers pressure in the portal vein because pressure is much lower in the general venous system.There are various types of portal-systemic shunt procedures. In one type, called transjugular intrahepatic portal-systemic shunting (TIPS), an x-ray-guided needle is passed through the liver to create a shunt connecting the portal vein directly with one of the hepatic veins. Shunt procedures are usually successful in stopping the bleeding but pose certain risks, such as hepatic encephalopathy.The TIPS procedure, although less dangerous than other portal-systemic shunt procedures, may need to be repeated periodically because the shunt narrows in some people.
Glad your husband got tested.
Hector
I don't know how often you should go.... but my doctor said I became very talkative while going under....some folks loose all inhibition.......
which has happened to me before....I usually tell jokes in these instances..rattle off medical questions...., or in this case would have sang the roto- rooter song....which means I won't be back for a while!!!!!!!. Blush.
which has happened to me before....I usually tell jokes in these instances..rattle off medical questions...., or in this case would have sang the roto- rooter song....which means I won't be back for a while!!!!!!!. Blush.
ff: I'm glad the world's looking a bit better and that you're set up with another dr. My hunch, based on your results so far, would be to get ready to jump in with soc and possibly alinia, unless the new dr can find a convincing alternative explanation for those varices.
Here's some follow from the last post. Not sure why the mh censors in their infinite wisdom have decided that some links to pubmed citations are not safe for viewing, but the pubmed ID for the link above is 15646423
Diagnosis and treatment of portal hypertension.
Dig Liver Dis. 2004 Dec;36(12):787-98.
(you can type the pmid in the pubmed search dialog to access the article).
Direct measurement of portal vein pressure (HPVG) seems the "gold standard" for assessing portal hypertension. However, while accurate, it appears to be rarely used:
"The pros of HVPG are that it is a safe and reproducible procedure: when a correct technique is used, the coefficient of variation of the method is 2.6 ± 2.6% . However, at present, HVPG measurement is not applicable on a routine basis, because it is invasive, relatively expensive and requires highly trained personnel."
They go on to discuss, pros and cons of the US and endoscopy, the latter being the technique most commonly used.
Discussion of a study from last year
http://www.ncbi.nlm.nih.gov/pubmed/17464984
comparing FS/TE (which they called LSM - liver stiffness measurement) with HPVG found pretty good agreement:
"In this issue of HEPATOLOGY, Vizzutti et al.[21] aimed to evaluate the role of transient elastography in predicting clinically significant portal hypertension, as measured by the HVPG and endoscopic evidence for varices. Sixty-one consecutive patients with clinical or histopathologic evidence of cirrhosis underwent transient elastography after an overnight fast, followed immediately by direct measurement of HVPG in the hepatic hemodynamic laboratory. Among individuals without prior histologic examination, a transjugular liver biopsy specimen was obtained. Subjects proceeded to undergo an upper endoscopy the following day, with a laboratory profile obtained within one week of study enrollment. Within this cohort, a positive correlation between HVPG and liver stiffness measurement (LSM) was observed (r = 0.81). The sensitivity and specificity of LSM in diagnosing clinically significant portal hypertension, as defined by HVPG 10 mm Hg, was 97% and 92%, respectively, using a cutoff threshold of 13.6 kPa. The negative predictive value and sensitivity of LSM in predicting severe portal hypertension (HVPG 12 mm Hg) was also favorable at 91% and 94%, respectively. However, similarly to the HVPG, its ability to predict and distinguish between grades of esophageal varices was poor, suggesting a plateau effect in which further increases in liver stiffness are not reflected in the development of late complications of portal hypertension."
It sounds like short of actually seeing varices on an endoscopy/ct , fs of 14 or above may be the best indicator.
Here's some follow from the last post. Not sure why the mh censors in their infinite wisdom have decided that some links to pubmed citations are not safe for viewing, but the pubmed ID for the link above is 15646423
Diagnosis and treatment of portal hypertension.
Dig Liver Dis. 2004 Dec;36(12):787-98.
(you can type the pmid in the pubmed search dialog to access the article).
Direct measurement of portal vein pressure (HPVG) seems the "gold standard" for assessing portal hypertension. However, while accurate, it appears to be rarely used:
"The pros of HVPG are that it is a safe and reproducible procedure: when a correct technique is used, the coefficient of variation of the method is 2.6 ± 2.6% . However, at present, HVPG measurement is not applicable on a routine basis, because it is invasive, relatively expensive and requires highly trained personnel."
They go on to discuss, pros and cons of the US and endoscopy, the latter being the technique most commonly used.
Discussion of a study from last year
http://www.ncbi.nlm.nih.gov/pubmed/17464984
comparing FS/TE (which they called LSM - liver stiffness measurement) with HPVG found pretty good agreement:
"In this issue of HEPATOLOGY, Vizzutti et al.[21] aimed to evaluate the role of transient elastography in predicting clinically significant portal hypertension, as measured by the HVPG and endoscopic evidence for varices. Sixty-one consecutive patients with clinical or histopathologic evidence of cirrhosis underwent transient elastography after an overnight fast, followed immediately by direct measurement of HVPG in the hepatic hemodynamic laboratory. Among individuals without prior histologic examination, a transjugular liver biopsy specimen was obtained. Subjects proceeded to undergo an upper endoscopy the following day, with a laboratory profile obtained within one week of study enrollment. Within this cohort, a positive correlation between HVPG and liver stiffness measurement (LSM) was observed (r = 0.81). The sensitivity and specificity of LSM in diagnosing clinically significant portal hypertension, as defined by HVPG 10 mm Hg, was 97% and 92%, respectively, using a cutoff threshold of 13.6 kPa. The negative predictive value and sensitivity of LSM in predicting severe portal hypertension (HVPG 12 mm Hg) was also favorable at 91% and 94%, respectively. However, similarly to the HVPG, its ability to predict and distinguish between grades of esophageal varices was poor, suggesting a plateau effect in which further increases in liver stiffness are not reflected in the development of late complications of portal hypertension."
It sounds like short of actually seeing varices on an endoscopy/ct , fs of 14 or above may be the best indicator.
When I had mine they put me to sleep, he also told me he would fix anything then and there while I was asleep, any variances and so on.
They also gave me color pictures and a menu of what it meant, (the colors)
Foo, you do need to advocate for yourself, I know it is hard, I have never done a trial.
Anyway good luck
Deb
They also gave me color pictures and a menu of what it meant, (the colors)
Foo, you do need to advocate for yourself, I know it is hard, I have never done a trial.
Anyway good luck
Deb
I wasn't told about the results. They sent a letter saying, tests are fine, we will let you know about the Vertex trial. I read the CT impressions and my bummer bloodwork after I picked up my records for HR before the Fibroscan.
They pretty much blow off every concern, question, suggestion, you name it. I am scheduled to meet the head man at a university liver and transplant clinic at the end of June. It may turn out that my first guy is right and that there is no reason to be concerned, but maybe not. I will finally have that second opinion that everyone has ALWAYS told me to get.
Don't like the sound of that old test. Maybe they don't measure it anymore. I don't think I have ever read of anyone here having a test for it. Just that they know they have it because they were diagnosed with varicies and have a spleen that is "all blowed up."
Yeah, I think I have accepted all the results that have contradicted my biopsy as accurate. It will be interesting to see if my new guy has me treating so fast it makes my head spin, or if he will have me wait as I TRY to lose more weight. Has been really hard as I have been super gut sick which is scary and also really sad. Exercise, which would help my depression and my weight, I just can't get up to do.!
Just started feeling better yesterday, thank goodness. And hopefully the last snow of the season will be tomorrow. Looking forward to getting outside to do some walking and gardening.
Finally--here comes the sun!
They pretty much blow off every concern, question, suggestion, you name it. I am scheduled to meet the head man at a university liver and transplant clinic at the end of June. It may turn out that my first guy is right and that there is no reason to be concerned, but maybe not. I will finally have that second opinion that everyone has ALWAYS told me to get.
Don't like the sound of that old test. Maybe they don't measure it anymore. I don't think I have ever read of anyone here having a test for it. Just that they know they have it because they were diagnosed with varicies and have a spleen that is "all blowed up."
Yeah, I think I have accepted all the results that have contradicted my biopsy as accurate. It will be interesting to see if my new guy has me treating so fast it makes my head spin, or if he will have me wait as I TRY to lose more weight. Has been really hard as I have been super gut sick which is scary and also really sad. Exercise, which would help my depression and my weight, I just can't get up to do.!
Just started feeling better yesterday, thank goodness. And hopefully the last snow of the season will be tomorrow. Looking forward to getting outside to do some walking and gardening.
Finally--here comes the sun!
deb: thanks - always good to know what you're walking into.
ff: yeah - I think we have something in common in the sense that our fs came out worse than other indicators. BTW, I owe you an apology; when you posted your results I meant to congratulate you on getting the test done, not on the results.
Here's a recent review of diagnostic methods:
http://www.****.gov
I'm not sure what's specifically involved in directly measuring the pressure, but in principle it seems straightforward. Here's an older '54 surgery article complete with a picture of the manometer on the guy's stomach.
http://www.pubmedcentral.ni****.gov
Hopefully, technology has improved. I think HR's comments may indicate that cm/sec as measured by US may not be that reliable. (The comment on my last US was "normal monotonous hepatopetal flow" with no flow measurement).
However, I would think both the CT-detected spleen enlargement and the splenic varices would be consistent with the fs - did your doc's office give any explanation why they didn't think these were not cause for concern?
ff: yeah - I think we have something in common in the sense that our fs came out worse than other indicators. BTW, I owe you an apology; when you posted your results I meant to congratulate you on getting the test done, not on the results.
Here's a recent review of diagnostic methods:
http://www.****.gov
I'm not sure what's specifically involved in directly measuring the pressure, but in principle it seems straightforward. Here's an older '54 surgery article complete with a picture of the manometer on the guy's stomach.
http://www.pubmedcentral.ni****.gov
Hopefully, technology has improved. I think HR's comments may indicate that cm/sec as measured by US may not be that reliable. (The comment on my last US was "normal monotonous hepatopetal flow" with no flow measurement).
However, I would think both the CT-detected spleen enlargement and the splenic varices would be consistent with the fs - did your doc's office give any explanation why they didn't think these were not cause for concern?
Yes, this is a subject that I am going back and forth on. I have had a couple recommendations to be safe and do it and a couple saying maybe not that big a rush.
Also here is a bit of discussion I had with HR, and his response in all caps. I try to glean info from all my reports and I still end up not knowing what to do. My doc's office got this report and they had no concerns. Have never ordered an endoscopy in spite of the stage 4.
To HR:
I noticed that on Feb 1 of 2007 my doc ordered an ultrasound that had my portal vein flow at 24 cm/sec but they have not checked that again. The CT they did last month says "a few splenic varicies" and one of the impressions said "Splenomegaly, findings could indicate portal venous hypertension."
Maybe a portal vein flow of 24 cm/sec was not that good and they just didn't say anything.
From HR:
NOT A WELL DEFINED PARAMETER IN EVALUATING PORTAL HYPERTENSION, ALSO FLUCTUATES A LOT.
So there is one more thing that won't tell you anything... portal vein flow. And apparently splenic varicies is something that is not a red flag either.
How do they check portal vein pressure? Also until this last CT, my imaging studies always just said borderline splenomegaly.
FF
Also here is a bit of discussion I had with HR, and his response in all caps. I try to glean info from all my reports and I still end up not knowing what to do. My doc's office got this report and they had no concerns. Have never ordered an endoscopy in spite of the stage 4.
To HR:
I noticed that on Feb 1 of 2007 my doc ordered an ultrasound that had my portal vein flow at 24 cm/sec but they have not checked that again. The CT they did last month says "a few splenic varicies" and one of the impressions said "Splenomegaly, findings could indicate portal venous hypertension."
Maybe a portal vein flow of 24 cm/sec was not that good and they just didn't say anything.
From HR:
NOT A WELL DEFINED PARAMETER IN EVALUATING PORTAL HYPERTENSION, ALSO FLUCTUATES A LOT.
So there is one more thing that won't tell you anything... portal vein flow. And apparently splenic varicies is something that is not a red flag either.
How do they check portal vein pressure? Also until this last CT, my imaging studies always just said borderline splenomegaly.
FF
Some serious good info here.
Willing I had endoscopy in Nov, (it was fine) they did give me pictures. It was no big deal at all. I went to sleep woke up all done!
Deb
Willing I had endoscopy in Nov, (it was fine) they did give me pictures. It was no big deal at all. I went to sleep woke up all done!
Deb
thanks for the update - all a bit puzzling. In the context of fibrosis, it's not clear to me how varices can develop in the absence of portal hypertension ( I thought they were basically a response to the increased pressure). The definitive test for portal hypertension seems to be based on measuring pressure in the portal vein. I'll ask about this when I have my pre-endoscopy appointment, but from what I've read this measurement is not standard practice. Possibly, in certain individuals tension can develop without visible effects on spleen/vein dimension; your visit with the hepatologist may clarify. The bx sample definitely seems large enough to support the diagnosis on its own and the trace varices would provide at least one confirming indicator even if the blood and us/ct scan results don't.
The images in the article on the tomography-based technique Mike716 posted a while back
http://www.ncbi.nlm.nih.gov/pubmed/18098299
certainly support the view that the degree of fibrosis can be very heterogenous throughout the liver - I share your suspicions about sampling error.
The images in the article on the tomography-based technique Mike716 posted a while back
http://www.ncbi.nlm.nih.gov/pubmed/18098299
certainly support the view that the degree of fibrosis can be very heterogenous throughout the liver - I share your suspicions about sampling error.
Unfortunately, we were given neither pics nor text at the time, but we're due to meet with the Hepatologist in 2 weeks, and my understanding is that we'll get the report then (I am under the impression that it will be written summary, but I'll ask about pics when the time comes.)
My husband actually has had no evidence of enlarged spleen by all criteria: phys exam, Ultrasound or CT scan. There was no evidence of portal hypertension, either, on scans (hmm... but should we presume mild undetected portal hypertension because of the presence of 'trace' varices?). The difficulty and uncertainty (as I'm know you're struggling with some) is that, in my husband's case, there was no 'evidence' of cirrhosis on scans, either, so go figure. From my experience, the biopsy is the best we have ... but even there, I tend to think there is more 'sampling error' than is admitted to.
My husband's definitive diagnosis of cirrhosis Stage 4 was based on a 13x6x3 cm piece of adipose liver tissue removed at resection (left lobe removal) so in his case, gross and microscopic pathology had lots to work with, so there's no question. (I didn't post in your other thread about F3/F4, because I thought this was probably not really a great help to you... my husband seems to be rather atypical in that most of his bloodwork in the past 9 months has been high normal, too, so I think it sorta further reinforces your doubts about reliable indicators, rather than removing them. )
Wishing I could be more helpful. ~eureka
My husband actually has had no evidence of enlarged spleen by all criteria: phys exam, Ultrasound or CT scan. There was no evidence of portal hypertension, either, on scans (hmm... but should we presume mild undetected portal hypertension because of the presence of 'trace' varices?). The difficulty and uncertainty (as I'm know you're struggling with some) is that, in my husband's case, there was no 'evidence' of cirrhosis on scans, either, so go figure. From my experience, the biopsy is the best we have ... but even there, I tend to think there is more 'sampling error' than is admitted to.
My husband's definitive diagnosis of cirrhosis Stage 4 was based on a 13x6x3 cm piece of adipose liver tissue removed at resection (left lobe removal) so in his case, gross and microscopic pathology had lots to work with, so there's no question. (I didn't post in your other thread about F3/F4, because I thought this was probably not really a great help to you... my husband seems to be rather atypical in that most of his bloodwork in the past 9 months has been high normal, too, so I think it sorta further reinforces your doubts about reliable indicators, rather than removing them. )
Wishing I could be more helpful. ~eureka
thanks for sharing your husband's information. I'm about to have my 1st endoscopy and am not clear on what the "results" are: photographs of detected varices? a narrative summary? what gets entered into the medical record?
Also, was his absence of spleen enlargement confirmed by ultra-sound or only based on its not being palpable on exam? From recent posts from stage3/stage4s it seemed an enlarged spleen generally accompanies portal hypertension - but your experience indicates this is not always the case( I've gotten very different results regarding the stage of my fibrosis from bxs/fs/blood-marker tests and so am looking for indicators that reliably indicate stage 4/cirrhosis)
Also, was his absence of spleen enlargement confirmed by ultra-sound or only based on its not being palpable on exam? From recent posts from stage3/stage4s it seemed an enlarged spleen generally accompanies portal hypertension - but your experience indicates this is not always the case( I've gotten very different results regarding the stage of my fibrosis from bxs/fs/blood-marker tests and so am looking for indicators that reliably indicate stage 4/cirrhosis)
Love your post comment of the endo. Had to borrow some of it for one of our threads at the B forum:
http://www.medhelp.org/posts/show/447649
http://www.medhelp.org/posts/show/447649
LOL... wondered about that myself... when I asked the nurses what he said, she just grinned and said... "oh, you know, just talking..." (sheesh, now I'm thankful for HIPAA lol)
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