How often/When is endoscopy necessary?

[eureka254]

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.

[eureka254]

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!

[HectorSF]

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

[eureka254]

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.)

[HectorSF]

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

[merryBe]

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.

[willing]

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.