A new word for hope!

http://www.timesonline.co.uk/article/0,,2087-2372358.html

The Sunday Times September 24, 2006


Drug may heal livers of chronic alcoholics
Sarah-Kate Templeton, Health Correspondent

BRITISH scientists have discovered a drug that could cure liver disease, even in alcoholics who continue drinking.

The medicine, found by a team of doctors and scientists at Newcastle University, could become a potential alternative to liver transplants.

Until now cirrhosis of the liver, caused by alcohol, obesity or the hepatitis C virus, was considered incurable in all but the rarest of cases. The only option for patients in the final stages of liver disease was to wait for a liver transplant. However, because of organ shortages many die while on the waiting list.

Clinical trials of the drug Sulphasalazine are expected to begin in Britain next year. If these prove successful, the drug could be used to treat heavy drinkers, whose plight was recently illustrated by George Best, the former Manchester United footballer who died from liver disease last year.

Sulphasalazine, which already has a licence to treat arthritis and inflammatory bowel disease, acts by preventing scarring from developing on the liver.

Tests carried out in the laboratory and on animals have shown that the medication can even reverse damage already inflicted on the liver.

The drug will initially be given to heavy drinkers who have given up alcohol, but too late for their liver to recover naturally. If this proves successful, the medicine will also be prescribed to alcoholics who continue to drink but show a determination to fight their addiction by reducing their intake.

Professor Christopher Day, who heads Britain’s biggest team of liver specialists at Newcastle University, said: “If you stop a drinker with cirrhosis of the liver from drinking, the cirrhosis will still be there. Even though we remove the cause of the liver scarring, by this stage that is not enough.

“The prospect is that you may be able to continue drinking. If the drug is not too expensive, I may say, of course we have to give these patients advice about drinking, but who are we to say, ‘Just because you are still drinking, we are not going to give you this drug’? I would be of the view that it should be tried in patients who are making an effort.

“I would not give it to someone who continues to drink heavily every day, but if someone had cut down to three pints a night and was really trying, why not give him this drug that might help his liver recover?”

Sulphasalazine may also relieve the ethical dilemmas of distributing scarce donated livers to the most needy and deserving. The decision to give Best a liver transplant was controversial because the late footballer continued drinking. Critics argued that the organ should have been given to someone whose illness was not self-inflicted.

If the drug is not prohibitively expensive, it could be given to all liver disease patients, regardless of whether the damage had been caused by a congenital disorder or years of alcohol abuse.

“This drug is not a finite resource, you are not stealing it from someone else — which is always a worry in public opinion. People are dying on the transplant list,” Day added.

After years of heavy drinking or obesity, so many scars appear on the liver that it can no longer carry out its normal tasks such as storing essential proteins and vitamins while cleaning up toxic substances.

The new use for the drug followed the discovery by Professor Derek Mann, a member of the team at Newcastle University, who identified the cells and proteins that may move the liver disease into reverse.

Mann found that when the liver is injured by a substance such as alcohol, proteins called nuclear factor kappa B encourage particular cells to multiply, which scars the organ. By switching off the nuclear factor kappa B protein, the scarring cells die and stop damaging the liver.

There are 45,000 deaths every year in Europe from cirrhosis of the liver but the number is decreasing.

In Britain, by contrast, where more than 4,000 die every year, the number of deaths from cirrhosis is increasing amid growing concern about the country’s so-called binge-drinking culture.

Doctors report that increasing numbers of young people, including women, are succumbing to liver disease caused by heavy drinking and poor diet.

Between 5% and 10% of people in the UK are unaware of having liver disease, which can be diagnosed by simple blood tests. Help is often sought when the symptoms become severe, which is too late for treatment.

Reseach spend per life lost for liver disease is amongst the lowest for all conditions — only respiratory medicine ranks lower.


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It's here!

At last – the clinic letter from Birmingham has arrived! It was worth the wait just for the sentence “Hannah is lovely [not very medical, but who cares] and is really very well compensated.” Compensated, in terms of liver disease, means that although the liver is damaged, it is functioning normally. Decompensation is when the liver begins to lose its function.

So, here is the long awaited ultrasound report, described by Dr McKiernan as “fine”, which will do very nicely, thank you.

Comparison has been made with the last scan dated 11.10.04. The liver is now slightly coarse in echotexture. No biliary dilatation. The PV measures 7.1 mm at the liver edge and has a flow of 31.6 cm/s into the liver. The HVs, IVC and SV are patent with normal directional flow. The hepatic artery RI = 0.69. The spleen is enlarged measuring 10.7 cm in length (previously 7.0 cm). No obvious spleno-renal shunt noted. The midline structures are obscured by overlying bowel gas. Both kidneys are normal. Right renal length = 7.3 cm (55th centile), previously 5.6 cm. Left renal length = 7.2 cm (55th centile), previously 5.9 cm. Normal urinary bladder. No free fluid.

Right, so overall this is good, and here is my attempt at interpretation:

The liver is now slightly coarse in echotexture Not great, this is indicative of a damaged liver, but at least it is only slightly.

No biliary dilatation I think this is good, and assume it means her bile ducts are not dilated.

The PV measures 7.1 mm at the liver edge and has a flow of 31.6 cm/s into the liver PV = Portal Vein. I haven’t found any normal values for this, but I think this is pretty good. If the portal vein flow is too slow, this is what causes portal hypertension.

The HVs, IVC and SV are patent with normal directional flow This is obviously good as it contains the words patent and normal. I’m guessing that this is about blood flow, and thinking that HVs = Hepatic Veins, IVC = Inferior Vena Cava, SV = Superior Vena [Cava].

The hepatic artery RI = 0.69 RI = resistance index. I think that this is good, although have not managed to find out much about it apart from above 1.0 or below 0.5 is bad.

The spleen is enlarged measuring 10.7 cm in length Not great, as this is the spleen size for a 10 year old child.

No obvious spleno-renal shunt noted Good; new pathways are not forming to cope with restricted blood flow.

The midline structures are obscured by overlying bowel gas The last US said this too, and I still have no clue what it means.

Both kidneys are normal. Right renal length = 7.3 cm (55th centile), previously 5.6 cm. Left renal length = 7.2 cm (55th centile), previously 5.9 cm. Normal urinary bladder Obviously good.

No free fluid No ascites, so good.

So, no nasty surprises lurking inside then! It feels very good to look at Hannah and know that what I can see on the outside is not too far off what is happening inside. I am very thankful that there is no diagnosis of portal hypertension.

Of course, being me, I am still left with questions, and things I would like to know more about. How is Hannah’s spleen so enlarged without being detectable by physical examination? I thought it followed the same rule as the liver, that it should match up with the bottom of the ribcage; and if it can be felt, then it is enlarged and vice versa. I also thought the enlarged spleen was a symptom of portal hypertension, which she does not appear to have. Could she have had PH when her liver was more inflamed when she was younger, which then resolved when the inflammation went down? I’m also keen to properly understand the portal vein flow and hepatic artery numbers; I just can’t help myself. I will be asking those questions of my knowledgeable buddies over at Liver Families.

The follow up at Birmingham will be next summer; no ultrasound scheduled, so there is plenty to smile about.

BIG sigh of relief.

No ultrasound report yet...

...but hopefully soon! I rang Dr McKiernan's secretary; the poor woman was on holiday for two weeks with no-one to cover, and she seems to have far too much to do anyhow. I wanted to check that it hadn't gone astray, as problems with our post are fairly common occurances, but no, she hadn't typed it up yet. I bet it will arrive and not contain the full US report, and I will have to ring Liver Direct and ask them to send me one out.

I am very proud that I have managed to add a photo strip to the blog (I needed help from Andy with the HTML to position it in the middle) and I love the contrast between the tiny sick yellow baby and the fun loving healthy toddler. Unfortunately the photos are in backwards order and I'm not sure how to fix that, but I'm sure I'll be a multimedia blogging queen in no time.

Hannah has a few things coming up in the next couple of months...flu and pneumococcal jabs, and bloods at the end of October. Then, hopefully, a quiet six months.