back to basics – liver problems

[boss_hogg]

Hii All,

The forums and info on the site are fantastic, but sometimes a little technical, especially if you 'join' them in the middle of a thread. So, i'd like some information if someone is kind enough, on liver readings. What has this got to do with gout, what should i be looking for?

Background: I'm 43, very overweight, heavy drinker, high blood pressure. I'm doing things about it – lost 20kg (45lbs) in the last year, started exercising again etc etc. Still drink too heavy though (can be half bottle vodka a night, most nights). I've had a few gouty niggles, but only 2 acute attacks in the past 8 years. My third one has been this week, one of those crippling ones/can't walk.

This attack was my first on colchicine 1mg – 3 tab first 2 days, 2 tabs for next couple days, then one per day for next 7 days. After 1 week, flareup has almost gone. (and NO side effects!)  The attack came because the last 2 months I've let things go – diet and exercise went out the window, then went on holiday to an “all inclusive” hotel deal and really took the piss. Also, i ran out of blood pressure tablets for 2 weeks, and pressure soared from 150/90 to 180/130. I think this was the main contribution to the flare up.

Ive never took allupurinol. I've only had 2 blood test for UA in 8 years (7.4 and 8.1), and they were right at the beginning when i only had a sore toe.

So, today here is the new me. Back on diet, loads of fruit/veg. Started using urine PH strips, ordering a UA meter, going back to the docs to ask for a blood test and to get AP prescribed. This got me thinking about the liver readings that i've seen mentioned on the forums. So, after all that longwinded intro, what i want to know is what liver readings i should be asking for, are they taken by blood or urine, and what i should be concerned about?

Thanks !

[zip2play]

You just ask for a “Liver Panel.” 

It's done with a small blood draw and usually includes around 5 items, always including ALT,  AST, and bilirubin.

If you want to familiarize yourself with some of the specifics, here's a good overview:

http://www.labtestsonline.org/understanding/analytes/liver_panel/test.html

[odo]

apas.org.uk/liver-function-tests.asp [link now invalid]

Alcohol can also make Allopurinol less effective due to it being expelled quicker.

[zip2play]

Odo,

Do you have a source for that alcohol – allopurinol excretion increase connection?

Allopurinol is usually eliminated by rapidly being oxidized to oxypurinol by xanthine oxidase, and permanently tying up the enzyme. rather than by urinary excretion…although it DOES occur. 

Then the oxypurinol is slowly excreted by the kidneys.

[odo]

Only the best

http://www.goutpal.com/allopurinol.html

PS. Your query prompted me to have another search: found this (but no date):

“A continued high alcohol intake may also impair the response to allopurinol therapy by inhibiting the conversion of the drug to its active metabolite, oxipurinol. This results in reduced oxipurinol plasma levels, increased urinary excretion of unmetabolized allopurinol, and hence reduced urate-lowering effects. It follows that urate-lowering drugs are often less effective in patients with gout who continue to drink.”

https://www.jrheum.com/subscribers/02/07/1350.html

[zip2play]

Thanks odo,

I'll add that to my gout lexicon.

A natural follow-up thought/question/musing. If alcohol “inhibits the conversion of allopurinol to oxypurinol” can we assume it interferes with the action of xanthine oxidase? That would seem logical.  Interfering with the action of the enzyme might also decrease the more  ”normal ” action of XA, the conversion  xanthine and guanine to uric acid. If so the net result of alcohol might be positive or negative.

I have a vaguely  similar situation with losartan…the drug eliminates uric acid and all it's homologues, thus it dumps uric acid, allopurinol, zanthine, oxypurinol. But the net effect is a slight lowering of SUA. so it is considered uricosuric.

I guess the question would be answered with a good study of gouties on 300 mg. allopurinol. Measure SUA before the study and have half the group party hearty with copious cocktails for a month…and the other have teetoal while they watch TV. After 30 days measure everyone's SUA again. With a big enough group you could have 1/3 of the drinkers on wine, 1/3 on beer, and 1/3 on hard stuff.

(If the booze is good I would be HAPPY to volunteer, unless they put me in the control group…that would cost them money.)

An interesting thought: both alcohol and allpurinol are found to benefit patients in long term heart failure. A reasonable premise is that perhaps each of these agents interferes with xanthine oxidase, thus sparing blood vessels from damage…both agents may this be protective fpor the same reason.

A good study:

Effects of Xanthine Oxidase Inhibition With Allopurinol on Endothelial Function and Peripheral Blood Flow in Hyperuricemic Patients With Chronic Heart Failure Results From 2 Placebo-Controlled Studies

Wolfram Doehner, MD^*; Nina Schoene, MD^*; Mathias Rauchhaus, MD; Francisco Leyva-Leon, MD; Darrell V. Pavitt, MSc; David A. Reaveley, PhD; Gerhard Schuler, MD; Andrew J.S. Coats, DM; Stefan D. Anker, MD, PhD; Rainer Hambrecht, MD

From Clinical Cardiology, National Heart and Lung Institute, Imperial College School of Medicine (W.D., M.R., F.L.-L., A.J.S.C., S.D.A.), and the Department of Clinical Chemistry, Charing Cross Campus, Imperial College School of Medicine (D.V.P., D.A.R.), London, UK; and the Franz-Volhard-Klinik (Charité, Campus Berlin Buch) at Max Delbrück Centrum for Molecular Medicine, Berlin (W.D., S.D.A.), and the University of Leipzig, Division of Cardiology, Heart Center, Leipzig (N.S., G.S., R.H.), Germany.

Correspondence to Stefan D. Anker, MD, PhD, Clinical Cardiology, NHLI London, Dovehouse Street, London, SW3 6LY, UK. E-mail [email protected]

Background— In patients with chronic heart failure (CHF), hyperuricemia is a common finding and is associated with reduced vasodilator capacity and impaired peripheral blood flow. It has been suggested that the causal link of this association is increased xanthine oxidase (XO)–derived oxygen free radical production and endothelial dysfunction. We therefore studied the effects of XO inhibition with allopurinol on endothelial function and peripheral blood flow in CHF patients after intra-arterial infusion and after oral administration in 2 independent placebo-controlled studies.

Methods and Results— In 10 CHF patients with normal serum uric acid (UA) levels (315±42 µmol/L) and 9 patients with elevated UA (535±54 µmol/L), endothelium-dependent (acetylcholine infusion) and endothelium-independent (nitroglycerin infusion) vasodilation of the radial artery was determined. Coinfusion of allopurinol (600 µg/min) improved endothelium-dependent but not endothelium-independent vasodilation in hyperuricemic patients (P<0.05). In a double-blind, crossover design, hyperuricemic CHF patients were randomly allocated to allopurinol 300 mg/d or placebo for 1 week. In 14 patients (UA 558±21 µmol/L, range 455 to 743 µmol/L), treatment reduced UA by >120 µmol/L in all patients (mean reduction 217±15 µmol/L, P<0.0001). Compared with placebo, allopurinol improved peak blood flow (venous occlusion plethysmography) in arms (+24%, P=0.027) and legs (+23%, P=0.029). Flow-dependent flow improved by 58% in arms (P=0.011). Allantoin, a marker of oxygen free radical generation, decreased by 20% after allopurinol treatment (P<0.001). There was a direct relation between change of UA and improvement of flow-dependent flow after allopurinol treatment (r=0.63, P<0.05).

Conclusions— In hyperuricemic CHF patients, XO inhibition with allopurinol improves peripheral vasodilator capacity and blood flow both locally and systemically.

If XO inhibition occurs with alcohol, then the same concusion is likely. It may very well be the route of cardiac protection seen for drinkers.

[trev]

Three cheers for Grog Blossom then,  🙂 🙂 🙂

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