Ethanol gout with

The risk of gout increases as the serum uric acid concentration increases, and approximately 30% of patients with levels greater than 10 mg/dL (greater than 595 pmol/L) develop symptoms of gout within 5 years. However, most patients with hyperuricemia are asymptomatic. Other risk factors for gout include obesity, ethanol use, and dyslipidemia. Gout is seen frequently in patients with type 2 diabetes mellitus and coronary artery disease, but a causal relationship has not been established. 

DETAILS - Colchicine is a plant drug used in the treatment of gout. It is a very efficient poison in view of its very low toxic dose and the fact that an autopsy will show only the symptoms of acute gastroenteritis. This does not, however, mean it is undetectable. It only means that it is likely to be overlooked. It is also very useful as a dart poison, especially when nicotine is used as a binder. Colchicine is great for small caliber (,22)bullets, as they usually won t hold enough of most other poisons to do any good. It dissolves slowly in water, but faster in dilute ethanol (liquor). As with any plant alkaloid, it is best to harvest the... 

Ethanol has also been implicated as the cause of acute gout in four patients with unstable angina who received intravenous infusions of glyceryl trinitrate (104). 

Fig. 13 Sensor output voltage Gout and change Ad of the gel layer thickness during the reswelling process of an initially water-swollen PNlPAAm (MBAAm 4) gel in solutions with different ethanol contents. Reprinted from (Guenther et al. 2008) with kind permission from Elsevier...

Acute gout is triggered by the tissue deposition of sodium urate crystals which cause an inllammatory response. In the chronic situation, tophaceous deposits of sodium urate may form in the tissues (Fig. 4). Gout is exacerbated by alcohol. The reason for this is twofold. Ethanol increases the turnover of ATP and urate production. Ethanol in excess may cause the accumulation of organic acids w hich compete with the tubular secretion of uric acitl. Disorders such as ethanol intoxication, diabetic ketoacidosis and starvation lead to elevations of lactic acid. (3-hydroxybutyric acid and acetoacetic acid, and will cause hyperuricaemia. 

Another consequence of the very high NADH/NAD ratio is that the balance in the lactate dehydrogenase reaction is shifted toward lactate, resulting in a lacticacido-sis (see Fig. 25.6, circle 6). The elevation of blood lactate may decrease excretion of nric acid (see Fig. 25.6, circle 7) by the kidney. Consequently patients with gout (which results from precipitated uric acid crystals in the joints) are advised not to drink excessive amounts of ethanol. Increased degradation of purines also may contribnte to hyperuricemia. 

Five patients with primary gout and an equal number of normo-uricaemic volunteers were studied in a metabolic ward. Prior to admission they received a low purine, alcohol-free diet for one week and gout patients discontinued all medication apart from colchicine. In hospital they were maintained on an iso-caloric, constant purine diet for five days. On days 3 and 4 they drank 2.8 litres of beer between 12.00 - 16.00 h. containing 1.Immol total purines and 53g ethanol. Days 1, 2 and 5 were control... 

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