[Excretion of phenol and p-cresol in the urine in fasting obese individuals and in persons treated with total enteral nutrition]. / Vylucování fenolu a p-krezolu mocí u hladovejících obézních a u osob lécených úplnou enterální výzivou.

In the literature it is maintained that phenol and p-cresol are produced in humans in the gut by bacteria from dietary protein. Both substances are absorbed from the small intestine and excreted in the urine. If the urinary output of phenol and p-cresol depends really on the dietary protein intake it should decline to zero values during fasting and correlate with the protein supply into the gut. The objective of the present work was therefore to investigate the urinary phenol and p-cresol excretion in fasting obese subjects (21 fasting subjects, 7 subjects with modified fasts--Nutramine R-350) and in subjects treated by complete enteral nutrition by a nasojejunal tube (8 patients with Crohn's disease, 8 with another disease of the gastrointestinal tract). Phenol and p-cresol in 24-hour urine specimens were assessed by gas chromatography in all four groups always on the 1st, 7th and 14th day. In fasting obese subjects the phenol and p-cresol values did not decline (the difference of values from the assumed zero value is significant z = 0.000055). There was no difference between patients with a complete and modified fast. The phenol and p-cresol values did not correlate mutually, nor with the protein intake, nitrogen balance and cumulated nitrogen balance. There are great individual differences in the urinary phenol and p-cresol excretion and it does not depend on the oral dietary protein intake, as hitherto assumed. It has most probably more complex causes and the decisive factor seems to be the metabolic activity of the intestinal bacterial microflora.

[Urinary excretion of phenol in Crohn disease during total parenteral nutrition]. / Vylucování fenolu mocí u Crohnovy choroby v prubehu totální parenterální výzivy.

Urinary phenol is a product of dietary tyrosine metabolism generated in the gut by bacteria. In our previous study we found in 42 patients with Crohn's disease a significantly higher level of urinary phenol in terminal ileitis and ileal resection when compared with Crohn's segmental colitis. Urinary phenol is believed to be extensively influenced by diet. For this purpose our present paper investigated urinary phenol in Crohn's disease before and after two weeks of total parenteral nutrition. Spectrophotometric analysis of urinary phenol was carried out in 10 patients (7 males, 3 females). They ranged from 24 to 40 (average 34.9) years of age. The patients received on an average 1.45 g of amino acids/kg/day (no tyrosine; 0.022 g of L-phenyl-alanine/kg/day), 25-30 kcal/kg/day (105-125 kJ/kg/day) in non-protein sources of energy, and fat-emulsions (80 g/day) twice a week. There was a significant decrease in the urinary phenol after two weeks of total parenteral nutrition (median 79.5, interquartile range 41.5 to 288.5 mumols/24 hours vs. median 37.5, interquartile range 0-93.5 mumols/24 hours), p = 0.032 using the paired t-test. In two patients with severe involvement of the gut, urinary phenol, though decreased, remained at higher levels (above 300 mumols/24 hours). A significant decrease of the urinary phenol can be explained in particular by exclusion of dietary proteins, although clinical and nutritional improvement was observed, too. However, persisting higher levels of urinary phenol in some patients with serious involvement of the gut may reflect the severity of Crohn's disease.