Improved method for the estimation of plasma ammonia by ion exchange

Fenton, J. C. B.; Williams, A. H.

doi:10.1136/jcp.21.1.14

Cited by 29 publications

(9 citation statements)

References 4 publications

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“…9 We have no experience of measuring ammonia levels in healthy preterm and term babies. However, using a microversion ofthe cation exchange column, Oberholzer et al10 found the plasma ammonia level for venous samples from neonates was 60 ,umol/l (SD ± 20) and for capillary samples 86 Vmol/l (SD ± 20).…”

Section: Discussionmentioning

confidence: 99%

Plasma ammonia levels in newborn infants admitted to an intensive care baby unit.

Beddis¹,

Hughes²,

Rosser³

et al. 1980

Archives of Disease in Childhood

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suMMARY A fatal case associated with severe hyperammonaemia is described in which no urea cycle enzyme deficiency could be found. This prompted further investigation of blood ammonia levels in neonates admitted to the premature baby unit at Hammersmith Hospital. 102 specimens were taken from 42 babies within the first 3 weeks of life; the babies had a variety of clinical conditions. The mean ammonia level was 94.5 ,mol/l (132.3 ±g/ 100 ml) (range 32-255 ,umol/l (44.8-357 jig/ 100 ml), SD ± 41.0). These results, although higher than the range for older babies in hospital,were not as high as in the baby with severe hyperammonaemia. Serial levels in 10 babies suggested that the range of blood ammonia levels was greatest in the first 2 weeks of life and narrowed considerably after this period. Great care is needed in collecting blood samples and measuring them if accurate results are to be obtained.In 1977 a fatal case associated with severe hyperammonaemia was seen at Hammersmith Hospital. A plasma ammonia level taken 3 hours before death was 3000 ,umol/l (4200 ,ug/100 ml) and cerebrospinal fluid taken shortly before death showed a level of 4000 tumol/l (5600 Fg/100 ml). A liver biopsy was taken immediately after death, but no enzyme defect of the urea cycle could be found, and investigations for organic aciduria did not show an inborn error in branch-chain amino-acid metabolism. The clinical details are given below.Three cases of severe hyperammonaemia in the neonatal period were reported by Pollack et al.l and 5 more were reported by Ballard et al.2 In none of these babies was an enzyme defect observed, and no explanation for the cause could be found, but it was suspected that hyperammonaemia in the neonatal period might not be a rare occurrence. Case historyA boy was born normally to a 22-year-old primigravida at 35 weeks' gestation after spontaneous onset of labour. The Apgar score at one minute was 9. The birthweight was 2-58 kg (10th centile) and, apart from slight grunting, no abnormalities were noted initially. Milk feeds were started via nasogastric tube at 2 hours. The grunting continued for 14 hours and at this stage the baby was noted to be irritable but no cause for this was apparent.At 24 hours his skin became mottled and he developed gasping respirations; blood sugar, urea and electrolytes, calcium, magnesium, and cerebrospinal fluid were all normal. The only abnormal finding was a metabolic acidosis. At 26 hours the baby had generalised convulsions which could not be controlled satisfactorily. In seeking an explanation for the deteriorating condition, a metabolic disorder was considered and a plasma ammonia level estimated with the result already mentioned above.However, the urea cycle enzyme activities measured in the liver biopsy (taken shortly after death) by the method of Brown and Cohen,3 as described by Levin,4 did not show any defect. The analysis of urine for organic acids by gas chromatographic and mass spectrometric methods of Chalmers et al.5 also failed to show an inborn error of orga...

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Section: Discussionmentioning

confidence: 99%

Plasma ammonia levels in newborn infants admitted to an intensive care baby unit.

Beddis¹,

Hughes²,

Rosser³

et al. 1980

Archives of Disease in Childhood

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“…Urea concentration was estimated by the urease method. Ammonia concentration before and after incubation with urease was estimated by a modification of the method of Fenton & Williams (1968) with 5 ml of sodium hydroxide (100 mmol/l) for elution and Nessler's reagent for colour development. The pH of samples incubated with urease was first adjusted to pH 6.6 with Sorensen's phosphate buffer [ K H z PO4 (0-067 mol/l) adjusted to pH 6.6 with NazHP04 (0-067 mol/l)] and 0.1 ml of jack-bean urease suspension (25 mg in 5 ml of ammonia-free water) was added.…”

Section: Zleostomy Ureamentioning

confidence: 99%

The Role of the Colon in Urea Metabolism in Man

et al. 1976

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1. The urea content of ileostomy effluent has been measured by the urease method as an indirect estimate of the urea concentration in the lumen of the normal ileum. 2. The plasma disappearance of intravenously administered[14C]urea was used to study intestinal urea breakdown. Normal subjects on high and low protein diets and patients with either excised (i.e. with ileostomies) or excluded colons were studied. 3. The 24 h intestinal urea breakdown was considerably greater than the quantity of urea estimated to be entering the colon from the ileum and across the colonic mucosa. 4. Intestinal urea breakdown increased with increase in dietary protein and decreased with, but was not abolished by, exclusion or excision of the colon. 5. Our results suggest that the colonic lumen is not the only site of intestinal ureolysis and that significant quantities of urea must be broken down either at a juxtamucosal site or in the ileum.

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“…Where required urea was added to the tube when the pump was switched on. AMMONIA AND UREA MEASUREMENT Ammonia was estimated as described by Fenton and Williams (1968). Urea was measured by the diacetyl monoxime technique on the AutoAnalyzer.…”

Section: Continuous Culturementioning

confidence: 99%