1466 alone needs a dozen such courses. The provision of ENB courses of all types is quite inadequate, while nurses who have graduated from them receiv...

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1466 alone needs a dozen such courses. The provision of ENB courses of all types is quite inadequate, while nurses who have graduated from them receive no extra reward for their efforts. This is the problem to be addressed-many more courses are needed in all branches of intensive care. These should certainly cover the care of children as well as of adults. Addenbrooke’s Hospital, Cambridge CB2 2QQ



SiR,—Dr Anne Simmonds has drawn our attention to the frequent misdiagnosis of 2,8-dihydroxyadenine stones as "uric acid" stones.l Both these urinary stones are radiolucent; and they give identical results with routine colorimetric tests (phosphomolybdate and murexide) and on thermogravimetric analysis. Their ultraviolet absorption spectra in alkaline media are identical. It is therefore not surprising that adenine phosphoribosyltransferase deficiency is misdiagnosed or that there is much delay in diagnosis. As the prognosis for this hereditary disease depends on the renal function at the time of diagnosis, early recognition is important. We report here a simple test to distinguish between urate and 2,8-dihydroxyadenine. One drop of an aqueous solution of each is put on a piece of filter paper. This is placed in a metal dish and liquid nitrogen is poured over it. The filter paper is then exposed to ultraviolet light (366 nm) for a few seconds. When the light is switched off, the 2,8-dihydroxyadenine spot glows brightly .with a sky-blue phosphorescence lasting 21 s. Uric acid does not phosphoresce. also

University Department of Therapeutics, Royal Hallamshire Hospital, Sheffield S10 2JF 1. Simmonds HA.

2,8-dihydroxyadenuria, 1979; 12: 195.

J. L.



a unc




not a uric


stone? Clin Nephrol


SIR,-Parvovirus B 19 infection has been associated with aplastic crisis in patients with chronic haemolytic anaemias and erythema infectiosum (fifth disease) in children. In adults, and in women especially, arthralgia is a common manifestation of parvovirus B 19’ infection. The B19 parvovirus may also pose a serious risk to the fetus after maternal infection. We report a serologically proven B 19 infection associated with an acute pseudosurgical illness. A 27-year-old man was admitted to hospital on May 4,1987, with fever (39’6°C) and an intense abdominal pain in the right lower quadrant with irradiation to the lumbar region, the pain had begun 1 day before examination. There was no history of diarrhoea, vomiting, cough, or coryza. Physical examination revealed an easily palpated abdomen except for the right lower quadrant where the pain with irradiation to the back was intense but not associated with guarding. Rectal examination was unremarkable. An X-ray and ultrasound scan of the abdomen were normal. The leucocyte count on admission was 18 000/1 (differential not done) and the

haemoglobin was 15g/dl. Urineanalysis was normal. Serum amylase was 71 IU/1. Bacterial enteropathogens were not recovered from faecal specimens. During the next 48 h, the abdominal pain disappeared and the leucocyte count became 6900/il with 58% segmented neutrophils, 21 % lymphocytes, 19% monocytes, and 2% eosinophils. Diagnosis of acute viral mesenteric lymphadenitis advocated. There was no serological evidence, in a serum specimen taken on May 6, of the man having been infected with Yersinia pseudotuberculosis, Y enterocolitica, adenovirus, cytomegalovirus, Epstein-Barr virus, influenza viruses A and B, measles virus, or chlamydia. However, solid-phase enzyme immunocapture assay for human parvovirus infection (monoclonal antibody to B 19 was a gift of Dr B. J. Cohen, Central Public Health Laboratory, London) revealed virus-specific IgM. No rheumatoid factor was detected by a latex agglutination test (Behring). Sera before and after May 6 were unavailable.

There are many illnesses which may mimic the symptoms and the signs of an "acute abdomen". Adenovirus and enterovirus have been circumstantially associated with mesenteric adenitis and pseudoappendicitis.1-2 Our case does not provide definitive evidence for a pathogenic relationship between B19 and acute mesenteric lymphadenitis, in the absence of detection of B 19 antigen or DNA in blood or mesenteric lymph-nodes. Nevertheless some animal parvoviruses do infect lymphatic cells,3canine parvovirus enteritis has been associated with enlarged mesenteric lymph-nodes,4 and a higher titre B 19 viraemia was detected by looking at buffy coat cells rather than serum.s Abdominal pain and lymphadenopathy have been reported during outbreaks of fifth disease’ and in cases of aplastic crisis.’ The case described here suggests a possible role for parvovirus B 19 in the pathogenesis of pseudoappendicitis or acute mesenteric lymphadenitis. F. MORINET Laboratory of Bacteriology-Virology, and Departments of Medicine J. J. MONSUEZ and Surgery, P. ROGER Hôpital Saint-Louis, 75010 Pans, France Y. PEROL TM, Steyn JH Viruses in lymph nodes of children with mesenteric adenitis and intussusception. Br Med J 1962; ii. 700-02. Liebman WM, St Geme JW. Enteroviral pseudoappendicitis. AmJ Dis Child 1970,

1. Bell 2.

120: 77-78. 3.

Siegl G. Biology and pathogenicity of autonomous parvovirus. In: Berns KI, ed The parvoviruses. New York: Plenum, 1984: 297-362.

4. Afshar A Canine parvovirus infections: a review. Vet Bull 1981; 51: 605-12 5 Kurtzman GJ, Ozawa K, Cohen B, Hanson G, Oseas R, Young NS. Chronic bone marrow

failure due to persistent B19 parvovirus

infection. N Engl J Med 1987; 317:


Cramp HE, Armstrong BDJ. Erythema infectiosum: an outbreak of "slapped cheek" disease in north Devon. Br Med J 1976; i 885-86. 7. Bertrand Y, Lefrère JJ, Leverger G, et al. Autoimmune haemolytic anaemia revealed by human parvovirus linked erythroblastopenia. Lancet 1985; ii: 382. 6.


SIR,—The prolonged administration to rats of powerful inhibitors of acid gastric secretion has resulted in sustained high plasma levels of gastrin.l,2 We report a case in which nearly continuous treatment for 6 years with Hz-blockers resulted in a reversible hypergastrinaemia and an increase in basal and stimulated gastric acid secretion. A 29-year-old man in whom duodenal ulcer disease had started at the age of 13 years, came to our outpatient clinic in 1981. Gastric acid secretion and serum gastrin response to a meal were normal. The patient did not drink coffee or alcohol and he did not smoke. He had severe pain with frequent relapses. After 8 weeks of successful treatment with full-dose cimetidine he was prescribed a long-term maintenance dose. During the first 3 years he was put on full-dose therapy two or three times a year because of clinical and/or endoscopic recurrences that often followed a few days of treatment discontinuation. For the next 3 years the patient continued the treatment on his own. He came back to our clinic in November, 1986, with a severe recurrence. For the 6 years 1981-86 he had been on cimetidine 400 mg daily for 27 months, ranitidine 300 mg and 150 mg for 34 months, and lastly famotidine 40 mg for 2 months. We discontinued the treatment for 7 days and measured gastric acid secretion, basal serum gastrin, and gastrin response to a meal. His basal serum gastrin (250 pmol/1) was 2-5 times the upper limit of normal (100 pmol/1).’ The gastrin response to meal was abnormal


Basal and meal stimulated and 1986 (open).



gastrin in