Azapropazone--a treatment for hyperuricaemia and gout?

In a metabolic ward study of five patients, azapropazone lowered plasma uric acid but exerted only a modest and variable uricosuric effect without altering urinary xanthine and hypoxanthine levels. An alternative mechanism other than uricosuria or xanthine oxidase inhibition must account for some of the hypouricaemic action of this drug. During the first day of treatment urine volume and pH declined sharply. In a separate investigation, 22 patients were given azapropazone and 18 were given allopurinol combined with colchicine for 3 months. Allopurinol reduced plasma uric acid more quickly but at the end of the study there was little difference in the hypouricaemic results achieved by both drugs. Recurrent gout occurred more frequently with allopurinol but side-effects were confined to those taking azapropazone. A slight rise in blood urea and creatinine and a fall in haemoglobin were also features of long-term azapropazone treatment.     

High resolution ultrasound characterization of soft tissue masses in children

Forty-two soft tissue masses in infants and children were examined with high resolution ultrasonography. Sonography was diagnostically specific in 17/42 (40%), useful but not diagnostic in 24/42 (58%), and misleading in 1/42 (2%) of soft tissue masses. Lesions with diagnostic sonographic features included cystic hygroma, fibromatosis colli, lymphadenopathy with abscess formation, and one case of osteomyelitis.     

Anomalous leukopoiesis in two patients with Crohn's disease.

Crohn's disease is a major form of chronic inflammatory bowel disease in the western world. The molecular genetic basis of Crohn's disease is unknown. In this study, we present evidence for anomalous leukopoiesis-namely, the generation of a leukocyte subset characterized by aberrant expression of gammadelta T cell receptor (gammadeltaTCR) with or without CD19 on a myeloid background-in two patients with Crohn's disease. The aberrant cells of patient 1 have the surface phenotype gammadeltaTCR + CD19 - CD14 + CD64 +. The aberrant cells of patient 2 have the surface phenotype gammadeltaTCR + CD19 + CD14 - CD64 + CD16 + CD13 + CD33 +. The results presented here are significant both in light of recent speculation that a critical defect in Crohn's disease may be at the level of hematopoiesis and because the CD19 gene lies within the region on chromosome 16 that corresponds with the Crohn's disease susceptibility locus IBD1.     

Fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis.

Recently attempts have been made to demonstrate the possible role of hypergastrinemia in the production of congenital hypertrophic pyloric stenosis in infants. Eleven infants with congenital hypertrophic pyloric stenosis, ranging in age from three to 11 weeks, were evaluated for fasting and postprandial serum gastrin levels. Two to ten weeks following successful pyloromyotomy, a similar evaluation was undertaken to demonstrate the possible role of elevated serum gastrin levels in the etiology of congenital hypertrophic pyloric stenosis. The average fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis did not differ significantly from levels noted in control infants. Similarly, no statistically significant difference was noted between the pre- and postoperative levels of serum gastrin in the affected infants. Several experimental studies have been reported within the past few years describing the production of hypertrophic pyloric stenosis in the offspring of dogs injected with pentagastrin during pregnancy. The results of our study minimize the direct importance of serum gastrin in the production of congenital hypertrophic pyloric stenosis. The role of the hormone secretin in the etiology of this condition is hypothesized.