Duodenal ulcer complicating intraarterial chemotherapy.
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Biomedical subjects
Publications and source records attributed to A Eliakim.
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Synthesis of prostaglandin E2 and 6-keto prostaglandin F1 alpha by cultured antral and fundic gastric mucosa obtained from 86 patients with active duodenal ulcer who were not receiving medication was 50% lower (p less than 0.01) than their respective synthesis by cultured gastric mucosa in normal subjects. Antral and fundic prostanoid synthesis in patients receiving chronic therapy with nonsteroidal antiinflammatory drugs was almost completely inhibited. The decreased synthesis of antral and fundic prostaglandin E2 and 6-keto prostaglandin F1 alpha in duodenal ulcer patients was not affected following ulcer healing achieved after 4 wk of therapy with placebo, arbacet, misoprostol, sucralfate, and pirenzepine. In contrast, following 4 wk of therapy with ranitidine, both antral and fundic prostaglandin E2 synthesis were significantly increased when compared with their respective synthesis before therapy. These results confirm that gastric prostanoid synthesis is decreased in patients with active duodenal ulcer and in subjects treated with nonsteroidal antiinflammatory drugs, suggesting that decreased endogenous prostanoid synthesis may contribute to the pathogenesis of mucosal damage. The induction of endogenous prostanoids by ranitidine may contribute to its therapeutic effect.
We reviewed 14 randomized controlled trials that involved long-term treatment of patients after myocardial infarction with beta-blockers. Studies in which randomization was carried out at the time of hospital admission were excluded because of a very high rate of early withdrawal before hospital discharge. Seven studies were found methodologically acceptable, and their results were analyzed according to the "intention-to-treat" principle to avoid bias caused by late withdrawals. Although only two of the trials found a significant reduction in total deaths in the beta-blocker groups, pooling the data from all seven studies showed a highly significant treatment benefit (p less than 0.001). The best estimate of the magnitude of the reduction in mortality rates is 26%. Pooling of the data revealed similarly significant reductions in the rates of reinfarction (p less than 0.001) and sudden death (p less than 0.001).
The concept of pituitary refractory period for GH secretion has been previously described. To measure the length of this refractory period we performed an exercise provocation test for GH secretion immediately following multiple overnight GH blood sampling. In addition, we correlated the magnitude of the GH response to a single exercise input with mean overnight GH, IGF-I and circulating IGFBP levels. 23 healthy adolescent females (15-17 yr) performed 10-min constant cycle ergometry at a power normalized to each subject's aerobic and anaerobic capacity. GH was measured every 10 min starting 10 min before exercise and then for 60 min after the exercise bout. Mean nocturnal GH was calculated from overnight values obtained every 20 min over a 12-h period. Pre-exercise GHBP, IGF-I and IGFBPs 1-5 were assessed using standard techniques. In five subjects, a spontaneous GH peak had preceded the exercise test by 1 hour or less, and no response to exercise was found. In the remaining 18 subjects, a GH peak (6.8 +/- 1.3 ng/ml, p < 0.0001) was observed at 32 +/- 4 min after the onset of exercise. The GH response to exercise was not correlated with fitness, mean GH or IGF-I but was correlated with IGFBP-3 (r = 0.65, p < 0.05). Spontaneous GH pulses may acutely render the pituitary refractory to exercise stimuli. The length of this refractory period is approximately 1 hour. The data corroborate the idea that while relationships exist among the various components of the GH-IGF-I axis, no single factor identified to date fully reflects GH-IGF-I "tone".
The purpose of this study was to determine whether growth-related changes in bone properties can be detected in prepubertal boys using quantitative ultrasound (QUS) and to determine whether resistance training stimulates bone changes. Two groups, each of thirty 9-10 year-old boys, participated in regular physical education classes or in resistance training. Tibial speed of sound (SOS) (SoundScan 2000, Myriad) was assessed at the beginning of the school year and after 8 months. At baseline, there were no differences between groups in tibial SOS, anthropometric measures or pubertal development. At the end of the year, the tibial SOS increased (p<0.001) in both groups to a similar extent. In addition, there were no differences in the increases in height between the two groups. This indicates that resistance training during the physical education program did not induce changes in bone beyond what would be expected by the mere effect of growing. We conclude that changes in tibial SOS, as obtained with QUS, can be detected in groups of prepubertal boys over a period of 8 months.
BACKGROUND: The prevalence of urinary tract infection (UTI) in premature infants ranges from 4% to 25%. It is surprising, however, that scant information exists regarding management of UTI in premature infants, particularly the need for radiologic evaluation of the urinary tract and the use of preventive antibiotic therapy after the first episode of UTI occurs. The aim of this study was to answer these questions. PATIENTS AND METHODS: Twenty-seven (8%) premature infants (< 1750 gm birth weight) born during the period from 1990 through 1993 had UTI. Eleven of them were of extreme low birth weight (ELBW) (birth weight < 1000 gm). Ultrasound examination of the urinary tract was performed in all premature infants 7 days after a diagnosis of UTI was made and was repeated 1 month later, if disease was detected. Voiding cystography was performed in 21 premature infants (8 with ELBW) 6 to 8 weeks after a diagnosis of UTI was made. RESULTS: The mean birth weight of premature infants with UTI was 1112 +/- 294 gm. The prevalence of UTI was significantly higher (p < 0.01) in infants with ELBW (13%) compared with that in premature infants with birth weight >1000 gm (6%). The male/female ratio in all premature infants was 2.9:1 and was significantly higher in infants with ELBW (10:1; p < 0.01). Organisms involved were Klebsiella (59%), Candida albicans (15%), Escherichia coli (15%), and Enterobacter (11%). Only premature infants with ELBW had Candida UTI. Five premature infants (four with ELBW) had mild transient hydronephronis, and one had persistent hydronephrosis and hydroureter. Voiding cystography showed that three premature infants had vesicoureteral reflux and that one had a bladder diverticulum. All premature infants with pathologic voiding cystography had birth weight >1000 gm and had normal ultrasound examination. CONCLUSIONS: Premature infants with birth weight 1000 to 1750 gm should be given preventive antibiotic therapy at least until imaging evaluation (ultrasonography and voiding cystography) is complete. Premature infants with ELBW are more susceptible to fungal infection and do not seem to have underlying urinary tract abnormalities. Prophylactic therapy and voiding cystography may be unwarranted in this population subset.