Search

Background: Prospective follow-up of heroin users is known to be difficult due to their unstable lifestyle, and high follow-up rates have usually demanded major tracking efforts. In Sweden, mobile telephones are commonly used by heavy drug users for drug trading., Objectives: This methodology study aims to examine the efficacy of mobile telephone contact for prospective follow-up interviews with injecting heroin users recruited at the syringe exchange program of Malmö, Sweden., Methods: Seventy-eight heroin users with mobile telephone numbers were included. Subjects reported using heroin for 28 days of the previous 30 days, and only 8% reported they had recently been engaged in work or studies. Clients were contacted between 15 and 21 times over 2 years, with each contact attempt generally involving two telephone calls on consecutive days., Results: During follow-up, 68% of subjects had been successfully contacted for at least one follow-up interview (on average 6.9 interviews), and 25% of follow-up attempts were successful. In 23% of the sample (n=18), at least 50% of follow-up attempts were successful, and these subjects tended to be older (p=.05) and more likely to be female (p=.07), whereas follow-up rates were unrelated to baseline heroin use., Conclusions and Scientific Significance: Despite limited effort, and despite the severe situation of intravenous heroin users, mobile telephone contact can be used with heavy drug users in the present setting., (Copyright © Informa Healthcare USA, Inc.)

Background: Glucocorticosteroid enemas are equally effective as 5-ASA enemas in the treatment of active distal ulcerative colitis (UC). With the introduction of budesonide, the risk of systemic side effects may be reduced. We investigated whether budesonide enema, 2 mg/100 ml, administered twice daily (b.i.d.) could increase the remission rate in comparison with the once daily (o.d.) standard regimen. Furthermore, we evaluated whether 2 mg budesonide enema, given twice weekly, could have a relapse preventing effect., Methods: 149 patients with active distal UC were treated in a controlled, double-blind multicentre study with two parallel groups: placebo enema in the morning and budesonide enema in the evening (i.e. 2 mg/day) or budesonide enema b.i.d. (i.e. 4 mg/day) until remission (absence of clinical symptoms and endoscopic healing) or at most 8 weeks. Patients in remission were randomized to either budesonide enema or placebo enema twice weekly for 24 weeks or until relapse., Results: The remission rates at 4 weeks were 33% for o.d. and 41% for b.i.d. regimens (NS) and correspondingly 51% and 54% at 8 weeks (NS). The b.i.d. group had an increased frequency of impaired adrenal function, 32% versus 4.8% (P = 0.001). The relapse rates during maintenance treatment with budesonide enema and placebo were 15% versus 24% after 8 weeks, 31% versus 27% after 16 weeks and 41% versus 51% after 24 weeks (NS)., Conclusion: Budesonide enema 2 mg o.d. appears to be the optimal dosage in active distal UC. We could not show that budesonide enema twice weekly is sufficient to maintain remission.

The effect of fat emulsion in the upper intestine on the maximal gastric acid response to pentagastrin was studied in chronic gastric fistula (GF) rats with a 4-cm blind loop of the duodenum anastomosed to the jejunum (Roux-en-Y). Fat emulsion in the loop inhibited the acid response by 85%. To localize the site of the inhibitory mechanism, GF rats were provided with Thirty-Vella loops of the duodenum (bile and pancreatic ducts transplanted to the proximal jejunum) or with Thirty-Vella loops of the proximal jejunum and a Roux-en-Y loop of the duodenum to prevent gastric juice from entering the duodenum. Perfusion of the duodenal loop with fat emulsion mixed with bile and pancreatic juice reduced the acid response by 49%, but perfusion of the proximal jejunal loop did not alter the response. It is concluded that the intestinal mechanism for inhibition of acid secretion by fat is located in the duodenum in rats.

In chronic gastric fistula rats 0.20 M HCl and 1200 mOsm X kg-1 solution of polyethylene glycol (PEG) infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced maximal inhibition of pentagastrin-stimulated acid secretion, which amounted to 60% and 50%, respectively. In the present study in Roux-en-Y rats with gastric fistula, perfusion of the loop with hyperosmolal (1200 mOsm X kg-1 of PEG solution) 0.20 M HCl produced a greater reduction of the maximal response to pentagastrin (91% inhibition) than perfusion with 0.20 M HCl (64%), suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. The maximal acid response to histamine was more resistant to inhibition than that to pentagastrin; 0.20 M HCl inhibited secretion by 43%, 1200 mOsm X kg-1 of PEG solution by 42%, and hyperosmolal 0.20 M HCl by 60%. The results suggest that HCl and hyperosmolal solution also inhibit histamine-stimulated secretion by different mechanisms. The anatomical sites of the mechanisms remain to be established.

The effect of duodenal acid perfusion on pentagastrin-stimulated gastric acid secretion was studied in Sprague-Dawley rats provided with a chronic gastric fistula, gastroenterostomy, and a 4-cm blind duodenal loop anastomosed to the jejunum. During maximal acid stimulation with intravenous pentagastrin (16 micrograms X kg-1 h-1) the loop was perfused with 0.15 M NaCl or 0.05 M, 0.10 M, or 0.20 M HCl at a rate of 2 ml X h-1. Perfusion with 0.05 M HCl did not significantly alter pentagastrin-stimulated secretion. 0.10 M and 0.20 M HCl reduced the 2-h acid response by 56% and 63%, respectively. Acid secretion returned to control level after cessation of acid perfusion. It is concluded that physiological amounts of HCl in the duodenum inhibits maximal acid secretion stimulated by pentagastrin in rats.

In chronic gastric fistula (GF) rats, HCl and a hyperosmolal solution of polyethylene glycol (PEG) in the upper intestine inhibit pentagastrin-stimulated gastric acid secretion by different mechanisms, but their anatomic sites have not yet been established. In the present study GF rats were provided with Thiry-Vella loops of the duodenum and the bile and pancreatic ducts transplanted to the proximal jejunum, or with Thiry-Vella loops of the proximal jejunum. In the latter rats the duodenum was anastomosed as a blind loop to the jejunum to prevent any gastric juice from entering the duodenum. Duodenal loop perfusion with 0.20 M HCl inhibited the acid response to pentagastrin by 62%, but perfusion with 1200 mOsmol x kg-1 of PEG solution did not alter the response. In contrast, acidification of the proximal jejunal loop did not alter but hyperosmolality inhibited the response by 41%. The study shows that the mechanism for inhibition by intestinal acidification is confined to the duodenum and that for inhibition by hyperosmolality is located in the proximal jejunum--but whether only to the proximal part is unknown.