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Prevention of Pneumocystis pneumonia
Notes
142
females whose carrierstate can be diagnosed from 79technique allows diagnosis to be made with 89 uracy. 99 PRWinship(1)
University of Oxford, oxfGrd0x13RE.UK epithelium OSpatients This in vivo study showed that the jejunum of patients
with cystic fibrosis fails to respond to a cholinergic secretory agent, pilocarpine, and a CAMP mediated secretory agent, prostaglandinE2, and that the wavelike changes of the jejtmaltransmucosalpotentialdifference normally associeted with intestinal motor activity in man and animals arc absent in cystic fibrosis. The absent response to secretoryagents corroborates previous in vitro results and confirms that the small bowel shares the defect in CA P-mediated chloride secretion seen in sweat gland and airway epithelia. which is believed to constitute part of the pathophysiology of cystic fibrosis. However, sweat glands can respond to cholinergic agents, which suggests that these agents cause secretion by different mechanisms in the two epithelia. The absence of PD waves with motor activity suggests that these reflect secretion associated with motility. PD traces from patients look strikingly differentto those from healthy controls and could be a useful aid to diagnosis. PSBaxter (2) TheUniversityof Sheffield, SheffieldSIO2TH,UK vtmtim ok?
OCJJS& pneumonk
Pneumocysfis carinii pneumonia occurs in 60% of
patients with AIDS and is the major cause of mortality in these patients. We have previously demonstrated (Ann Inrern Med. Ckt 1987. 107 (4). 495-498) that aerosolized pentamidine is effective for the treatmentof acute pneumocystis pneumonia. We believe that the data published in t5s Lcrncerdemonstratesthat aerosolized pentamidine,given once monthly, is also probably effective for the prevention of Pneumocystis carinii pneumonia. The study suggests that the attack rate is reduced by approximately50% and the time to onset of PCP is prolonged by approximately‘6 months. This effect is independentof zidovudine (AET) administration. We are presently performingdose escalation studies in order to determinewhether PCP is completely preventableby aerosolized pentamidinewithout inducing additional significant toxicity. JEConte(3) TheMedicalCenterat theUniversityof Catifemia, SanFrancis~~ CA94143.USA (1) fmcef (1989)‘i. 631. (2) Lancer(1989) i. 464. (3) Lamer (1989) i, 654.
enal ulcer aad Campylobacterpylorl. Campylobacter pyfori. a Gram-negativespiralorganism,
colonizes the gastric mucosa of most patients with peptic ulcer disease (gastric ulcer SO%,duodenal ulcer 95%) and it is suggested that by causing gastritis, C pyfori weakens the gastric mucosa allowing acid and pepsin to form ulcers. In this study we treated 100 patients with C pylori and duodenal ulcer proven by endoscopy. Half the patients received Tagamet or Tagarnet plus tinidazole (an antibiotic similar to metronidazole):the other klf received De-no1 (bismuth subcitrate) or De-no1 plus tinidazole. The Tagamet or De-no1 were given in standardulcer healing doses for 8 weeks. The antibiotic or a matching placebo were administered concurrently with the ulcer healing drug from day 1 to day 10. During week 10 (2 weeks after finishing treatment)patients were endoscoped to see if the ulcers had healed and if the C pyfori had been eradicated. When C pylori had been eradicated,ulcers healed in 92% of cases us only 65% of cases when the Campylobacter had persisted (P c 0.001). Patients who healed were then followed up without maintenance therapy for 12 months. The relapse rate for patients who still had C pylori was 85%. In contrast, when C pylori had been eradicated,the relapse rate was a very low 20% (P c 0.0001). Although the number of patients in whom C pylori was eradicatedwas small .(24 patients followed up for 12 months), the study demonstrates that C pyfori is probably the most important factor predisposing patients to duodenal ulcer relapse. The study also suggests that C pylori impairs ulcers healing and that C pylori infected patients have a more severe clinical course than patients without C pylori. The best combination therapy was De-no1 plus tinidazole 1 g daily. The authors recommend that patients with C pylori and duodenal ulcer initially be treated with De-no1 for one month and be given concurrenttinidazole 1 g daily from day I-10. Biopsies to assess eradicationof C pylori should be performedone month after the patient has completed this therapy. If C pylori has been eradicated,then maintenancetherapy with H2 blockers is unnecessary. BJ Marshall(4) Departmentof InternalMedicine, Virginia22908, USA Sim
tin in hyperlipidaemia.
In a cross-over study in 10 patients with hyperlipidaemia due to unremitting nephrotic syndrome, we compared the efficacy of the HMG CoA reduGtaR!inhibitor SimvasNtin with that of the bile-acid binding resin cholestyramine. Simvastatin produced a 36% decrease in total cholesterol, a 39% decrease in LDL cholesterol, and a 30% decrease in apo B, whereas Gholestyramine reduced LDL cholesterol by 19% and (4) Luncel (1988) ii, 1438.
142
females whose carrierstate can be diagnosed from 79technique allows diagnosis to be made with 89 uracy. 99 PRWinship(1)
University of Oxford, oxfGrd0x13RE.UK epithelium OSpatients This in vivo study showed that the jejunum of patients
with cystic fibrosis fails to respond to a cholinergic secretory agent, pilocarpine, and a CAMP mediated secretory agent, prostaglandinE2, and that the wavelike changes of the jejtmaltransmucosalpotentialdifference normally associeted with intestinal motor activity in man and animals arc absent in cystic fibrosis. The absent response to secretoryagents corroborates previous in vitro results and confirms that the small bowel shares the defect in CA P-mediated chloride secretion seen in sweat gland and airway epithelia. which is believed to constitute part of the pathophysiology of cystic fibrosis. However, sweat glands can respond to cholinergic agents, which suggests that these agents cause secretion by different mechanisms in the two epithelia. The absence of PD waves with motor activity suggests that these reflect secretion associated with motility. PD traces from patients look strikingly differentto those from healthy controls and could be a useful aid to diagnosis. PSBaxter (2) TheUniversityof Sheffield, SheffieldSIO2TH,UK vtmtim ok?
OCJJS& pneumonk
Pneumocysfis carinii pneumonia occurs in 60% of
patients with AIDS and is the major cause of mortality in these patients. We have previously demonstrated (Ann Inrern Med. Ckt 1987. 107 (4). 495-498) that aerosolized pentamidine is effective for the treatmentof acute pneumocystis pneumonia. We believe that the data published in t5s Lcrncerdemonstratesthat aerosolized pentamidine,given once monthly, is also probably effective for the prevention of Pneumocystis carinii pneumonia. The study suggests that the attack rate is reduced by approximately50% and the time to onset of PCP is prolonged by approximately‘6 months. This effect is independentof zidovudine (AET) administration. We are presently performingdose escalation studies in order to determinewhether PCP is completely preventableby aerosolized pentamidinewithout inducing additional significant toxicity. JEConte(3) TheMedicalCenterat theUniversityof Catifemia, SanFrancis~~ CA94143.USA (1) fmcef (1989)‘i. 631. (2) Lancer(1989) i. 464. (3) Lamer (1989) i, 654.
enal ulcer aad Campylobacterpylorl. Campylobacter pyfori. a Gram-negativespiralorganism,
colonizes the gastric mucosa of most patients with peptic ulcer disease (gastric ulcer SO%,duodenal ulcer 95%) and it is suggested that by causing gastritis, C pyfori weakens the gastric mucosa allowing acid and pepsin to form ulcers. In this study we treated 100 patients with C pylori and duodenal ulcer proven by endoscopy. Half the patients received Tagamet or Tagarnet plus tinidazole (an antibiotic similar to metronidazole):the other klf received De-no1 (bismuth subcitrate) or De-no1 plus tinidazole. The Tagamet or De-no1 were given in standardulcer healing doses for 8 weeks. The antibiotic or a matching placebo were administered concurrently with the ulcer healing drug from day 1 to day 10. During week 10 (2 weeks after finishing treatment)patients were endoscoped to see if the ulcers had healed and if the C pyfori had been eradicated. When C pylori had been eradicated,ulcers healed in 92% of cases us only 65% of cases when the Campylobacter had persisted (P c 0.001). Patients who healed were then followed up without maintenance therapy for 12 months. The relapse rate for patients who still had C pylori was 85%. In contrast, when C pylori had been eradicated,the relapse rate was a very low 20% (P c 0.0001). Although the number of patients in whom C pylori was eradicatedwas small .(24 patients followed up for 12 months), the study demonstrates that C pyfori is probably the most important factor predisposing patients to duodenal ulcer relapse. The study also suggests that C pylori impairs ulcers healing and that C pylori infected patients have a more severe clinical course than patients without C pylori. The best combination therapy was De-no1 plus tinidazole 1 g daily. The authors recommend that patients with C pylori and duodenal ulcer initially be treated with De-no1 for one month and be given concurrenttinidazole 1 g daily from day I-10. Biopsies to assess eradicationof C pylori should be performedone month after the patient has completed this therapy. If C pylori has been eradicated,then maintenancetherapy with H2 blockers is unnecessary. BJ Marshall(4) Departmentof InternalMedicine, Virginia22908, USA Sim
tin in hyperlipidaemia.
In a cross-over study in 10 patients with hyperlipidaemia due to unremitting nephrotic syndrome, we compared the efficacy of the HMG CoA reduGtaR!inhibitor SimvasNtin with that of the bile-acid binding resin cholestyramine. Simvastatin produced a 36% decrease in total cholesterol, a 39% decrease in LDL cholesterol, and a 30% decrease in apo B, whereas Gholestyramine reduced LDL cholesterol by 19% and (4) Luncel (1988) ii, 1438.