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1.
Gastroenterology ; 121(5): 1088-94, 2001 Nov.
Article in English | MEDLINE | ID: mdl-11677200

ABSTRACT

BACKGROUND & AIMS: We evaluated etanercept, a human soluble tumor necrosis factor receptor: Fc fusion protein, for the treatment of active Crohn's disease. METHODS: Forty-three patients with moderate to severe Crohn's disease were enrolled in an 8-week placebo-controlled trial. Patients were randomized to subcutaneous etanercept 25 mg or placebo twice weekly. The primary outcome measure was clinical response at week 4, defined as a decrease in the baseline Crohn's Disease Activity Index score > or =70 points or a Crohn's Disease Activity Index score <150 points. RESULTS: At week 4, 39% of etanercept-treated patients had clinical response as compared with 45% of placebo-treated patients (P = 0.763). The frequency of common adverse events including headache, new injection site reaction, asthenia, abdominal pain, Crohn's disease-related anemia, and skin disorders was similar in both groups. Likewise, the frequency of severe or serious adverse events was similar in both groups. CONCLUSIONS: Subcutaneous etanercept at a dose of 25 mg twice weekly is safe, but not effective, for the treatment of patients with moderate to severe Crohn's disease. The dose of etanercept administered in this study is that approved for rheumatoid arthritis. Higher doses or more frequent dosing may be required to attain a response in patients with active Crohn's disease.


Subject(s)
Crohn Disease/drug therapy , Gastrointestinal Agents/therapeutic use , Immunoglobulin G/therapeutic use , Receptors, Tumor Necrosis Factor/therapeutic use , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adult , Aged , Antibodies, Monoclonal/therapeutic use , Double-Blind Method , Etanercept , Female , Humans , Immunoglobulin G/adverse effects , Infliximab , Male , Middle Aged
2.
Aliment Pharmacol Ther ; 15(7): 927-35, 2001 Jul.
Article in English | MEDLINE | ID: mdl-11421866

ABSTRACT

BACKGROUND: Esomeprazole, the S-isomer of omeprazole, is the first proton pump inhibitor to be developed as an optical isomer. In patients with erosive oesophagitis, esomeprazole has produced significantly greater healing rates and improved symptom resolution vs. omeprazole. AIM: This study assesses the efficacy of esomeprazole for preventing relapse in patients with healed oesophagitis. METHODS: In this 6-month US multicentre randomized double-blind placebo-controlled trial, 375 Helicobacter pylori-negative patients with endoscopically healed oesophagitis received esomeprazole 40 mg, 20 mg, 10 mg, or placebo once daily. The primary efficacy end-point was maintenance of healing at 6 months. Secondary end-points assessed changes in symptoms, and long-term safety and tolerability. RESULTS: Significantly (P < 0.001) more patients remained healed with esomeprazole 40 mg (87.9%), 20 mg (78.7%), or 10 mg (54.2%), than with placebo (29.1%). Relapse, when it occurred, was later with esomeprazole. Sustained resolution of heartburn was observed in the 40 mg and 20 mg groups; there was a high correlation between absence of heartburn and maintenance of healing. Adverse effects were mild, infrequent and not significantly different between groups. CONCLUSIONS: Esomeprazole is effective and well-tolerated in the maintenance of healing of erosive oesophagitis. Esomeprazole 40 mg and 20 mg offer significant clinical benefit to patients.


Subject(s)
Esomeprazole/administration & dosage , Esophagitis, Peptic/drug therapy , Gastroesophageal Reflux/drug therapy , Proton Pump Inhibitors/administration & dosage , Administration, Oral , Adolescent , Adult , Aged , Aged, 80 and over , Dose-Response Relationship, Drug , Double-Blind Method , Esomeprazole/adverse effects , Esophagitis, Peptic/pathology , Female , Gastroesophageal Reflux/complications , Heartburn , Humans , Isomerism , Male , Middle Aged , Placebos , Proton Pump Inhibitors/adverse effects , Recurrence , Treatment Outcome
4.
J Clin Invest ; 50(6): 1309-21, 1971 Jun.
Article in English | MEDLINE | ID: mdl-4325312

ABSTRACT

It is generally recognized that glucocorticoid administration may diminish calcium absorption in vivo as well as the active transport of calcium by the intestine in vitro. Recent studies by others have emphasized the possibility of an alteration in the metabolism of vitamin D to 25-hydroxycholecalciferol in accounting for the steroid effects on calcium absorption. The results obtained in the present studies fail to support this hypothesis. The present studies confirm that the administration of cortisone or other glucocorticoids to the rat interferes with the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to an alteration in the permeability of the intestine to calcium, and it cannot be corrected by the administration of either massive doses of vitamin D(2) or modest doses of 25-hydroxycholecalciferol. Experiments concerned with the effects of cortisone on the level of the vitamin D-dependent duodenal calcium-binding protein, the amount of bioassayable vitamin D activity in the mucosa, and the distribution and metabolism of (3)H-vitamin D(3), did not provide evidence in favor of a harmone-related defect in either the localization of vitamin D or its metabolism to 25-hydroxycholecalciferol. Alterations in the transport of iron and D-galactose, not dependent on vitamin D, suggest that cortisone treatment may be responsible for more than a simple antagonism to the effects of vitamin D. The results of the present studies indicate that cortisone administration affects the cellular mechanisms mediating calcium transport in a manner that is opposite to the effects of vitamin D, but seems to be independent of any direct interaction with the parent vitamin or its metabolites. If a disorder in vitamin D metabolism is at all involved, it is at a step subsequent to 25-hydroxylation.


Subject(s)
Biological Transport, Active/drug effects , Calcium/metabolism , Cortisone/pharmacology , Drug Antagonism , Intestine, Small/physiology , Vitamin D/antagonists & inhibitors , Animals , Biological Assay , Calcium Chloride , Calcium Isotopes , Cholecalciferol/pharmacology , Duodenum , Galactose/metabolism , Ileum , Intestinal Mucosa/analysis , Leucine/metabolism , Male , Rats , Sarcoidosis/metabolism , Vitamin D/analysis
7.
J Clin Invest ; 49(6): 1288-300, 1970 Jun.
Article in English | MEDLINE | ID: mdl-5422027

ABSTRACT

The intestinal absorption of calcium is often depressed in patients with chronic renal insufficiency. Furthermore, the malabsorption of calcium and the osteodystrophy which occur in association with chronic renal disease are often "resistant" to vitamin D; the basis for this resistance remains uncertain however. Recent studies by others have emphasized the role of an abnormality in the metabolism of vitamin D in accounting for the alterations in the calcium absorption and the apparent vitamin D-resistance which accompany the uremic syndrome. The present studies with an experimentally uremic animal model demonstrate a defect in the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to the semistarvation associated with renal insufficiency and cannot be corrected by the administration of physiologic amounts of vitamin D(3): it is reversed by massive doses of the vitamin. Neither the metabolism of vitamin D(3) nor the levels of calcium binding protein activity in the duodenal mucosa are affected by renal insufficiency under the conditions employed in the present studies. The results of the present studies strongly suggest that in addition to the recently proposed mechanism involving an interference with the metabolism of vitamin D renal insufficiency also affects the cellular mechanisms for calcium transport in a manner which, while opposite in direction to that of vitamin D, is independent of a direct interaction with the vitamin or its metabolites.


Subject(s)
Biological Transport, Active , Calcium/metabolism , Intestine, Small/metabolism , Kidney/physiopathology , Uremia/physiopathology , Animals , Calcium/analysis , Creatinine/analysis , Duodenum/physiopathology , Glucose/analysis , Intestinal Absorption , Intestinal Mucosa/metabolism , Jejunum/physiopathology , Kidney Failure, Chronic/physiopathology , Lactates/analysis , Nephrectomy , Protein Binding , Radiometry , Rats , Vitamin D/administration & dosage , Vitamin D/analysis , Vitamin D/metabolism
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