ger time than patients in the placebo maintenance group. Among patients who were not in response by Week 12, therapy continued beyond 12 weeks did not result in significantly more responses.
Ulcerative Colitis
The safety and efficacy of Humira were assessed in adult patients with moderately to severely active ulcerative colitis (Mayo score 6 to 12 on a 12 point scale, with an endoscopy subscore of 2 to 3 on a scale of 0 to 3) despite concurrent or prior treatment with immunosuppressants such as corticosteroids, azathioprine, or 6-MP in two randomized, double-blind, placebo-controlled clinical studies (Studies UC-I and UC-II). Both studies enrolled TNF-blocker naïve patients, but Study UC-II also allowed entry of patients who lost response to or were intolerant to TNF-blockers. Forty percent (40%) of patients enrolled in Study UC-II had previously used another TNF-blocker.
Concomitant stable doses of aminosalicylates and immunosuppressants were permitted. In Studies UC-I and II, patients were receiving aminosalicylates (69%), corticosteroids (59%) and/or azathioprine or 6-MP (37%) at baseline. In both studies, 92% of patients received at least one of these medications.
Induction of clinical remission (defined as Mayo score ≤ 2 with no individual subscores > 1) at Week 8 was eva luated in both studies. Clinical remission at Week 52 and sustained clinical remission (defined as clinical remission at both Weeks 8 and 52) were eva luated in Study UC-II.
In Study UC-I, 390 TNF-blocker naïve patients were randomized to one of three treatment groups for the primary efficacy analysis. The placebo group received placebo at Weeks 0, 2, 4 and 6. The 160/80 group received 160 mg Humira at Week 0 and 80 mg at Week 2, and the 80/40 group received 80 mg Humira at Week 0 and 40 mg at Week 2. After Week 2, patients in both Humira treatment groups received 40 mg every other week (eow).
In Study UC-II, 518 patients were randomized to receive either Humira 160 mg at Week 0, 80 mg at Week 2, and 40 mg eow starting at Week 4 through Week 50, or placebo starting at Week 0 and eow through Week 50. Corticosteroid taper was permitted starting at Week 8.
In both Studies UC-I and UC-II, a greater percentage of the patients treated with 160/80 mg of Humira compared to patients treated with placebo achieved induction of clinical remission. In Study UC-II, a greater percentage of the patients treated with 160/80 mg of Humira compared to patients treated with placebo achieved sustained clinical remission (clinical remission at both Weeks 8 and 52) (Table 13).
Table 13. Induction of Clinical Remission in Studies UC-I and UC-II and Sustained Clinical Remission in Study UC-II
(Percent of Patients)
Study UC-I Study UC-II
Placebo
N=130 Humira
160/80 mg
N=130 Treatment Difference
(95% CI) Placebo
N=246 Humira
160/80 mg
N=248 Treatment Difference
(95% CI)
Induction of Clinical Remission (Clinical Remission at Week 8) 9.2% 18.5% 9.3%*
(0.9%, 17.6%) 9.3% 16.5% 7.2%*
(1.2%, 12.9%)
Sustained Clinical Remission (Clinical Remission at both Weeks 8 and 52) N/A N/A N/A 4.1% 8.5% 4.4%*
(0.1%, 8.6%)
Clinical remission is defined as Mayo score ≤ 2 with no individual subscores > 1.
CI=Confidence interval
* p<0.05 for Humira vs. placebo pairwise comparison of proportions
In Study UC-I, there was no statistically significant difference in clinical remission observed between the Humira 80/40 mg group and the placebo group at Week |
