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DAS28: DMARD Change and Biologic Groups

Adapted from Bombardier C, et al: Presented at CRA 2010; poster #17.presmedic.com [email protected] (917) 856-0582

Before

0

1

2

3

4

5

6

7

8

Biologic DMARD Change

Mea

n S

core

DAS28: DMARD Change and Biologic Groups

Biologic (baseline)Biologic (6 Mth)

DMARD Change (baseline)DMARD Change (6 Mth)

Adapted from Bombardier C, et al: Presented at CRA 2010; poster #17.presmedic.com [email protected] (917) 856-0582

After

Patient Agreement With Statements Regarding Adherence Support

Adapted from Olszynski W, et al: Presented at CRA 2010; poster #201.presmedic.com [email protected] (917) 856-0582

Before

0 2

25

2 2

20

5 510

3428

19

5963

26

0

10

20

30

40

50

60

70

I feel satisfied with theoverall support I get from

family and friends

I feel satisfied with theoverall support I get from

the HUMIRAPROGRESS program

May family and friendshelp me remember totake my medication

Coh

ort

(%)

Patient Agreement With Statements Regarding Adherence Support

Adapted from Olszynski W, et al: Presented at CRA 2010; poster #201.

Strongly Disagree Disagree Undecided Agree Strongly agree


After

Bevacizumab Alone and With Irinotecan: Progression-free Survival

PFS-6BV alone: 42.6%BV + Iri: 50.3%

Adapted from Friedman HS, et al: J Clin Oncol 2009; 27(28):4733-40presmedic.com [email protected] (917) 856-0582

Before

Bevacizumab Alone and With Irinotecan: Progression-free Survival

Adapted from Friedman HS, et al: J Clin Oncol 2009; 27(28):4733-40

0.0

0.2

0.4

0.6

0.8

1.0

0 2 4 6 8 10 12 14

Pro

gre

ssio

n-F

ree

Su

rviv

al(p

rop

ort

ion

)

Time (months)

BV + CPT-11 (n = 82) median PFS 5.6 months (95% CI, 4.4 to 6.2)

PFS-6BV alone: 42.6%BV + Iri: 50.3%

BV (n = 85) median PFS 4.2 months (95% CI, 2.9 to 5.8)

No. at risk85 61 39 26 14 4 1 082 65 47 24 15 7 1 0


After

Recurrence by MMR Status:dMMR Attenuated Risk of Recurrence

All Patients Stage II Colon

Risk ratio: 0.53 (95% CI 0.40-0.70) Risk ratio: 0.49 (95% CI 0.36-0.68)

p<0.00001 p<0.00001

MMR, mismatch repair; dMMR, defective mismatch repairAdapted from Hutchins G, et al. J Clin Oncol 28:7s, 2010 (suppl; abstr 3517)

Before

Recurrence by MMR Status:dMMR Attenuated Risk of Recurrence

MMR, mismatch repair; dMMR, defective mismatch repairAdapted from Hutchins G, et al. J Clin Oncol 28:7s, 2010 (suppl; abstr 3517)

Risk ratio: 0.53 (95% CI 0.40-0.70)p<0.00001

Risk ratio: 0.49 (95% CI 0.36-0.68)p<0.00001

All Patients Stage II Colon

0

10

20

30

40

50

60

70

80

90

100

0 1 2 3 4 5 6 7 8 9 10Years from randomization

% w

ith

recu

rren

ce

At risk:Deficient 218 201 195 189 174 146 112 94 69 47 37Proficient 1695 1563 1405 1286 1127 921 750 608 479 327 214

0

10

20

30

40

50

60

70

80

90

100

0 1 2 3 4 5 6 7 8 9 10Years from randomization

% w

ith

recu

rren

ceAt risk:Deficient 199 187 181 176 162 136 105 90 67 45 35Proficient 1097 1014 918 850 744 613 501 398 304 204 131

No.Patients

No. EventsObs. Exp.

Deficient 218 25 56.9Proficient 1695 438 406.1

Deficient Proficient

2P < 0.0000131%

14%

2P < 0.00001

27%

11%

No.Patients

No. EventsObs. Exp.

Deficient 199 18 43.8Proficient 1097 245 219.2

Deficient Proficient

After

Rapid Desensitization to Chemotherapy


Before

Rapid Desensitization to Chemotherapy

278 hadno reaction111 had a

mild reaction

24 hada severereaction

67%

27%

6%

Castells, et al. J Allergy Clin Immunol 2008;122:574-80.

Severe: Including at least 1 of:• Chest pain • Changes in BP• Dyspnea • O2 desaturation • Throat tightness

Mild: Absence of any of the above


After

Peterson LR et al Circulation 2004; 109: 2192-2196

Effect Of Obesity And Insulin Resistance On Myocardial Substrate Metabolism And Function In Young Women

• Increased hemodynamic load and neurohormonal activation

• Increased FFA uptake, utilization and oxidation • Increased ceramide production and apoptosis • Increased oxidative stress and myocellular injury

• Similar cardiac phenotype as hypertensive heart but different mechanisms

• May help explain greater risk for CHF in women compared to men


Before

Effect of Obesity And Insulin Resistance on Myocardial Substrate Metabolism and Function in Young Women

Peterson LR et al Circulation 2004; 109: 2192-2196

Increased hemodynamic load and neurohormonal activation

Increased FFA uptake, utilization and oxidation

Increased ceramide production and apoptosis

Increased oxidative stress and myocellular injury

Similar cardiac phenotype as hypertensive heart but different mechanisms

May help explain greater risk for CHF in women compared to men

0.00.51.01.52.02.53.03.54.04.55.0

MVO

2 (j/g

/min

)

0 20 40 60BMI (kg/m2)

0

5

10

15

20

25

30

35

Effic

ienc

y (%

)

0 20 40 60BMI (kg/m2)

0.00.10.20.30.40.50.6

7,500 10,000 12,500 15,000 17,500

MFA

Up

(mL/

g/m

in)

Glucose AUC (mg/dL x 120 min)

0

100

200

300

400

7,500 10,000 12,500 15,000 17,500

MFA

U (m

mol

/g/m

in)


0

100

200

300

400

7,500 10,000 12,500 15,000 17,500

MFA

O (m

L/g/

min

)


r = .55P < .005

r = .62P < .001

r = .58P < .005

r = .58P < .0006

r = .40P < .05

A

B

A

B

C


After

20050829

Low dose Lasix relieves Dyspnea well and equal to high Dose w.r.t. Dyspnea: VERITAS


Before

Low Dose Lasix Relieves Dyspnea Well and Equal to High Dose W.R.T. Dyspnea: VERITAS

3,000

900

2,000

1,000

0

-1,000

-2,000

-3,000

8007006005004003002001000Maximum in-hospital diuretic dose

Dys

pn

ea v

as


After


Before

Study or Subgroup

AS Control

WeightRisk Ratio

M-H, Random, 95% CIRisk Ratio

M-H, Random, 95% CIEvents Total Events Total

Han 2006 122 1843 391 7372 39.8% 1.25 [1.03, 1.52]

Peters 2009 17 383 922 75333 36.0% 3.63 [2.27, 5.80]

Sukenik 1987 7 40 5 40 24.2% 1.40 [0.48, 4.04]

Total (95% CI) 2266 82745 100.0% 1.88 [0.83, 4.26]

Total events 46 1318

0.2 0.5 2 51Heterogeneity: Tau2 = 0.43; Chi2 = 17.28; df = 2 (P = 0.0002); I3 = 88%Test for overall effect Z = 1.51 (P = 0.13)


After


Before

ParameterAdjusted Effect Size

(96% CI)Adjusted Treatment Difference,

Units (SD)

ASDAS 0.80 units (0.88)

C-reactive protein 8.61 mg/L (11.59)

Nocturnal back pain 16.41 mm (VAS) (24.83)

Stiffness 13.81 mm (VAS) (22.93)

Back pain 14.73 mm (VAS) (24.48)

Disease Activity Patient Global Assessment 14.51 mm (VAS) (24.16)

Length of stiffness 14.13 mm (VAS) (23.90)

Disease Activity Physician Global Assessment 11.44 mm (VAS) (19.35)

BASDAI 12.08 mm (VAS) (20.93)

ASQoL 2.52 units (4.53)

Level of stiffness 13.56 mm (VAS) (24.81)

Peripheral Joint Arthritis Patient Global Assessment 13.19 mm (VAS) (24.88)

BASR 9.92 mm (VAS) (20.89)

Peripheral Joint Arthritis Physician Global Assessment 7.90 mm (VAS) (16.63)

Derived EQ-50 score 0.11 units (0.24)

BASMI 0.59 mm (VAS) (1.33)

SF-36 PCS 3.70 units (8.55)

SF-36 MCS 3.38 units (9.33)

VAS EQ-5D 6.82 mm (VAS) (20.51)

Modified Schober’s Test 0.49 cm (1.57)

Inter??? distance 4.55 cm (16.47)

HADS total score 1.28 units (5.46)

HADS depression score 0.66 units (3.02)

HADS anxiety score 0.64 units (3.03)

Cervical rotation 2.51 degrees (12.66)

Tender joint count 0.79, n (70 joints) (4.16)

Lateral flexion 0.69 cm (3.68)

Swollen joint count 0.40, N (68 joints) (2.37)

Tragus-to-wall distance 0.28 cm (2.24)

Chest expansion 0.18 cm (3.05)

Occiput-to-wall distance 0.28 cm (4.55)

From an ANCOVA model, adjusted for the endpoint’s baseline and pooled site: adjusted effect size is the adjusted difference between etanercept and sulfasalazine, divided by ANCOVA model-based SD estimate. Effect sizes <0.4 were considered small; 0.4-0.7moderate; and ≥0.7 large. The width of the 95% CI for ASQoL is attributable to the smaller sample size relative to other endpoints.

Sulfasalazine > Etanercept Etanercept > Sulfasalazine

-0.2 0 0.2 0.4 0.6 0.8 1 1.2


After

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