The AlphaNet® Alpha-1 Disease Management and Prevention Program (ADMAPP) is the only fully integrated disease management program shown to improve patient outcomes1,2*

Disease management health outcomes study results:


Significant improvements in health outcomes after intervention year (n=878)2
10%
reduction in exacerbations2 Ρ<0.001
12%
reduction in unscheduled physician visits2 Ρ=0.03
21%
reduction in emergency room visits2 Ρ=0.02
10%
increase in the use of long-term oxygen therapy (>16 hours/day)2 Ρ<0.01
15%
increase in use of long-acting bronchodilator2 Ρ<0.001
  • Translates into more optimal medication use
Reduction in the use of systemic steroids2 Ρ=0.02
Significant improvements in health outcomes after intervention year (n=878)2
10%
reduction in exacerbations2 Ρ<0.001
12%
reduction in unscheduled physician visits2 Ρ=0.03
21%
reduction in emergency room visits2 Ρ=0.02
10%
Increase in the use of long-term oxygen therapy (>16 hours/day)2 Ρ<0.01
15%
increase in long-acting bronchodilator use2 Ρ<0.001
  • Translates into more optimal medication use
Reduction in the use of systemic steroids2 Ρ=0.02

*2-year study comparing outcomes in a 12-month observation period with augmentation therapy alone and a 12-month intervention period with augmentation therapy plus ADMAPP2.

  • Participants were members of AlphaNet, a not-for-profit health management company founded by alphas to provide comprehensive care solely for alphas
  • 97% of ADMAPP study participants were taking PROLASTIN® (alpha1-proteinase inhibitor [human])2

Enrolled patients immediately start receiving ADMAPP benefits through AlphaNet1


PROLASTIN®-C (alpha1-proteinase inhibitor [human]) is indicated for chronic augmentation and maintenance therapy in adults with clinical evidence of emphysema due to severe hereditary deficiency of alpha1-PI (alpha1-antitrypsin deficiency).

The effect of augmentation therapy with any alpha1-proteinase inhibitor (alpha1-PI), including PROLASTIN-C, on pulmonary exacerbations and on the progression of emphysema in alpha1-antitrypsin deficiency has not been conclusively demonstrated in randomized, controlled clinical trials. Clinical data demonstrating the long-term effects of chronic augmentation or maintenance therapy with PROLASTIN-C are not available.

PROLASTIN-C is not indicated as therapy for lung disease in patients in whom severe alpha1-PI deficiency has not been established.

PROLASTIN-C is contraindicated in IgA-deficient patients with antibodies against IgA due to the risk of severe hypersensitivity and in patients with a history of anaphylaxis or other severe systemic reactions to alpha1-PI.

Hypersensitivity reactions, including anaphylaxis, may occur. Monitor vital signs and observe the patient carefully throughout the infusion. Should hypersensitivity symptoms be observed, promptly stop infusion and begin appropriate therapy. Have epinephrine and other appropriate therapy available for the treatment of any acute anaphylactic or anaphylactoid reaction.

PROLASTIN-C may contain trace amounts of IgA. Patients with known antibodies to IgA, which can be present in patients with selective or severe IgA deficiency, have a greater risk of developing potentially severe hypersensitivity and anaphylactic reactions.

The most common drug-related adverse reaction observed at a rate of >5% in subjects receiving PROLASTIN-C was upper respiratory tract infection. The most serious adverse reaction observed during clinical trials with PROLASTIN-C was an abdominal and extremity rash in 1 subject.

Because PROLASTIN-C is made from human plasma, it may carry a risk of transmitting infectious agents, eg, viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. This also applies to unknown or emerging viruses and other pathogens.

Please click here for full Prescribing Information for PROLASTIN-C.


References

  1. Data on file, PROLASTIN DIRECT program.
  2. Campos MA, Alazemi S, Zhang G, Wanner A, Sandhaus RA. Effects of a disease management program in individuals with alpha-1 antitrypsin deficiency. COPD. 2009;6(1):31-40.