Shire Recognizes HAE Day with Launch of Interactive Website Calling for Inspirational Wishes

Shire Recognizes HAE Day with Launch of Interactive Website Calling for Inspirational Wishes

May 15, 2015

HAE-Day-2015Shire plc (LSE: SHP, NASDAQ: SHPG) today announced, in recognition of the fourth annual hae day :-) (16 May), the launch of a new educational website as part of its hereditary angioedema (HAE) awareness campaign Me, Not HAE. The interactive site supports the HAE community by enabling the sharing of stories of inspiration and helping raise awareness of the realities of living with HAE. The Me, Not HAE campaign, which was initially launched on hae day :-) in 2014, focuses on finding innovative ways to share personal stories from people living with HAE to help inspire the community at large while also driving education and awareness of this rare condition.

In conjunction with the campaign and to recognize hae day :-) 2015, Shire is inviting all site visitors to share a wish or message of inspiration with the HAE community from 16 to 30 May. Each wish submitted online will add a leaf to a virtual HAE Wish Tree, building a picture of hope for those living with this condition. Wishes can be made at:

“Shire is dedicated to raising awareness of HAE and recognizes the importance of sharing inspirational messages and stories as a way to encourage and show our support for those living with this challenging condition,” said Emmanuel Dulac, Head of the Rare Disease Business Unit at Shire. “We are very pleased to launch this new site in support of this rare disease community on the occasion of hae day.”

HAE is a rare and life-threatening genetic condition affecting about 1 in 10,000 to 1 in 50,000 people.1-4 Symptoms include unpredictable swelling in various parts of the body including the extremities, face, abdomen and upper airways.1-5

“People living with HAE often feel isolated, so sharing personal stories and messages of hope will help unite the community and strengthen its collective voice,” said Anthony Castaldo, president of the International Patient Organization for C1 Inhibitor Deficiencies (HAEi). “This new site not only offers visitors the chance to learn more about HAE, but to also contribute messages of hope for the community in support of hae day.”

HAEi is an advocacy organization dedicated to raising awareness of HAE around the world. Each year on 16 May, hae day :-) aims to raise global awareness of this condition among the general public and medical community, to help ensure better care, and earlier and more accurate diagnosis for those living with HAE.6

“We are proud to help unite the global HAE community and to foster increased awareness of the condition on hae day,” said Henrik Balle Boysen, executive director of the HAEi. “It is our hope that hae day, along with supportive initiatives including this new educational website, will ultimately help lead to more accurate diagnoses.”

About HAE

HAE is a rare, genetic disorder that results in recurring attacks of edema (swelling) in parts of the body.1,2 HAE mainly affects the skin, abdomen and less frequently causes life-threatening attacks, due to obstruction in the upper airways.1-2,5,7-8

Patients with HAE are prone to swelling due to an underlying deficiency in a protein called C1 esterase inhibitor (C1-INH).1,9-11 C1-INH is part of a pathway in the body which controls the production of the protein bradykinin.9-15 During a swelling attack, the overproduction of bradykinin increases the permeability of blood vessels, causing fluids to ‘leak’ into the surrounding tissue and results in swelling.12

For further information please contact:


Lauren O’Brien [email protected]
+41 44 288 4040
Gwen Fisher  [email protected]
+1 484 595 9836


Shire enables people with life-altering conditions to lead better lives.

Our strategy is to focus on developing and marketing innovative specialty medicines to meet significant unmet patient needs.

We focus on providing treatments in Rare Diseases, Neuroscience, Gastrointestinal and Internal Medicine and we are developing treatments for symptomatic conditions treated by specialist physicians in other targeted therapeutic areas, such as Ophthalmics.


Statements included herein that are not historical facts are forward-looking statements. Such forward-looking statements involve a number of risks and uncertainties and are subject to change at any time. In the event such risks or uncertainties materialize, Shire’s results could be materially adversely affected. The risks and uncertainties include, but are not limited to, that:

  • Shire’s products may not be a commercial success; 
  • product sales from ADDERALL XR and INTUNIV are subject to generic competition; 
  • the failure to obtain and maintain reimbursement, or an adequate level of reimbursement, by third-party payers in a timely manner for Shire's products may affect future revenues, financial condition and results of operations;
  • Shire conducts its own manufacturing operations for certain of its products and is reliant on third party contract manufacturers to manufacture other products and to provide goods and services. Some of Shire’s products or ingredients are only available from a single approved source for manufacture. Any disruption to the supply chain for any of Shire’s products may result in Shire being unable to continue marketing or developing a product or may result in Shire being unable to do so on a commercially viable basis for some period of time;
  • the manufacture of Shire’s products is subject to extensive oversight by various regulatory agencies. Regulatory approvals or interventions associated with changes to manufacturing sites, ingredients or manufacturing processes could lead to significant delays, an increase in operating costs, lost product sales, an interruption of research activities or the delay of new product launches;
  • Shire has a portfolio of products in various stages of research and development. The successful development of these products is highly uncertain and requires significant expenditures and time, and there is no guarantee that these products will receive regulatory approval;
  • the actions of certain customers could affect Shire's ability to sell or market products profitably. Fluctuations in buying or distribution patterns by such customers can adversely affect Shire’s revenues, financial condition or results of operations;
  • investigations or enforcement action by regulatory authorities or law enforcement agencies relating to Shire’s activities in the highly regulated markets in which it operates may result in significant legal costs and the payment of substantial compensation or fines;
  • adverse outcomes in legal matters and other disputes, including Shire’s ability to enforce and defend patents and other intellectual property rights required for its business, could have a material adverse effect on Shire’s revenues, financial condition or results of operations;
  • Shire faces intense competition for highly qualified personnel from other companies and organizations. Shire is undergoing a corporate reorganization and was the subject of an unsuccessful acquisition proposal and the consequent uncertainty could adversely affect Shire’s ability to attract and/or retain the highly skilled personnel needed for Shire to meet its strategic objectives; 
  • failure to achieve Shire’s strategic objectives with respect to the acquisition of NPS Pharmaceuticals Inc. may adversely affect Shire’s financial condition and results of operations; and other risks and uncertainties detailed from time to time in Shire’s filings with the Securities and Exchange Commission, including those risks outlined in “Item 1A: Risk Factors” in Shire’s Annual Report on Form 10-K for the year ended December 31, 2014.


  1. Donaldson V, Evans R. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C1-esterase. Am J Med. 1963; 35: 37-44
  2. Bork K, et al. Hereditary angioedema: New findings concerning symptoms, affected organs, and course. Am J Med. 2006; 119(3): 267-74
  3. Agostoni A, Aygoren-Pursun E, Binkley KE, et al. Hereditary and acquired angioedema: problems and progress: proceedings of the third C1 esterase inhibitor deficiency workshop and beyond. J Allergy Clin Immunol 2004; 114(3 Suppl): S51-131 
  4. Bowen T, Cicardi M, Bork K, et al. Hereditary angioedema: a current state-of-the-art review, VII: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema. Ann Allergy Asthma Immunol 2008; 100(1 Suppl 2): S30-40
  5. Bork K, et al. Clinical studies of sudden upper airway obstruction in patients with hereditary angioedema due to C1 esterase inhibitor deficiency. Arch Intern Med. 2003; 163: 1229-1235
  6. International Patient Organization for C1 Inhibitor Deficiencies. (HAEi). About hae day.
  7. Bork K, et al. Asphyxiation by laryngeal edema in patients with hereditary angioedema. Mayo Clin Proc. 2000; 75: 349-354
  8. Bork K. Fatal laryngeal attacks and mortality in hereditary angioedema due to C1-INH deficiency. JAACI. 2012; DOI:
  9. Circardi M, et al. Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group. Allergy. 2014; 69: 602–616
  10. Craig T, et al. WAO guideline for the management of hereditary angioedema. World Allergy Organ Journal. 2012; 5 (12): 182-99
  11. Nussberger J, et al. Plasma bradykinin in angio-edema. The Lancet. 1998; 351: 1693-1697
  12. Donaldson V. Kinin formation in hereditary angioneurotic edema (HANE) plasma. Int Arch Allergy Appl Immunol. 1973; 45: 206-209
  13. Curd J, et al. Detection of active kallikrein in induced blister fluids of hereditary angioedema patients. Journal of experimental medicine. 1980; 153 (3): 742-747
  14. Lung C, et al. Analysis of an exon 1 polymorphism of the B2 bradykinin receptor gene and its transcript in normal subjects and patients with C1 inhibitor deficiency. J. Allergy, Asthma Clin Immunol. 1997; 99 (1): 134-146
  15. Nussberger J, et al. Local bradykinin generation in hereditary angioedema. J. Allergy Asthma Clin Immunol. 1999; 104 (6): 1321-1322

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