#ecrs

New Post has been published on https://sydneyentclinic.com/richard-harvey/2021/02/16/patient-selection-prognostic-markers-and-outcomes-in-inflammatory-airway-disease/

Patient selection, prognostic markers and outcomes in inflammatory airway disease

Patient selection, prognostic markers and outcomes in inflammatory airway disease

Created and Presented by: Rhinology And Skull Base Research Group, Continuing Medical Education Dinner Meeting

A live webinar and dinner educational event.

Agenda: • Prof Richard Harvey: Biologics – Responders and non-responders of the upper airway • A/Prof Janet Rimmer: Biologics – Responders and non-responders of the lower airway • Prof Constance Katelaris: Heterogeneity and similarities of action between biologics

Venue: ZEST Waterfront – 21 Wunulla Road Point Piper 2027 (located at the Royal Motor Yacht club)

Date: 22.02.2021 Time: Dinner meeting: 7:00pm – 9:30pm Webinar session: 7:30pm – 9:30pm

PRIVACY STATEMENT: Your personal information (“Information”) will be collected and used by AstraZeneca Pty Ltd (“AstraZeneca”) to register you for this event, for follow up purposes and for any other purpose described in AstraZeneca’s Privacy Policy. AstraZeneca may disclose your Information to our related entities or service providers (including IT support/service providers), some of which may be located overseas including in the US, European Union and Asia Pacific. If you do not provide your Information, AstraZeneca will not be able to register you for this event. Please refer to our Privacy Policy at http://www.astrazeneca.com.au/privacy-policy for more information about how your Information is handled and how you may seek to access or correct your Information, or submit a privacy complaint. AU-9861, February 2021.

For enquiries please contact: Marie Urriste

New Post has been published on https://sydneyentclinic.com/richard-harvey/2021/02/16/patient-selection-prognostic-markers-and-outcomes-in-inflammatory-airway-disease/

Patient selection, prognostic markers and outcomes in inflammatory airway disease

Patient selection, prognostic markers and outcomes in inflammatory airway disease

Created and Presented by: Rhinology And Skull Base Research Group, Continuing Medical Education Dinner Meeting

A live webinar and dinner educational event.

Agenda: • Prof Richard Harvey: Biologics – Responders and non-responders of the upper airway • A/Prof Janet Rimmer: Biologics – Responders and non-responders of the lower airway • Prof Constance Katelaris: Heterogeneity and similarities of action between biologics

Venue: ZEST Waterfront – 21 Wunulla Road Point Piper 2027 (located at the Royal Motor Yacht club)

Date: 22.02.2021 Time: Dinner meeting: 7:00pm – 9:30pm Webinar session: 7:30pm – 9:30pm

PRIVACY STATEMENT: Your personal information (“Information”) will be collected and used by AstraZeneca Pty Ltd (“AstraZeneca”) to register you for this event, for follow up purposes and for any other purpose described in AstraZeneca’s Privacy Policy. AstraZeneca may disclose your Information to our related entities or service providers (including IT support/service providers), some of which may be located overseas including in the US, European Union and Asia Pacific. If you do not provide your Information, AstraZeneca will not be able to register you for this event. Please refer to our Privacy Policy at http://www.astrazeneca.com.au/privacy-policy for more information about how your Information is handled and how you may seek to access or correct your Information, or submit a privacy complaint. AU-9861, February 2021.

For enquiries please contact: Marie Urriste

New Post has been published on https://sydneyentclinic.com/richard-harvey/2020/03/08/sinusitis-better-classified-by-rhinologists-and-the-sinus-specialist/

Sinusitis better classified by rhinologists and the sinus specialist

Chronic sinusitis is a very mixed bag of disease entitites to a sinus specialist.

Chronic rhinosinusitis (CRS) is a broadly defined process that has previously been used to describe many different sinonasal pathologies from odontogenic sinusitis, allergic fungal sinusitis, to the more contemporary definition of broad inflammatory airway diseases. Previous classification systems have dichotomized these patients into CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP).

In clinical practice, treatment decisions are often based upon clinical history, presumed disease process and molecular pathophysiology. The proposed classification system by EPOS 2020  is simple and practical. It proposes that the functional anatomical compartments involved create the first level of separation into local and diffuse. These are usually unilateral or bilateral in distribution. Diffuse does not imply ‘pan-sinusitis’ but simply that the disease does not confine to a known functional anatomical unit. This takes into account whether local anatomical factors are contributing to pathogenesis. Then the inflammatory endotype dominance separates into a Th2 skewed inflammation as this has both etiologic and treatment implications. The non-Th2 encompasses everything else we don’t know yet about inflammation and may change over time. The phenotypes or clinical examples are CRS entities that have been described and how they align with this system.

The range of conditions that encompass chronic rhinosinusitis to a sinus specialist:

Primary CRS Classificaiton system (Grayson JW, Hopkins C, Mori ES, B. Contemporary Classification of Chronic Rhinosinusitis: Movingbeyond CRSwNP and CRSsNP. JAMA Otolaryngol Head Neck Surg. 2020; )

  Less commonly, CRS is secondary to an established systemic disease (mucocillary dysfunction, autoimmune or immunodeficiency) or local pathology (odontogenic, neoplasm). Secondary CRS represents a group of clinical entities in which the sinus disease observed is part of ‘another’ disease process. Secondary CRS is simply an expression of another condition and correction of that mechanism will results in resolution of the CRS. The sinus specialist will look for other conditions that affect the human body, either locally or broadly to explain why a patient develops chronic sinus disease. If there is an underlying ‘secondary process’ then this is addressed but otherwise it is considered primary CRS.

Secondary CRS Classificaiton system (Grayson JW, Hopkins C, Mori ES, B. Contemporary Classification of Chronic Rhinosinusitis: Movingbeyond CRSwNP and CRSsNP. JAMA Otolaryngol Head Neck Surg. 2020; )

Hear a sinus specialist explain the diversity of conditions that encompass chronic rhinosinusitis:

New Post has been published on https://sydneyentclinic.com/richard-harvey/2020/03/08/sinusitis-better-classified-by-rhinologists-and-the-sinus-specialist/

Sinusitis better classified by rhinologists and the sinus specialist

Chronic sinusitis is a very mixed bag of disease entitites to a sinus specialist.

Chronic rhinosinusitis (CRS) is a broadly defined process that has previously been used to describe many different sinonasal pathologies from odontogenic sinusitis, allergic fungal sinusitis, to the more contemporary definition of broad inflammatory airway diseases. Previous classification systems have dichotomized these patients into CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP).

In clinical practice, treatment decisions are often based upon clinical history, presumed disease process and molecular pathophysiology. The proposed classification system by EPOS 2020  is simple and practical. It proposes that the functional anatomical compartments involved create the first level of separation into local and diffuse. These are usually unilateral or bilateral in distribution. Diffuse does not imply ‘pan-sinusitis’ but simply that the disease does not confine to a known functional anatomical unit. This takes into account whether local anatomical factors are contributing to pathogenesis. Then the inflammatory endotype dominance separates into a Th2 skewed inflammation as this has both etiologic and treatment implications. The non-Th2 encompasses everything else we don’t know yet about inflammation and may change over time. The phenotypes or clinical examples are CRS entities that have been described and how they align with this system.

The range of conditions that encompass chronic rhinosinusitis to a sinus specialist:

Primary CRS Classificaiton system (Grayson JW, Hopkins C, Mori ES, B. Contemporary Classification of Chronic Rhinosinusitis: Movingbeyond CRSwNP and CRSsNP. JAMA Otolaryngol Head Neck Surg. 2020; )

  Less commonly, CRS is secondary to an established systemic disease (mucocillary dysfunction, autoimmune or immunodeficiency) or local pathology (odontogenic, neoplasm). Secondary CRS represents a group of clinical entities in which the sinus disease observed is part of ‘another’ disease process. Secondary CRS is simply an expression of another condition and correction of that mechanism will results in resolution of the CRS. The sinus specialist will look for other conditions that affect the human body, either locally or broadly to explain why a patient develops chronic sinus disease. If there is an underlying ‘secondary process’ then this is addressed but otherwise it is considered primary CRS.

Secondary CRS Classificaiton system (Grayson JW, Hopkins C, Mori ES, B. Contemporary Classification of Chronic Rhinosinusitis: Movingbeyond CRSwNP and CRSsNP. JAMA Otolaryngol Head Neck Surg. 2020; )

Hear a sinus specialist explain the diversity of conditions that encompass chronic rhinosinusitis:

หลัก 3 Mu คือ อะไร ?

ทำความรู้จัก Muda Mura และ Muri หรือหลัก 3 Mu ว่าหลัก 3 Mu คือ อะไร ? (more…)

New Post has been published on http://sydneyentclinic.com/richard-harvey/2018/07/20/severe-asthma-and-sinusitis-nasal-polyps/

Controlling severe asthma and sinusitis (nasal polyps)

Successful management of severe asthma and sinusitis relies on understanding the disease process. For the majority of patients, a disordered inflammatory response is responsible and this is often an eosinophilic reaction. The nature of severe eosinophilic airway inflammation is still debated and the initiating factors still elude us. The perception of a threat by the host mucosa (us!) is at the heart of many theories for the origins of the eosinophilic inflammation and is thought to occur when the micro-environment is normal or only minimally distorted. The result is inflammation causing severe asthma and sinusitis despite those affected patients affected living in and exposed to the same environment as the rest of us.

Some of the mechanisms that are activated in eCRS (eosinophilic asthma and sinusitis/nasal polyps)

Many of our patients with severe asthma and sinusitis (eosinophilic airway disease) are well controlled by the effective use of locally delivered corticosteroids. This often requires a radical reshape of the sinus cavity and the use of a nasal irrigation for the upper airway (https://www.ncbi.nlm.nih.gov/pubmed/29394004). The lower airway is more easily accessible with inhaled therapies.

Controlling severe asthma and sinusitis

However, not everyone is controlled with topical-only treatments and we used to rely on cautious use of systemic or oral corticosteroids and other immune suppressing agents. All of which have side-effects that have to be carefully monitored as some are more susceptible than other to them.

Today, there are several biologic therapies available to patients with severe eosinophilic disease of their airway. These biologic agents are often human mono-clonal antibodies. They are directed to a specific signalling protein of the inflammation process and deplete the body of that signal mechanism.

Mepoluzimab (Anti-IL5) is one example that is currently available in Sydney both as a PBS supported medication for certain forms of lower airway involvement and under our clinical trials program for sinusitis.

Mepolizumab

hypereosinophilic syndrome (HES), eosinophilic esophagitis (EoE), nasal polyposis, eosinophilic granulomatosis with polyangiitis (EGPA) and chronic obstructive

New Post has been published on http://sydneyentclinic.com/richard-harvey/2018/07/20/severe-asthma-and-sinusitis-nasal-polyps/

Controlling severe asthma and sinusitis (nasal polyps)

Successful management of severe asthma and sinusitis relies on understanding the disease process. For the majority of patients, a disordered inflammatory response is responsible and this is often an eosinophilic reaction. The nature of severe eosinophilic airway inflammation is still debated and the initiating factors still elude us. The perception of a threat by the host mucosa (us!) is at the heart of many theories for the origins of the eosinophilic inflammation and is thought to occur when the micro-environment is normal or only minimally distorted. The result is inflammation causing severe asthma and sinusitis despite those affected patients affected living in and exposed to the same environment as the rest of us.

Some of the mechanisms that are activated in eCRS (eosinophilic asthma and sinusitis/nasal polyps)

Many of our patients with severe asthma and sinusitis (eosinophilic airway disease) are well controlled by the effective use of locally delivered corticosteroids. This often requires a radical reshape of the sinus cavity and the use of a nasal irrigation for the upper airway (https://www.ncbi.nlm.nih.gov/pubmed/29394004). The lower airway is more easily accessible with inhaled therapies.

Controlling severe asthma and sinusitis

However, not everyone is controlled with topical-only treatments and we used to rely on cautious use of systemic or oral corticosteroids and other immune suppressing agents. All of which have side-effects that have to be carefully monitored as some are more susceptible than other to them.

Today, there are several biologic therapies available to patients with severe eosinophilic disease of their airway. These biologic agents are often human mono-clonal antibodies. They are directed to a specific signalling protein of the inflammation process and deplete the body of that signal mechanism.

Mepoluzimab (Anti-IL5) is one example that is currently available in Sydney both as a PBS supported medication for certain forms of lower airway involvement and under our clinical trials program for sinusitis.

Mepolizumab

hypereosinophilic syndrome (HES), eosinophilic esophagitis (EoE), nasal polyposis, eosinophilic granulomatosis with polyangiitis (EGPA) and chronic obstructive