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Relationship of Endoplasmic Reticulum Stress and Adenoid Diseases

Relationship Between Apoptosis and er Stress in Chronic Adenoiditis and Adenoid Hypertrophy

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT04583631
Enrollment
54
Registered
2020-10-12
Start date
2018-11-01
Completion date
2019-08-01
Last updated
2021-09-27

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Adenoiditis Acute Infective

Keywords

Adenoidectomy, ; Endoplasmic Reticulum

Brief summary

Adenoid tissue is a significant organ for the performing of immune systems in children. The Endoplasmic Reticulum (ER), is an organelle needed for the care of a stable function of cells. The purpose of the study was to explore the correlation among ER stress and adenoid tissue disorders and to explain the structure of diseases related to the immune system.

Interventions

All patients underwent adenoidectomy under general anesthesia by routine curettage method and adenoid tissues were put in formaldehyde and sent to the genetics department for the exploration of ER stress and apoptosis markers.

Sponsors

Selcuk University
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
3 Years to 9 Years
Healthy volunteers
No

Inclusion criteria

\- Patients with the clinical diagnosis of chronic adenoiditis and adenoid hypertrophy.

Exclusion criteria

* Systemic diseases * Other otolaryngological

Design outcomes

Primary

MeasureTime frameDescription
Correlation of ER stress and apoptosis with chronic adenoiditis and adenoid hypertrophy2018-2019 (1 year)Our primary outcome was to evaluate providing that ER stress and apoptosis reaction performing in chronic adenoiditis and adenoid hypertropy, which is related with the immune system of children.

Countries

Turkey (Türkiye)

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026