Antecedent Disease Is Less Prevalent in Amyotrophic Lateral Sclerosis
Background/Aims: Recent studies suggest that antecedent disease could impact the pathophysiology of the motoneuron disease Amyotrophic Lateral Sclerosis (ALS). We performed a case-control study to examine the prevalence of 11 antecedent diseases in ALS. Methods: Prevalence of antecedent disease in a...
Gespeichert in:
Veröffentlicht in: | Neuro-degenerative diseases 2015-01, Vol.15 (2), p.109-113 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Background/Aims: Recent studies suggest that antecedent disease could impact the pathophysiology of the motoneuron disease Amyotrophic Lateral Sclerosis (ALS). We performed a case-control study to examine the prevalence of 11 antecedent diseases in ALS. Methods: Prevalence of antecedent disease in a 1,288 patient ALS population (Emory University ALS Clinic, Atlanta, Ga., USA) is compared to an age, gender, and geography-matched 7,561 subject control population using a statistical odds ratio (OR) with 95% confidence interval. Results: Association of ALS with odds of arthritis (OR = 0.14); non-ALS neurological disease (OR = 0.14); liver disease (OR = 0.19); chronic obstructive pulmonary disorder or COPD (OR = 0.23); kidney disease (OR = 0.32); adult asthma (OR = 0.39); diabetes (OR = 0.47); hypertension (OR = 0.56); obesity (OR = 0.6); hyperlipidemia or hypercholesterolemia (OR = 0.62); and thyroid disease (OR = 0.78). Conclusions: The prevalence of antecedent disease was overall less in the ALS population. We present two potential lines of inquiry to explain these results: (1) ‘Other disease as ALS protection' - antecedent diseases infer biochemical neuroprotection to ALS; (2) ‘ALS as other disease protection' - the underpinnings of ALS could infer protection to other diseases, possibly via the mechanism hypervigilant regulation or ‘too-high' regulatory feedback gains. |
---|---|
ISSN: | 1660-2854 1660-2862 |
DOI: | 10.1159/000369812 |