Clinical trial NCT00331812: Mitochondrial Functions and Oxidative Stress in ALS Patients
Official title: Study of Mitochondrial Functions and Oxidative Stress in ALS Patients.
Study type: OBSERVATIONAL
Overall status: UNKNOWN
Conditions: Amyotrophic Lateral Sclerosis
Keywords: Hypermetabolism
Mitochondrial abnormalities
Oxidant/antioxidant status
Lead sponsor: University Hospital, Clermont-Ferrand
Sponsor class: OTHER
Collaborators: name: University Hospital, Limoges
name: Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement
First posted: 2006-05-31
Enrollment: 40
Sex: ALL
Minimum age (years): 30
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Three groups of patients will be studied : 20 hypermetabolic ALS patients, 20 normometabolic ALS patients and 20 healthy volunteers paired for age and sex.

Brief summary: In Amyotrophic Lateral Sclerosis (ALS), malnutrition is frequent (16 to 50 % of the patients) and is an independent prognostic factor. One of the implicated factors is the increase of resting energy expenditure (REE) which can be found in about 50 % of ALS patients. The origin of this hypermetabolism is currently unknown but could be located in the mitochondria. In fact, some studies have found mitochondrial abnormalities and the existence of an oxidative stress. Thus, the aim of this study is to characterize the mitochondrial abnormalities and the oxidant/antioxidant status of ALS patients and to determine their relationship with the metabolic status, hypermetabolism or normometabolism. Three groups of patients will be studied : 20 hypermetabolic ALS patients, 20 normometabolic ALS patients and 20 healthy volunteers paired for age and sex.

Detailed description: In Amyotrophic Lateral Sclerosis (ALS), malnutrition is frequent (16 to 50 % of the patients) and is an independent prognostic factor. One of the implicated factors is the increase of resting energy expenditure (REE) which can be found in about 50 % of ALS patients. The origin of this hypermetabolism is currently unknown but could be located in the mitochondria. In fact, some studies have found mitochondrial abnormalities and the existence of an oxidative stress. Thus, the aim of this study is to characterize the mitochondrial abnormalities and the oxidant/antioxidant status of ALS patients and to determine their relationship with the metabolic status, hypermetabolism or normometabolism. Three groups of patients will be studied : 20 hypermetabolic ALS patients, 20 normometabolic ALS patients and 20 healthy volunteers paired for age and sex.

Eligibility criteria: Inclusion Criteria:

* male or female
* age \> 30 years
* definite or probable ALS according to the El Escorial criteria, bulbar or spinal form, ALS diagnosis \< 1 year and treatment by riluzole.

Exclusion Criteria:

* family history of ALS,
* oral, enteral or parenteral nutritional supply,
* vitamin or trace element supplementation
* confusing illness (cancer, diabetes, chronic infectious or inflammatory disease,thyroid disorders, recent surgery...),
* current tobacco use,
* alcoholism
* treatment by corticosteroids,
* diuretics,
* anorectics
* NSAIDs
* cytotoxics
* anticoagulants...

Primary outcomes:
measure: relationship between these abnormalities and the metabolic status (hypermetabolism or normometabolism).
Secondary outcomes:
Other outcomes:
Locations:
city: Clermont-Ferrand
country: France
facility: Clermont-Ferrand University Hospital
state: Auvergne
Study officials:
affiliation: University Hospital, Clermont-Ferrand
name: Corinne Bouteloup, Dr
role: PRINCIPAL_INVESTIGATOR
References:
citation: Desport JC, Preux PM, Magy L, Boirie Y, Vallat JM, Beaufrere B, Couratier P. Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis. Am J Clin Nutr. 2001 Sep;74(3):328-34. doi: 10.1093/ajcn/74.3.328.
citation: Ferrante RJ, Browne SE, Shinobu LA, Bowling AC, Baik MJ, MacGarvey U, Kowall NW, Brown RH Jr, Beal MF. Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis. J Neurochem. 1997 Nov;69(5):2064-74. doi: 10.1046/j.1471-4159.1997.69052064.x.
citation: Menzies FM, Ince PG, Shaw PJ. Mitochondrial involvement in amyotrophic lateral sclerosis. Neurochem Int. 2002 May;40(6):543-51. doi: 10.1016/s0197-0186(01)00125-5.