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Diane Check

Cooper Institute | USA

Title: Dextroamphetamine sulphate provides marked improvement for patients suffering from chronic fatigue even when the etiology is unexplained

Biography

Biography: Diane Check

Abstract

Statement of problem: Dextroamphetamine sulfate is an approved drug for chronic fatigue associated with cancer and multiple sclerosis.  The question that the present study was designed to answer is whether the sympathomimetic amine therapy only helps chronic fatigue associated with cancer, and multiple sclerosis, or could it be used in patients in apparent good health but plagued by severe unexplained chronic fatigue.

Methods: Dextroamphetamine sulfate extended release capsules were administered to 50 patients with unexplained chronic fatigue (thyroid, adrenal, infectious and autoimmune etiologies excluded).  The dosage could be increased on a monthly basis to a maximum of 60mg/day.  Six months following the final dosage the patients answered a questionnaire:  fatigue – 1) worse, 2) stable but no better, 3) slightly better, 4) moderately better, 5) markedly better.

Results: Forty-eight of 50 patients (96%) stated markedly better and 2 patients moderately better.

Conclusions: Dextroamphetamine sulfate not only improves the chronic fatigue for patients with cancer and multiple sclerosis, but also very effective relieves chronic fatigue in otherwise physically normal patients.  Thus, this study will hopefully encourage palliative care specialists to consider this treatment for chronic fatigue for other debilitating conditions besides cancer and multiple sclerosis.  Furthermore, through approved for chronic fatigue for cancer patients, the drug is likely underutilized by palliative care specialists for patients with cancer.  Hopefully this study will generate more interest in treating patients with cancer with dextroamphetamine sulfate.  The mechanism is likely related to stimulating the release of dopamine from sympathetic nerve fibers. Dopamine decreases cellular permeability and it has been hypothesized that chemicals permeating into mitochondria may cause dysfunction of the mitochondria in muscles leading to fatigue.

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