Serum Levels of Carnitine in Chronic Fatigue Syndrome: Clinical Correlates

Plioplys, Audrius V.; Plioplys, Sigita

doi:10.1159/000119226

Cited by 46 publications

(39 citation statements)

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“…Correlations between lower acylcamitine levels and worse clinical CFS symptomatology has been previously reported [12], Likewise, in a previous study, we reported decreased free and total carnitine serum levels being cor related with CFS symptomatology [13]. In the current treatment program we found decreased free carnitine lev els to be associated with the female sex, an observation that is well established in normals [32,33], Also, we found decreased acylcamitine levels to be associated with dis ease severity in two study psychometric parameters used, thus confirming previously reported results [12], Higher acylcamitine and total carnitine levels were also associat ed with longer duration of illness and with chronic onset of illness, observations that have not been previously reported.…”

Section: Discussionsupporting

confidence: 86%

“…Also, clinical correlations were noted between increases in acyl carnitine levels and improvement in fatigue symptoms [12]. We have found decreased total carnitine, free carni tine and acylcarnitine levels in 35 CFS patients (27 females and 8 males) [13]. We have also found a statisti cally significant correlation between serum levels of total and free carnitine and clinical symptomatology [13].…”

Section: Introductionsupporting

confidence: 53%

“…We have found decreased total carnitine, free carni tine and acylcarnitine levels in 35 CFS patients (27 females and 8 males) [13]. We have also found a statisti cally significant correlation between serum levels of total and free carnitine and clinical symptomatology [13]. Higher serum carnitine levels correlated with better func tional capacity.…”

Section: Introductionsupporting

confidence: 50%

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Amantadine and L-Carnitine Treatment of Chronic Fatigue Syndrome

Plioplys

1997

Neuropsychobiology

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Carnitine is essential for mitochondrial energy production. Disturbance in mitochondrial function may contribute to or cause the fatigue seen in Chronic Fatigue Syndrome (CFS) patients. Previous investigations have reported decreased carnitine levels in CFS. Orally administered L-carnitine is an effective medicine in treating the fatigue seen in a number of chronic neurologic diseases. Amantadine is one of the most effective medicines for treating the fatigue seen in multiple sclerosis patients. Isolated reports suggest that it may also be effective in treating CFS patients. Formal investigations of the use of L-carnitine and amantadine for treating CFS have not been previously reported. We treated 30 CFS patients in a crossover design comparing L-carnitine and amantadine. Each medicine was given for 2 months, with a 2-week washout period between medicines. L-Carnitine or amantadine was alternately assigned as fist medicine. Amantadine was poorly tolerated by the CFS patients. Only 15 were able to complete 8 weeks of treatment, the others had to stop taking the medicine due to side effects. In those individuals who completed 8 weeks of treatment, there was no statistically significant difference in any of the clinical parameters that were followed. However, with L-carnitine we found statistically significant clinical improvement in 12 of the 18 studied parameters after 8 weeks of treatment. None of the clinical parameters showed any deterioration. The greatest improvement took place between 4 and 8 weeks of L-carnitine treatment. Only 1 patient was unable to complete 8 weeks of treatment due to diarrhea. L-Carnitine is a safe and very well tolerated medicine which improves the clinical status of CFS patients. In this study we also analyzed clinical and laboratory correlates of CFS symptomatology and improvement parameters.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionsupporting

confidence: 53%

Section: Introductionsupporting

confidence: 50%

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Amantadine and L-Carnitine Treatment of Chronic Fatigue Syndrome

Plioplys

1997

Neuropsychobiology

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“…A primary genetic carnitine deficiency occurs in children with dilated cardiomyopathy, hypoglycemia, and low carnitine contents in plasma, liver and muscle, owing to a defect in a common high-affinity trans- Matsumoto/Sato/Ohashi/Araki/Tadokoro/ Osumi/Ito/Morita/Amano port system [21][22][23]. Acquired forms of carnitine deficiency are observed in women during pregnancy [24], patients receiving long-term total parenteral nutrition [25], patients with chronic fatigue syndrome [26,27], and chronic HD patients. HD is of particular note because it induces a substantial loss of carnitine from the skeletal and cardiac muscle.…”

Section: Discussionmentioning

confidence: 99%

Effects of L-Carnitine Supplementation on Cardiac Morbidity in Hemodialyzed Patients

Matsumoto

Sato

Ohashi³

et al. 2000

Am J Nephrol

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Cardiac diseases are well known among patients on maintenance hemodialysis (HD), and carnitine deficiency may be an important factor in cardiac morbidity. We studied the effects of low-dose L-carnitine treatment (500 mg/day) on chest symptoms (dyspnea on exertion, chest pain, palpitation), cardiac function, and left ventricular (LV) mass in 9 HD patients with reduced ejection fraction (EF). After 6 months of L-carnitine treatment, most patients had at least some improvement in chest symptoms, while LVEF was increased and LV mass was decreased. Carnitine fractions increased and reached plateaus at 2–3 times the baseline levels. These results suggest that prolonged low-dose L-carnitine treatment can improve the cardiac morbidity by restoring decreased carnitine tissue levels and impaired oxidation of FFA.

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“…A few case reports have described patients labeled with chronic fatigue syndrome (CFS) ultimately diagnosed with an energy metabolism disorder, based on measured deficiencies in respiratory chain or fatty acid oxidation enzymes, or on the basis of carnitine deficiency [88][89][90]. Although beyond the scope of this article, these earlier findings resulted in considerable interest among clinicians and patients to perform in-depth evaluations of those suffering with CFS.…”

Section: Chronic Fatiguementioning

confidence: 99%

Neuromuscular and Systemic Presentations in Adults: diagnoses beyond MERRF and MELAS

Cohen

2013

Neurotherapeutics

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Mitochondrial diseases are a diverse group of inherited and acquired disorders that result in inadequate energy production. They can be caused by inheritable genetic mutations, acquired somatic mutations, and exposure to toxins (including some prescription medications). Normal mitochondrial physiology is responsible, in part, for the aging process itself, as free radical production within the mitochondria results in a lifetime burden of oxidative damage to DNA, especially the mitochondrial DNA that, in turn, replicate the mutational burden in future copies of itself, and lipid membranes. Primary mitochondrial diseases are those caused by mutations in genes that encode for mitochondrial structural and enzymatic proteins, and those proteins required for mitochondrial assembly and maintenance. A number of common adult maladies are associated with defective mitochondrial energy production and function, including diabetes, obesity, hyperthyroidism, hypothyroidism, and hyperlipidemia. Mitochondrial dysfunction has been demonstrated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson disease, amyotrophic lateral sclerosis, and some cancers. Polymorphisms in mitochondrial DNA have been linked to disease susceptibility, including death from sepsis and survival after head injury. There is considerable overlap in symptoms caused by primary mitochondrial diseases and those illnesses that affect mitochondrial function, but are not caused by primary mutations, as well as disorders that mimic mitochondrial diseases, but are caused by other identified mutations. Evaluation of these disorders is complex, expensive, and not without false-negative and false-positive results that can mislead the physician. Most of the common heritable mitochondrial disorders have been well-described in the literature, but can be overlooked by many clinicians if they are uneducated about these disorders. In general, the evaluation of the classic mitochondrial disorders has become straightforward if the clinician recognized the phenotype and orders appropriate confirmatory testing. However, the majority of patients referred for a mitochondrial evaluation do not have a clear presentation that allows for rapid identification and testing. This article provides introductory comments on mitochondrial structure, physiology, and genetics, but will focus on the presentation and evaluation of adults with mitochondrial symptoms, but who may not have a primary mitochondrial disease.

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Serum Levels of Carnitine in Chronic Fatigue Syndrome: Clinical Correlates

Cited by 46 publications

References 10 publications

Amantadine and <i>L</i>-Carnitine Treatment of Chronic Fatigue Syndrome

Amantadine and <i>L</i>-Carnitine Treatment of Chronic Fatigue Syndrome

Effects of <i>L</i>-Carnitine Supplementation on Cardiac Morbidity in Hemodialyzed Patients

Neuromuscular and Systemic Presentations in Adults: diagnoses beyond MERRF and MELAS

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