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Acetyl‐L‐carnitine for the treatment of diabetic peripheral neuropathy

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Acetyl‐L‐carnitine for the treatment of diabetic neuropathy

The aim of this review

The aim of this review was to assess the effects of acetyl‐L‐carnitine (ALC) on diabetic peripheral neuropathy (DPN) in people with diabetes. We were particularly interested in whether ALC could relieve pain, and also aimed to identify any harmful effects.

Key messages

We are uncertain whether ALC reduces pain in DPN, as the evidence is sparse and of very low certainty. Adverse events may be no more common than with placebo, but the evidence here is also very uncertain.

What was studied in the review?

Diabetes is a condition where the amount of sugar in the blood is abnormally high. Damage to nerve fibres as a result of diabetes is called DPN. DPN is a frequent and severe complication of diabetes, affecting about 50% of people with long‐term diabetes. Overall, 16% to 24% of people with diabetes experience chronic pain due to nerve damage. The feet, legs, and hands are primarily affected by DPN.

There is a need for therapies to restore nerve function and relieve the symptoms of DPN. The Cochrane review authors searched for evidence from randomised trials on the effects of ALC in DPN. Evidence from randomised trials is usually more reliable than other study designs.

The main results of the review

The review authors found four relevant trials, which involved 906 adults with diabetes. Three studies compared ALC with a placebo (an inactive, dummy compound), and one compared ALC with methylcobalamin (a form of vitamin B12).

The certainty of the evidence from the studies ranged from low to very low, which means that we cannot be confident in the findings. The key reasons for this were that results were not always completely or clearly reported, the studies had serious limitations, and the results lacked precision.

In people with nerve damage due to diabetes, it is uncertain whether ALC reduces pain after 12 months of therapy, compared to placebo. The trials provided little or no information on the effects of ALC on functional impairment, sensory testing, and symptoms. Even when trials provided data, the quality of evidence was too low to draw reliable conclusions. The study that compared ALC with methylcobalamin did not assess pain. Functional impairment and symptoms may improve to a similar extent with ALC and methylcobalamin.

Harmful side effects may be no more frequent with ALC than with placebo. The evidence on adverse events from the trial comparing ALC with methylcobalamin was very uncertain.

Two of the four studies were funded by a manufacturer of ALC and the other two studies had at least one co‐author who was a consultant for an ALC manufacturer.

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