Alcohol Consumption as a Causator and/or an Accelerator of Neuropathy in People With Diabetes Is Regularly Overlooked

Author: David S. H. Bell & Edison Goncalves 

Abstract

Patients with diabetes and distal symmetrical polyneuropathy (DSP) are routinely evaluated for etiologies other than diabetes, including vitamin B12 deficiency, paraproteinemia, hypothyroidism and drug or autoimmune-induced neuropathy. However, the most common cause of DSP, next to that of diabetes, is alcohol intake, which is almost never evaluated. In addition to assessment of alcohol intake based on patient history, which often leads to an underestimation of alchohol intake, markers of a high alcohol intake (elevated liver enzymes, uric acid, triglycerides, low magnesium or low folic acid levels) should be obtained. However, the test that is most likely to detect surreptitious alcohol intake is urinary ethyl glucuronide (EtG), which will detect the intake of alcohol within the previous 90 h. Detection of alcohol use is important since if alcohol consumption is not discontinued, DSP, whatever the etiology, will not improve. In addition, the use of drugs to improve symptoms of DSP (tricyclics, anti-epileptics, serotonin, norepinephrine reuptake inhibitors and analgesics) may in combination with alcohol excessively suppress respiration and cognitive function such that these drugs should not be prescribed or utilized if use of alcohol continues. In the future, all patients with DSP, and especially those with symptomatic DSP, should be biochemically screened for excessive alcohol intake and appropriate action taken.