Disulfiram-induced neuropathy: a case report

Mohapatra, Satyakam; Sahoo, Manas Ranjan; Rath, Neelmadhav

doi:10.1016/j.genhosppsych.2014.09.015

Cited by 12 publications

(10 citation statements)

References 6 publications

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“…This suggests the involvement of small fiber sensory nerves but the sparing of large fiber sensory nerves. This is in contrast to prior literature that report large fiber involvement in disulfiram neuropathy [ 5 , 6 ]. Unfortunately, both of our patients declined repeat electrodiagnostic testing and hence it was not possible to document a correlation between clinical and electrophysiological findings.…”

Section: Case Presentationcontrasting

confidence: 97%

“…Disulfiram neuropathy occurs in patients who have a history of chronic alcohol use. The frequency with which it occurs is difficult to assess, though one quoted figure is 1:15,000 [ 5 , 7 ]. The challenge in determining disulfiram as the causative agent is that concomitant alcohol-related neuropathy is often a confounding factor; thus, disulfiram neuropathy is likely under-diagnosed and attributed to alcohol neuropathy.…”

Section: Discussionmentioning

confidence: 99%

“…Some observations that can help distinguish the two include a history of onset that occurs in a matter of weeks in disulfiram neuropathy as opposed to an insidious course over months in alcoholic neuropathy. Additionally, the progression is faster in disulfiram neuropathy [ 5 ]. Symptoms of both types of neuropathy can be similar, such as symmetrical distribution, worse severity distally, and depression of ankle jerk reflexes.…”

Section: Case Presentationmentioning

confidence: 99%

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Disulfiram neuropathy: two case reports

2016

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BackgroundNeuropathy is a rare adverse side effect of disulfiram therapy and is under-recognized. There have been few case reports documenting this side effect.Case presentationTwo cases of disulfiram peripheral neuropathy are discussed. The first case is that of a 25-year-old Caucasian woman who was exposed to disulfiram therapy for a total of 8 months and developed pain and stiffness that prevented her from walking. The second case is that of a 46-year-old Caucasian woman who developed sudden-onset numbness in her lower extremities with progression to pain. Her symptoms improved over the course of 2 months after cessation of disulfiram therapy. In both cases, symptoms improved after cessation of disulfiram therapy.ConclusionsDisulfiram neuropathy occurs in persons with a history of chronic alcohol use. It is under-recognized and often attributed to alcoholic neuropathy given its comorbidity with alcoholic neuropathy. A greater understanding of this side effect may reduce neurologic complications related to disulfiram neuropathy and aid in early withdrawal of this offending agent.

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Section: Case Presentationcontrasting

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Case Presentationmentioning

confidence: 99%

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Disulfiram neuropathy: two case reports

2016

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“…For the past 50 years disulfiram is the commonly prescribed drug for the treatment of alcohol dependence. Important side effects of disulfiram are hepatological, dermatological, neurological (polyneuritis, encephalopathy) 1 , 2) and psychiatric in nature. Psychiatric manifestations include confusion, loss of memory, psychosis, 3 – 6) mania with psychotic symptoms.…”

Section: Introductionmentioning

confidence: 99%

Disulfiram Induced Psychosis

Mohapatra

Rath

2017

Clin Psychopharmacol Neurosci

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Disulfiram is the commonly prescribed drug for the treatment of alcohol dependence. It’s major metabolite (diethyldithiocarbamate) is an inhibitor of dopamine-betahydroxylase, an enzyme that catalyzes the metabolism of dopamine to norepinephrine resulting in psychosis. We recommend that disulfiram should be used at the lowest effective dose, possibly 250 mg daily and caution should be taken while prescribing disulfiram for patients with personal and familial antecedents of psychosis.

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“…[10] Notably, a phase 2 clinical trial of disulfiram in mCRPC patients demonstrated significant toxicity without improvement in efficacy. [11] The failure of DSF in the clinical setting could be attributed to its lack of specificity along with its unwanted metabolites.…”

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confidence: 99%

Leveraging γ‐Glutamyl Transferase To Direct Cytotoxicity of Copper Dithiocarbamates against Prostate Cancer Cells

et al. 2018

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A prodrug approach is presented to direct copper-dependent cytotoxicity to prostate cancer cells. The prochelator GGTDTC requires activation by γ-glutamyl transferase (GGT) to release the metal chelator diethyldithiocarbamate from a linker that masks its thiol reactivity and metal binding properties. In vitro studies demonstrated successful masking of copper binding as well as clean liberation of the chelator by GGT. GGTDTC was stable to non-specific degradation when incubated with a series of prostate cancer and normal cell lines, with selective release of diethyldithiocarbamate only occurring in cells with measurable GGT activity. The antiproliferative efficacy of the prochelator correlated with cellular GGT activity, with 24 h inhibitory concentrations ranging from 800 nm in prostate cancer lines 22Rv1 and LNCaP to over 15 μm in normal prostate PWR-1E cells. These findings underscore a new strategy to leverage the amplified copper metabolism of prostate cancer by conditional activation of a metal-binding pharmacophore.

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Disulfiram-induced neuropathy: a case report

Cited by 12 publications

References 6 publications

Disulfiram neuropathy: two case reports

Disulfiram neuropathy: two case reports

Disulfiram Induced Psychosis

Leveraging γ‐Glutamyl Transferase To Direct Cytotoxicity of Copper Dithiocarbamates against Prostate Cancer Cells

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