Alcohol use disorder and muscle weakness: Original study of the effect of vitamin D supplementation in ambulatory participants with alcohol use disorder.

INTRODUCTION: Chronic alcohol-related myopathy presents with proximal muscle weakness. We studied the effect of vitamin D supplementation on muscle weakness in adults with alcohol use disorder. METHOD: Randomized controlled trial. Participants were community-dwelling adults with alcohol use disorder. Participants allocated to VIDIO, vitamin D intensive outreach, received bimonthly oral doses of 50,000‒100,000 IU cholecalciferol for 12 months. Participants allocated to CAU, care as usual, received prescriptions of once-a-day tablets containing 800 IU cholecalciferol and 500 mg calcium carbonate. Data included demographic variables, laboratory tests, alcohol use, and rating scales of help-seeking and support. Main outcomes were the participants' quadriceps maximum voluntary contractions (qMVC) and serum-25(OH)vitamin D concentrations, 25(OH)D. RESULTS: In 66 participants, sex ratio 50/16, mean age 51 year, alcohol use was median 52 [IQR 24‒95] drinks per week. Baseline qMVC values were 77% (SD 29%) of reference values. Laboratory tests were available in 44/66 participants: baseline 25(OH)D concentrations were 39.4 (SD 23.7) nmol/L. Thirty-one participants with 25(OH)D concentrations <50 nmol/L received either VIDIO or CAU and improved in qMVC, respectively with mean 51 (P<0.05) and 62 Newton (no P-value because of loss of follow-up) after one year of treatment. Vitamin D status increased with mean +56.1 and +37.4 nmol/L, respectively in VIDIO and CAU. CONCLUSION: The qMVC values improved during vitamin supplementation in adults with vitamin D deficiency and alcohol use disorder. Despite higher 25(OH)D concentrations in VIDIO, in terms of muscle health no advise could be given in favor of one vitamin strategy over the other. TRIAL REGISTRATION: Netherlands Trial Register (NTR) identifier: NTR4114.

[Thiamine in patients with alcohol use disorder and Wernicke's encephalopathy]. / Thiamine bij een alcoholstoornis en Wernicke-encefalopathie.

- Patients with alcohol use disorder frequently have a thiamine deficiency.- A potential life-threatening complication of thiamine deficiency is Wernicke's encephalopathy.- Since it is clinically difficult to recognize Wernicke's encephalopathy, this condition is often treated inadequately. - Early supplementation of thiamine is important to avoid irreversible neurological damage. - There are differences between the Dutch guidelines regarding the supplementation of thiamine for the treatment of alcoholic use disorder, and those for Wernicke's encephalopathy. - There are no solid evidence-based recommendations about the best dosage, route of administration and duration of thiamine supplementation for the treatment of alcohol use disorder and Wernicke's encephalopathy. - Based on the pharmacokinetic properties of thiamine, it is more appropriate to give patients with alcohol use disorder 25 mg four times a day rather than 50 mg twice a day. - Patients at high risk of Wernicke's encephalopathy should immediately receive an intravenous or intramuscular dose of thiamine; patients with suspected Wernicke's encephalopathy should preferably receive an intravenous dose.- Reports of anaphylactic reaction to parenteral administration of thiamine are rare and are not a reason to refrain from parenteral treatment.

Biomarkers of delirium as a clue to diagnosis and pathogenesis of Wernicke-Korsakoff syndrome.

BACKGROUND AND PURPOSE: Wernicke's encephalopathy (WE) and Korsakoff's syndrome are considered to be different stages of the same disorder due to thiamine deficiency, which is called Wernicke-Korsakoff syndrome (WKS). The earliest biochemical change is the decrease of α-ketoglutarate-dehydrogenase activity in astrocytes. According to autopsy-based series, mental status changes are present in 82% of WE cases. The objective of the present review is to identify possible underlying mechanisms relating the occurrence of delirium to WKS. METHODS: Studies involving delirium in WKS, however, are rare. Therefore, first, a search was done for candidate biomarkers of delirium irrespective of the clinical setting. Secondly, the results were focused on identification of these biomarkers in reports on WKS. RESULTS: In various settings, 10 biochemical and/or genetic biomarkers showed strong associations with the occurrence of delirium. For WKS three of these candidate biomarkers were identified, namely brain tissue cell counts of CD68 positive cells as a marker of microglial activation, high cerebrospinal fluid lactate levels, and MHPG, a metabolite of norepinephrine. Based on current literature, markers of microglial activation may present an interesting patho-etiological relationship between thiamine deficiency and delirium in WKS. CONCLUSIONS: In WKS cases, changes in astroglia and microglial proliferation were reported. The possible loss-of-function mechanisms following thiamine deficiency in WKS are proposed to come from microglial activation, resulting in a delirium in the initial phase of WKS.

[Neurological complications of infectious mononucleosis in 3 patients]. / Neurologische complicaties van mononucleosis infectiosa bij 3 patiënten.

Neurological complications of infectious mononucleosis were seen in three patients, a boy aged 18 months and two women aged 70 and 51 years respectively: a Bell's palsy, polyradiculitis and transverse myelitis. In a patient with acute neurological symptoms without indications of any other cause, infectious mononucleosis should be considered.