Concomitant occurrence of Wernicke’s encephalopathy and sarcopenia due to vitamin D depletion in patients with alcohol use disorder: a case report

Abstract

Individuals with alcohol use disorder frequently suffer from vitamin D deficiency, in addition to deficiencies in vitamins B12, folic acid and B1. This is due to inadequate dietary intake and behavioural changes. Each of these deficiencies results in different clinical symptoms. Subacute spinal cord degeneration, together with radicular and sensorimotor peripheral neuropathy, arises from B12 vitamin and folic acid deficiencies. B1 vitamin deficiency leads to Wernicke’s encephalopathy, which can include the classical triad of symptoms (i.e. cognitive changes, ataxia and ophthalmoplegia). Sarcopenia is a consequence of a long-term deficiency of vitamin D. This current case report describes a 43-year-old female patient with alcohol use disorder who complained of dizziness, postural disturbance and episodes of intermittent paraesthesia. She was subsequently shown to have concomitant Wernicke’s encephalopathy and sarcopenia due to vitamin D deficiency. This case report presents the diagnostic process undertaken to exclude conditions related to ataxia and paraparesis other than vitamins D and B1 deficiencies. It also emphasizes the importance of concomitant replacement of the depleted vitamins because the vitamin deficiency may occur simultaneously, which causes the accompanying manifestations of several clinical syndromes.

Keywords

Ataxia paraparesis sarcopenia vitamin B1 vitamin D

Introduction

Patients with alcohol use disorder, due to inadequate dietary intake and behavioural alterations, frequently suffer from vitamin D deficiency, in addition to a deficit of vitamin B12, folic acid and vitamin B1.^1,2 Each of these deficiencies results in different clinical symptoms. Subacute spinal cord degeneration, together with radicular and sensorimotor peripheral neuropathy, arises from B12 vitamin and folic acid deficiency.³ B1 vitamin deficits result in Wernicke’s encephalopathy, which can include the classical triad of symptoms (i.e. cognitive alteration, ataxia and ophthalmoplegia).⁴ Sarcopenia is a consequence of long-term vitamin D deficiency.⁵

This current case report describes a female patient with alcohol use disorder who was subsequently shown to have Wernicke’s encephalopathy and concomitant sarcopenia due to vitamin D deficiency.

Case report

In April 2021, a 43-year-old female patient was admitted to the Department of Neurology, Univerzita Pavla Jozefa Šafárika v Košiciach, Košice, Slovakia after repeatedly presenting to the department with right-sided lower limb weakness that had worsened over the past 6 months. With regard to her prior medical history, the patient reported epileptic seizures and chronic pancreatitis in relation to alcohol abuse in the past 5 years and local manifestations of psoriasis. She also presented a history of folic acid supplementation over the last 6 months, ordered by a haematologist who evaluated her in order to rule out hereditary thrombophilia.

One week prior to this case presentation, the patient had been admitted to the Department of Neurology, Univerzita Pavla Jozefa Šafárika v Košiciach presenting with dizziness, postural disturbance and episodes of intermittent paraesthesia with tingling during the week before her examination. She also complained of pain localized to the area of the right hip joint. During this previous admission, drowsiness and mild cognitive impairment with an inability to concentrate and memory problems were observed. During repeated clinical examinations, the patient was observed to have impaired posture and gait with a positive Romberg sign, dysmetria and intention tremor. There were no signs of L2–S2 root radiculopathy or funicular pain. The otorhinolaryngologist repeatedly excluded a vestibular origin of the complaints by electronystagmography.

During the current admission and round of investigations, the neurologist (M.F.) concluded the findings to be of progressive cerebellar ataxia and flaccid paraparesis of the lower limbs of unknown origin. On further review, a magnetic resonance imaging (MRI) examination undertaken 6 months previously showed frontal and parietal thickening of the meninges on the right side by 3.3 mm and three hyperintense lesions in T2-weighted fluid attenuated inversion recovery (FLAIR) MRI in the area of the pons Varolii, with a diameter of <5 mm. The lesions were described as demyelinating because they did not show either diffusion restriction or postcontrast enhancement. As a result of involutional changes, there was a subtle enlargement of the ventricles and the subarachnoid space. Due to the neurological findings, an MRI of the brain and a lumbar puncture were performed. When compared with the preceding MRI performed 6 months prior to hospitalization, the following changes were noted: supratentorial solitary white matter lesions 3 mm in diameter and in the pons Varolii area 5 mm in diameter with an accentuated T2-weighted FLAIR signal.

An MRI of the spinal cord, including the cervical, thoracic and lumbar regions, exhibited only a low grade of degenerative signs, with no sign of spinal cord or nerve root compression. It also revealed spondylolisthesis of the L4–L5 vertebrae with a diameter of <3.5 mm, which according to the neurosurgeon (M.O.) may not have had an effect on the development of paraparesis and the sensation of paraesthesia. No signs of hyperintense lesions on T2-weighted images of the spinal cord were recorded. Examination of the cerebrospinal fluid (CSF), including examination of specific antibodies, did not show inflammation in the central nervous system (CNS). These MRI findings, together with the CSF results (Table 1), were not indicative of spinal cord pathology, so her physicians did not proceed with a differential diagnosis of spinal cord disease.

Table 1.

Lumbar puncture findings in a 43-year-old female patient who was hospitalized after repeatedly presenting with right-sided lower limb weakness that had worsened over the past 6 months.

Qualitative analysis of the CSF	Clear, colourless cerebrospinal fluid; CSF glucose level: 3.5 mmol/l; CSF protein level: 312 mg/l; CSF Cl: 128 mmol/l; CSF lactate: 1.47 mmol/l.
Qualitative analysis of the CSF	CSF blood cells: mononuclear oligocytosis without cellular activity.
Analysis for the presence of antibodies in the CSF	Qualitative proof of immunoglobulin IgG oligoclonality.
	IEF method: type D (5/5) – reflecting image presented (CSF/serum) 5 IgG gradients.
	Conclusion: intrathecal oligoclonal IgG production in the CSF was not confirmed. Higher possibility of systemic inflammation.
Analysis for the presence of specific antibodies in the CSF	Anti-aquaporin IV: negative; L-anti-MOG: negative; NMDAR: negative; CASPR2: negative; AMPA R1/R2: negative; DPPX: negative; LGI 1: negative; GABAB-R: negative; CSF-TPHA: negative.
Serology	Measles, rubeola, VZV, EBNA and CMV: all negative; HSV (1 + 2) 1.4 IU/ml (normal range, 0.7–1.3 IU/ml), but HSV IgG was not confirmed (AI positivity above 1.5 IU/ml in intact HLB). Anti-Borrelia IgM 14 IU/ml.

CSF, cerebrospinal fluid; Ig, immunoglobulin; IEF, isoelectric focusing; MOG, myelin oligodendrocyte glycoprotein; NMDAR, N-methyl-D-aspartate receptor; CASPR2, contactin-associated protein-like 2; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; DPPX, dipeptidyl-peptidase-like protein 6; LGI, lactate-glucose index; GABAB-R, gamma-aminobutyric acid type B-receptor; CSF-TPHA, cerebrospinal fluid - Treponema pallidum hemagglutination assay; VZV, varicella-zoster virus; EBNA, Epstein Barr nuclear antigen; CMV, cytomegalovirus; HSV, herpes simplex virus; AI, active ingredient; HLB, hydrophilic-lipophilic balance.

Ultrasonography of the carotid arteries did not show any significant change in the diameter of the examined arteries, nor did it show the presence of atherosclerotic lesions. An electromyography examination did not confirm peripheral neuropathy.

In order to exclude a thrombophilic state, 6 months previously the patient was referred to a haematologist who ruled out hereditary thrombophilia, but registered slightly positive levels of anti- Annexin V. However, the patient presented no clinical or laboratory signs of a coagulation disorder. The haematologist repeatedly detected low levels of folic acid and started to substitute it once daily. Vitamin B12 levels were normal.

During routine laboratory screening, slightly decreased levels of transferrin, elevated levels of fibrinogen and carcinoembryonic antigen (CEA) were detected, which suggested systemic inflammation or neoplasia (Table 2). Abdominal computed tomography (CT), performed due to the elevated levels of CEA, described a pancreatic pseudocyst, which was determined to be a consequence of acute pancreatitis in her past medical history. The patient’s clinical state, biochemical findings and abdominal CT did not indicate liver cirrhosis.

Table 2.

Laboratory findings in a 43-year-old female patient who was hospitalized after repeatedly presenting with right-sided lower limb weakness that had worsened over the past 6 months.

Biochemistry:

Sodium: 133.6 mmol/l; potassium: 4.7 mmol/l; BUN: 4.2 mmol/l; creatinine: 50.6 µmol/l; glucose: 5.0 mmol/l; CRP: 3.5 mg/l; AST: 0.68 µkat/l; ALT: 0.58 µkat/l; bilirubin: 11 µmol/l; uric acid: 286 µmol/l; total proteins: 76.9 g/l; albumin: 42.0 g/l; magnesium: 0.80 mmol/l; ammonia: 22 µmol/l; CK: 0.97 µkat/l; CK MB: 0.31 µkat/l; LDH: 2.9 µkat/l; myoglobin: 21.0 μg/l; iron: 12.0 µmol/l; ferritin: 49.7µg/l; transferrin saturation: 18.2%; ceruloplasmin: 0.30 g/l; copper: 20.4 µmol/l; vitamin B12:171 pmol/l; vitamin B1: 158 nmol/l; vitamin B6: 108 nmol/l.

Blood count and coagulation status:

Haemoglobin: 13.7 g/dl; haematocrit: 0.41%; mean corpuscular volume: 97.2 fl; WBC count: 8.1 × 10⁹/l; platelet count: 246 × 10⁹/l; prothrombin time: 0.98 INR; fibrinogen: 4.76 g/l.

Endocrinological laboratory findings:

Calcium: 2.22 mmol/l (normal range, 2.2–2.65 mmol/l); phosphorus: 1.22 mmol/l (normal range, 0.8–1.45 mmol/l); vitamin D: 34.12 µg/l (normal range, 20–100 µg/l); parathormone: 7.46 pmol/l (normal range, 1.6–6.9 pmol/l); cortisol: 354 nmol/l; TSH: 2.4 IU/ml.

Autoimmune disease markers:

ANA: negative; ENA: negative; anti-dsDNA: negative; ANCA: negative; EMA: negative; LKM: negative; anti-CCP: negative.

Immunology and serology:

IgA: 3.8 g/l; IgG: 9.5 g/l; IgM: 1.0 g/l; serum protein electrophoresis: normal; IGRA (QFT-GIT): negative; Blastomyces EIA: negative; HIV ELISA: negative; HTLV 1 + 2 ELISA: negative;

Oncomarkers:

AFP: negative; CA-125: negative; CA-19-9: negative; B2M: negative; CEA: 3.08 μg/l (normal range, 0.01–3.0 μg/l) .

BUN, blood urea nitrogen; CRP, C-reactive protein; AST, aspartate-amino transferase; ALT, alanine-amino transferase; CK, creatine kinase; CK MB, MB fraction of creatine kinase; LDH, lactate-dehydrogenase; WBC, white blood cell; INR, international normalized ratio; TSH, thyroid-stimulating hormone; ANA, antinuclear antibody; ENA, extractable nuclear antigen; dsDNA, double stranded DNA ; ANCA, antineutrophil cytoplasmic antibodies; EMA, endomysial antibodies; LKM, liver-kidney microsomal antibodies; CCP, cyclic citrullinated peptide; Ig, immunoglobulin; IGRA, interferon gamma release assay; QFT, quantiferon test; GIT, gold in tube; EIA, enzyme immunoassay; HIV, human immunodeficiency virus; ELISA, enzyme-linked immunosorbent assay; HTLV, human T-cell lymphotrophic virus; AFP, alpha fetoprotein; CA, cancer antigen; B2M, beta-2-microglobulin; CEA, carcinoembyonic antigen.

The patient was referred to an endocrinologist (E.F.) who found a severe vitamin D (25-OH-cholecalciferol) deficiency, along with secondary hyperparathyroidism (Table 2). Other common forms of endocrine myopathies were also excluded (normal thyroid-stimulating hormone, free thyroxine, cortisol, insulin-like growth factor one levels) (Table 2). In terms of the differentiation of ataxia, copper and zinc levels were measured and found to be normal (Table 2). Serological examination regarding latent tuberculosis infection, viral infections, Borrelia (immunoglobulin [Ig]M and IgG) and Treponema pallidum (Clinical Laboratory Improvement Amendments) showed no specific agent (Table 2).

Due to the patient’s alcohol abuse in the past, Wernicke's encephalopathy was considered in the differential diagnosis. In accordance with the recommendations of the European Federation of Neurological Societies⁶ and the Royal College of Physicians,⁷ the patient was immediately administered 500 mg thiamine (vitamin B1) twice a day intravenously for 5 days, followed by 200 mg thiamine orally three times a day for 6 weeks.

The patient also had severe vitamin D deficiency that might have participated in the development of sarcopenia. In terms of the vitamin D deficiency, the patient was investigated to determine the severity of the sarcopenia, which was assessed on the basis of muscle strength, muscle quantity and physical performance according to the European Working Group on Sarcopenia in Older People 2 2019 guidelines, while each test was performed twice.⁸ Regarding muscle strength, both a grip strength test and chair stand-up test were positive. Muscle quantity evaluated by dual-energy X-ray absorptiometry showed a significant decrease in appendicular skeletal muscle mass. Physical performance assessed by the ‘Time up and go’ (TUG) test showed severe impairment as well. The results of these tests are presented in Table 3. In terms of vitamin D deficiency, a resorption disorder was excluded by tests for coeliac disease. Vitamin D (25-OH-cholecalciferol) replacement in the dose of 25 000 IU given three times a week was started for 1 month, with a subsequent reduction in the dose to 25 000 IU given twice a week. The tests of the severity of sarcopenia were repeated after 6 months of vitamin D administration, where improvements in the scores of all of the tests were observed (Table 3). The TUG test score decreased to normal values, which indicated that the extent of the sarcopenia was significantly reduced.

Table 3.

Results of the tests for the severity of the sarcopenia according to the European Working Group on Sarcopenia in Older People 2. 2019 guidelines in a 43-year-old female patient who was hospitalized after repeatedly presenting with right-sided lower limb weakness that had worsened over the past 6 months.⁸

Test used to measure the severity of the sarcopenia	Test type	Baseline values at the time of diagnosis	Values after 6 months of treatment	Reference values
Muscle strength	Grip strength test	13 kg	15 kg	>16 kg
Muscle strength	Chair stand-up test	21 s/5 stand-ups	16 s/5 stand-ups	<15 s/5 stand-ups
Muscle quality	DEXA scan	5.0 kg/m²	5.3 kg/m²	5.5 kg/m²
Physical performance	TUG test	25 s	19 s	<20 s

DEXA, dual-energy X-ray absorptiometry; TUG, time up and go.

Together with the diminished extent of the sarcopenia, there was also an improvement in the severity of the degree of paraparesis, a complete recovery in terms of dysmetria and intention tremor and a partial recovery of gait and ataxia. According to the neurosurgeon (M.O.), spondylolisthesis of the L4–L5 vertebrae with a diameter of <3.5 mm did not contribute to the incomplete resolution of ataxia, despite the treatment. Mental status gradually improved, but the patient experienced residual memory problems and learning deficits.

Ethical permission from the local Ethics Committee of the Univerzita Pavla Jozefa Šafárika v Košiciach, Košice, Slovakia was not required because it is a case report and no other interventions or procedures were performed on the patient except for standard diagnostic and therapeutic procedures. Written informed consent for publication of the case report was obtained from the patient after full explanation of the purpose. The reporting of this study conforms to CARE guidelines.⁹

Discussion

A diagnosis of Wernicke's encephalopathy due to alcohol abuse was considered in this current patient who had the symptoms of dizziness, ataxia and memory problems.¹⁰ However, the patient only exhibited two symptoms from the classic triad of symptoms of Wernicke's encephalopathy (i.e. confusion, ophthalmoplegia and ataxia) and showed only partial resolution of ataxia with thiamine administration,¹¹ which highlighted the need to consider an alternative diagnosis. Ataxia in people with alcohol use disorder can be caused by sensorimotor neuropathy or cerebellar atrophy. Other diseases that can cause ataxia are described in Table 4.¹² Nevertheless, flaccid paraparesis can also be attributed to conditions other than chronic alcohol abuse.¹³ In the current case, there was a partial recovery of sarcopenia following vitamin D supplementation, which resulted from the physiological effects of that vitamin. In parallel, there was also an improvement in the paraparesis due to an increase in muscle volume and strength, which was reflected in a better physical performance.¹⁴ Clinical recommendations and guidelines emphasise the importance of high dose vitamin D supplementation for patients with vitamin D deficiency regardless of the clinical conditions.^15,16 In contrast, a retrospective cohort study of 389 malnourished patients with alcoholic Wernicke–Korsakoff syndrome found an increased time-related risk of cancer development; with the temporal relationship between vitamin D supplementation and newly diagnosed cancer being significant when the administration was started within the year leading up to the diagnosis.¹⁷

Table 4.

The most common causes of cerebellar ataxia.¹²

Common causes of cerebellar ataxia
Acute alcoholic intoxication.
Toxins: mercury, thallium, toluene, solvents.
Chronic atrophy in alcohol abusers.
Cerebellar neoplasms and abscesses.
Paraneoplastic cerebellar degeneration.
Meningitis, particularly basilar meningitis; viral cerebellitis.
Medication: phenytoin, carbamazepine, phenobarbital, lithium.
Other metabolic disorders: anti-glutamic acid decarboxylase ataxia; ataxia associated with gluten sensitivity; superficial siderosis; Niemann–Pick type C; Tay–Sachs disease.
Psychogenic.
Inherited diseases: Spinocerebellar ataxia; Holmes–Adie syndrome; Refsum disease; Machado–Joseph disease; mitochondrial disease.
Multiple sclerosis.

With regard to the limitations of the current case report, there was no possibility to determine thiamine concentrations or measure the red blood cell transketolase activity in the patient.¹⁸ Another shortcoming of this case report was that the patient’s compliance with vitamin D administration could not be fully monitored after hospital discharge. Likewise, some data on the patient’s history were collected retrospectively and this might have caused information bias in some respects. Furthermore, the patient had a lean body mass index, which might have limited the ability to generalize the effect of vitamin D supplementation in overweight individuals. One of the clinically important aspects of this case presentation was that it focused attention on the fact that individuals with alcohol use disorder are mostly evaluated only in terms of their acute hepatic complications of alcohol misuse, or in terms of their cognitive outcomes, but neurological complications are neglected. Furthermore, patients, if ever, are not thoroughly and correctly evaluated from an endocrinological point of view. Ataxia and paraparesis may have different causes in these patients that may be present simultaneously. Furthermore, in these patients, the balance problems can range from mild walking disorders to complete inability to walk; and in the long term they show delayed improvement and residual gait disturbances.¹⁹ Moreover, patients with Wernicke’s encephalopathy often do not show the typical triad of symptoms and frequently have simultaneous deficiency of vitamins D, B1 and B12.²⁰ Therefore, screening for these vitamin deficiencies, as well as concomitant vitamin replacement, are required. It should be emphasized that vitamin D replacement requires high doses given in the long term to be effective with respect to the recovery of sarcopenia.

In conclusion, patients with alcohol use disorder may have a wide range of neurological symptoms and cognitive changes. Differential diagnosis of ataxia, paraparesis and muscular weakness should be based on the consideration of a wide variety of aetiological factors, including infectious agents and degenerative changes of the CNS. Due to an inadequate dietary intake by individuals with alcohol use disorder a concomitant occurrence of vitamin B1, B12 and D deficiencies should also be considered.

Supplemental Material

sj-pdf-1-imr-10.1177_03000605231182262 - Supplemental material for Concomitant occurrence of Wernicke’s encephalopathy and sarcopenia due to vitamin D depletion in patients with alcohol use disorder: a case report

Supplemental material, sj-pdf-1-imr-10.1177_03000605231182262 for Concomitant occurrence of Wernicke’s encephalopathy and sarcopenia due to vitamin D depletion in patients with alcohol use disorder: a case report by Emil Fraenkel, Michal Orlický, Miriam Fedičová, Zuzana Gdovinová and Ivica Lazúrová in Journal of International Medical Research

Footnotes

Acknowledgements

The authors are indebted to Mundher Abdulkareem Salman Aljubouri MD and Eva Šuverová PhD for their linguistic revision of the manuscript.

Declaration of conflicting interests

The authors declare that there are no conflicts of interest.

Funding

This research received no specific grant from funding agency in the public, commercial, or not-for-profit sectors.

ORCID iD

Emil Fraenkel

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