Thiamine Deficiency Research Articles

The prevalence of thiamine deficiency among elderly nursing home residents: A cross-sectional study.

Although thiamine deficiency (TD) can lead to Wernicke encephalopathy, the characteristics associated with TD in the elderly have not yet been clarified. We sought to clarify the frequency of TD among an institutionalized elderly population with a controlled dietary intake and to identify possible factors related to TD. We undertook a cross-sectional study of residents in three nursing homes for the elderly as of June 2020. Blood thiamine concentrations were measured using a high-performance liquid chromatography method, with TD defined as a concentration of <21.3ng/mL. Basic data (age, sex, height, weight, and BMI), dietary intake for the previous 3 weeks, degree of care (DOC), degree of independence in daily life for elderly with dementia (DIDLED), and comorbidities were analyzed using descriptive statistical methods. The mean age (±SD) was 86.9 years (±8.29), with 84 residents (70.0%) being female. The DIDLED varied from total independence to long-term care level 5 (full assistance), with 89.2% suffering dementia. The mean whole blood thiamine value was 36.18 (±17.58) ng/ml, with TD confirmed in 7 (5.8%) of the 120 residents. All TD patients suffered from dementia. No TD was observed in patients with a near-normal food intake, and no related factors were observed among the other items. Reduced food intake may at increase the risk of TD and symptoms of TD may be overlooked in those displaying symptoms of dementia; thus, it is important for clinicians working with the elderly to remain aware of the potential for TD.

Thiamine Pyrophosphate-Requiring Enzymes are Altered during Pyrithiamine-Induced Thiamine Deficiency in Cultured Human Lymphoblasts

The most common of the severe complications of thiamine deficiency are beriberi and Wernicke-Korsakoff syndrome. To help clarify the biochemical basis for these disorders, a cell culture system has been established in which pyrithiamine, a potent thiamine transport inhibitor, was used to mimic different degrees of thiamine deficiency within human lymphoblasts. Activities of both transketolase and α-ketoglutarate dehydrogenase (α-KGDH) decreased at the same rate and to roughly the same levels in response to thiamine deficiency within a given cell line. However, variation in sensitivity to thiamine deficiency, as judged by the relative percentage of loss of enzymatic activities, was found when different cell lines were compared. When exogenous thiamine pyrophosphate was added to the activity assays, differences between transketolase and α-KGDH became readily apparent. Only 25% of the lost transketolase activity was present as apo-enzyme, whereas 70% of the lost α-KGDH activity was present in the apo-enzyme form. For transketolase, the non-recoverable activity was due mainly to a decrease in the synthesis rate of the protein during thiamine deficiency, suggesting that thiamine has a direct effect on the expression of the transketolase gene and/or protein.

Maternal Blood, Egg and Larval Thiamin Levels Correlate with Larval Survival in Landlocked Atlantic Salmon (Salmo salar)

A link was previously established between the Cayuga syndrome, a condition causing 100% mortality in larval landlocked Atlantic salmon, Salmo salar, in several of New York’s Finger Lakes, and a maternal diet of alewife, Alosa pseudoharengus, a non-native thiaminase-rich Clupeid fish. We evaluated salmon larvae viability relative to maternal thiamin status, and investigated the putative link of the Cayuga syndrome to an alewife diet in fish from the geographic regions outside the Finger Lakes/lower Great Lakes watersheds. We identified Cayuga syndrome in Atlantic salmon from Otsego Lake in the Susquehanna River watershed and from Green Pond in New York’s Adirondack Mountains. In both systems alewife represent the major component of the diet for the salmon. Thiamin levels in the maternal blood of Otsego salmon with syndrome-negative progeny were three- to four-fold greater than those Otsego females whose progeny exhibited 100% mortality. Thiamin levels in eggs and larvae were directly related to thiamin levels in maternal blood in both syndrome-positive and syndrome-negative stocks. Thiamin bath treatments of syndrome-afflicted larvae eliminated mortality regardless of their lake stock of origin. Maternal blood levels of approximately 0.31 nmol thiamin pyrophosphate/g or 0.44 nmol total thiamin/g appear necessary to achieve egg threshold levels of approximately 0.8 and 1.1 nmol/g unphosphorylated and total thiamin, respectively; these egg thiamin levels should prevent significant syndrome-related mortality in landlocked Atlantic salmon larvae. These results confirm the role of thiamin in the etiology of the Cayuga syndrome and support the dietary link of this naturally occurring thiamin deficiency to the thiaminase-rich alewife.

A Systematic Review of How To Reduce Morbidity in HIV Patients With Cardiovascular Diseases.

The human immunodeficiency virus (HIV) is known to cause cardiovascular diseases in patients infected with HIV. The pathology ranges from atherosclerosis to cardiomyopathy. There are several factors that could possibly cause cardiovascular diseases in the HIV population, including malnutrition and vitamin deficiency (for example, thiamine, B12, and zinc deficiencies); a lifestyle including increased prevalence of alcoholism and illicit drug usage; viral infection; and medication combinations that could cause sudden cardiac deaths. Cardiovascular diseases contribute to major morbidity in these populations and could have a reflection on the global financial burden, thus emphasizing the importance of prevention strategies. In this article, we focused on several factors that contribute to coronary artery disease and other cardiovascular diseases. We found that HIV has direct and indirect effects on the development of coronary artery diseases; furthermore, antiretroviral therapy adds to the deleterious effects of HIV and increases the risk of cardiovascular diseases. We further assessed the causal relationships and associations to understand the research gaps. In conclusion, this paper acknowledges and summarizes the current management strategies and the need to develop future strategies focusing on the prevention of cardiovascular diseases and tailoring the regimens according to the patient's clinical and socio-economic background.

Fetal demise and Wernicke–Korsakoff syndrome in a patient with hyperemesis gravidarum: a case report

BackgroundWernicke–Korsakoff syndrome is a neuropsychiatric disorder caused by thiamine deficiency composed of two related disorders accounting for an acute presentation and chronic progression. Hyperemesis gravidarum presents a significant risk factor for Wernicke–Korsakoff syndrome as symptoms may rapidly progress in the setting of pregnancy. We present the first-reported case of hyperemesis-gravidarum-associated Wernicke encephalopathy in a patient in the first half of pregnancy in which a missed diagnosis led to septic shock, fetal demise, and eventual profound Korsakoff syndrome.Case presentationWe present the case of a 33-year-old primigravid African American woman at 15 weeks gestational age who initially presented at a community emergency department with nausea and vomiting that ultimately progressed to severe hyperemesis-gravidarum-associated Wernicke–Korsakoff syndrome, fetal demise, and septic shock. The patient received a total of 6 weeks of high-dose parenteral thiamine. Magnetic resonance imaging of the head and formal neuropsychological assessment following treatment plateau confirmed the diagnosis of Wernicke–Korsakoff syndrome.ConclusionsThe multisystem complications seen in severe thiamine deficiency can delay timely administration of high-dose thiamine, particularly in pregnancy, in which the classic triad of Wernicke–Korsakoff syndrome may not raise clinical suspicion due to rapid progression of neurological sequelae in this population. We advise a low threshold for parenteral thiamine repletion in pregnant women with persistent vomiting as hyperemesis gravidarum-induced severe thiamine deficiency can result in Wernicke–Korsakoff syndrome, sepsis, and fetal demise.

Annals for Hospitalists - February 2023

Annals for Hospitalists - February 2023

Limited effects of macro-nutrient ratios on thiamin content and transfer in phytoplankton and copepods.

Vitamin B1 (thiamin) is primarily produced by bacteria, phytoplankton and fungi in aquatic food webs and transferred to higher trophic levels by ingestion. However, much remains unknown regarding the dynamics this water-soluble, essential micronutrient; e.g. how it relates to macronutrients (carbon, nitrogen and phosphorous). Nutrient limitation has been found to be related to periods of thiamin deficiency as well as in models. Hence, thiamin transfer to copepods from three phytoplankton species from different taxa was investigated, along with the effect of various nutrient regimes on thiamin content. Nutrient levels did not affect thiamin content of phytoplankton nor the transfer to copepods. Instead, phytoplankton displayed species-specific thiamin and macronutrient contents and whilst a higher thiamin content in the prey lead to higher levels in copepods, the transfer was lower for Skeletonema compared to Dunaliella and Rhodomonas. In all, thiamin transfer to copepods is not only dependent on thiamin content of the prey, but also the edibility and/or digestibility is of importance. Thiamin is essential for all organisms, and this study offers insights into the limited effect of macronutrients on the dynamics and transfer of thiamin in the aquatic food webs.

Protocol and application of basal erythrocyte transketolase activity to improve assessment of thiamine status.

Thiamine (vitamin B1) is an essential micronutrient required as a cofactor in many metabolic processes. Clinical symptoms of thiamine deficiency are poorly defined, hence biomarkers of thiamine status are important. The erythrocyte transketolase activity coefficient (ETKac) is a sensitive measure of thiamine status, but its interpretation may be confounded where the availability of the transketolase enzyme is limited. Basal ETK activity per gram of hemoglobin provides a complementary biomarker of thiamine status; however, its measurement and calculation are poorly described. Here, we describe in detail the assessment of basal ETK activity, including the calculation of path length in microplates and the molar absorption coefficient of NADH specific to the assay, and the measurement of hemoglobin in sample hemolysates. To illustrate the application of the methods, we present ETKac and basal ETK activity from women in The Gambia and UK. In conclusion, we present a clear protocol for the measurement of basal ETK activity that will permit the harmonization of methods to improve replication between laboratories.

Protocatechuic Acid Prevents Some of the Memory-Related Behavioural and Neurotransmitter Changes in a Pyrithiamine-Induced Thiamine Deficiency Model of Wernicke-Korsakoff Syndrome in Rats.

The purpose of this research was to investigate the effects of protocatechuic acid (PCA) at doses of 50 and 100 mg/kg on the development of unfavourable changes in cognitive processes in a pyrithiamine-induced thiamine deficiency (PTD) model of the Wernicke-Korsakoff syndrome (WKS) in rats. The effects of PCA were assessed at the behavioural and biochemical levels. Behavioural analysis was conducted using the Foot Fault test (FF), Bar test, Open Field test, Novel Object Recognition test (NOR), Hole-Board test and Morris Water Maze test (MWM). Biochemical analysis consisting of determination of concentration and turnover of neurotransmitters in selected structures of the rat CNS was carried out using high-performance liquid chromatography. PTD caused catalepsy (Bar test) and significantly impaired motor functions, leading to increased ladder crossing time and multiplied errors due to foot misplacement (FF). Rats with experimentally induced WKS showed impaired consolidation and recall of spatial reference memory in the MWM test, while episodic memory related to object recognition in the NOR was unimpaired. Compared to the control group, rats with WKS showed reduced serotonin levels in the prefrontal cortex and changes in dopamine and/or norepinephrine metabolites in the prefrontal cortex, medulla oblongata and spinal cord. PTD was also found to affect alanine, serine, glutamate, and threonine levels in certain areas of the rat brain. PCA alleviated PTD-induced cataleptic symptoms in rats, also improving their performance in the Foot Fault test. In the MWM, PCA at 50 and 100 mg/kg b.w. improved memory consolidation and the ability to retrieve acquired information in rats, thereby preventing unfavourable changes caused by PTD. PCA at both tested doses was also shown to have a beneficial effect on normalising PTD-disrupted alanine and glutamate concentrations in the medulla oblongata. These findings demonstrate that certain cognitive deficits in spatial memory and abnormalities in neurotransmitter levels persist in rats that have experienced an acute episode of PTD, despite restoration of thiamine supply and long-term recovery. PCA supplementation largely had a preventive effect on the development of these deficits, to some extent also normalising neurotransmitter concentrations in the brain.

Genetic basis of thiaminase I activity in a vertebrate, zebrafish Danio rerio

Thiamine (vitamin B1) metabolism is an important driver of human and animal health and ecological functioning. Some organisms, including species of ferns, mollusks, and fish, contain thiamine-degrading enzymes known as thiaminases, and consumption of these organisms can lead to thiamine deficiency in the consumer. Consumption of fish containing thiaminase has led to elevated mortality and recruitment failure in farmed animals and wild salmonine populations around the world. In the North American Great Lakes, consumption of the non-native prey fish alewife (Alosa pseudoharengus) by native lake trout (Salvelinus namaycush) led to thiamine deficiency in the trout, contributed to elevated fry mortality, and impeded natural population recruitment. Several thiaminases have been genetically characterized in bacteria and unicellular eukaryotes, and the source of thiaminase in multicellular organisms has been hypothesized to be gut microflora. In an unexpected discovery, we identified thiaminase I genes in zebrafish (Danio rerio) with homology to bacterial tenA thiaminase II. The biochemical activity of zebrafish thiaminase I (GenBank NP_001314821.1) was confirmed in a recombinant system. Genes homologous to the zebrafish tenA-like thiaminase I were identified in many animals, including common carp (Cyprinus carpio), zebra mussel (Dreissena polymorpha) and alewife. Thus, the source of thiaminase I in alewife impacting lake trout populations is likely to be de novo synthesis.

Understanding and mitigating thiaminase activity in silver carp

A deficiency of thiamine (vitamin B1), an essential cofactor for enzymes involved in metabolic processes, can be caused by the enzyme thiaminase. Thiaminase in food stocks has been linked to morbidity and mortality due to thiamine depletion in many ecologically and economically important species. Thiaminase activity has been detected in certain bacteria, plants, and fish species, including carp. The invasive silver carp (Hypophthalmichthys molitrix) presents an enormous burden to ecosystems throughout the Mississippi River watershed. Its large biomass and nutritional content offer an attractive possibility as a food source for humans, wild animals, or pets. Additionally, harvesting this fish could alleviate some of the effects of this species on waterways. However, the presence of thiaminase would detract from its value for dietary consumption. Here we confirm the presence of thiaminase in several tissues from silver carp, most notably the viscera, and systematically examine the effects of microwaving, baking, dehydrating, and freeze-drying on thiaminase activity. Certain temperatures and durations of baking and microwaving reduced thiaminase activity to undetectable levels. However, caution should be taken when carp tissue is concentrated by processes without sufficient heat treatment, such as freeze-drying or dehydration, which results in concentration, but not inactivation of the enzyme. The effects of such treatments on the ease of extracting proteins, including thiaminase, and the impact on data interpretation using the 4-nitrothiophenol (4-NTP) thiaminase assay were considered.

Wernicke's Encephalopathy in Type 2 Achalasia: Case Report and Literature Review.

Achalasia is primarily a smooth muscle motility disorder of the esophagus driven by aberrant peristalsis and failure of sphincter relaxation. Notably, achalasia is a heterogeneous disease with primarily 3 possible pattern subtypes. According to the review of current cases and literature regarding achalasia, patients primarily present with dysphagia, usually to solids and, if progressed, to solids and liquids. Rarely, untreated achalasia may result in thiamine deficiency and present as Wernicke-Korsakoff syndrome (WKS). This acute neurologic condition primarily affects the central and peripheral nervous system and is known by the triad of ataxia, ophthalmoplegia, and confusion. Individuals who present with WKS typically have a notable history of chronic alcohol abuse with decreased thiamine intake and metabolism. Although less common, individuals with WKS may have a pertinent history of starvation, anorexia nervosa, and malnutrition. This case highlights a unique presentation of Wernicke's encephalopathy (WE) in a 30-year-old woman with severe type II achalasia complicated by a 60-pound weight loss in a span of 2 months. According to our literature review, there have only been 2 previously reported cases of severe achalasia leading to the development of WE. Considering the limited number of case reports available, WE must be in the differentials in patients with underlying achalasia, and our case report highlights this unusual presentation with corresponding brain imaging and manometry testing.

Virtual Reality in Korsakoff’s Syndrome

Purpose - Korsakoff’s syndrome (KS) is a severe neuropsychiatric disorder following thiamine deficiency often resulting from chronic alcohol consumption. KS is characterized by cognitive problems, such as impaired memory, decreased organization and planning skills, and confabulations. Patients diagnosed with KS often require long-term care, because of the severity of their cognitive problems and psychiatric problems. Case description - In this project, virtual reality techniques were administered to a Korsakoff’s syndrome population in a long-term (residential) treatment setting. Following an overview of the technique, three vignettes that illustrate how virtual reality techniques can ameliorate the mood, felt sense of control and activity levels of KS patients. Outcomes - Actively engaging in virtual reality settings encouraged KS patients to decrease their apathy, matched their individual needs, and increased laughing behavior. Conclusions – Virtual reality techniques can actively engage patients diagnosed with KS in activities that are normally not initiated because of apathy. More systematic research on virtual reality techniques in KS should be conducted to test for possible benefits on quality of life, autonomy and reduction in neuropsychiatric symptoms

Clinical Practice Guidelines for Assessment and Management of Patients with Substance Intoxication Presenting to the Emergency Department.

Clinical Practice Guidelines for Assessment and Management of Patients with Substance Intoxication Presenting to the Emergency Department.

Generalized vestibular hyporeflexia and chronic upbeat nystagmus due to thiamine deficiency.

Ocular motor and vestibular manifestations of Wernicke's thiamine deficiency (WTD) are frequent and heterogeneous. Previous neuropathological and neuroimaging findings identified brainstem and cerebellar lesions responsible for these findings, however, peripheral vestibular lesions are probably uncommon in human WTD, though noted on an avian thiamine deficient study. Single case study of a WTD patient post-gastric bypass who developed ataxia, oscillopsia and nystagmus, with low serum thiamine, and increased MRI T2 signal in the thalami, but normal brainstem and cerebellum. Vestibular evaluation showed significant vestibular hyporreflexia affecting all six canals, and a chronic upbeat nystagmus, now for 14months after WTD onset. Serial clinical, video head impulse, nystagmus analysis, cervical and ocular vestibular evoked responses. She is undergoing treatment with Memantine, Clonazepam and vestibular rehabilitation, and feels improvement. This report shows a novel combination of central and peripheral vestibular findings, of relevance for diagnosis and treatment, in addition to the development of a coherent hypothesis on the ocular motor and vestibular findings in WTD.

500: DIAGNOSIS OF WERNICKE ENCEPHALOPATHY IN A PATIENT WITH UNDERLYING PSYCHIATRIC ILLNESS

Introduction: Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome caused by thiamine deficiency. Common causes include alcohol use, bariatric surgery, and hemodialysis. Description: Our case involves a 65-year-old female who initially presented with seizure-like activity. Subsequent presentations over months included dysphagia, behavioral changes, and confusion. Initial workup with EEG, CT head, MRI brain, CT soft tissue neck, and endoscopy was unremarkable. Further history revealed that after her mother’s death four months prior, she began to self-isolate and reduce oral intake. Patient was evaluated by psychiatry and was diagnosed with conversion disorder. The clinical course was complicated by worsening neurological symptoms and respiratory distress requiring mechanical ventilation. Repeat MRI brain showed increased T2 FLAIR signal in the periaqueductal gray matter and along the dorsomedial thalamus consistent with WE. Patient was started on thiamine and showed symptomatic improvement. Discussion: WE is a triad of oculomotor dysfunction, ataxia, and confusion. In an observational study by Chamorro et al, 92.7% of cases were due to excessive alcohol intake, 47.1% due to malnutrition, and 5.9% due to psychiatric illness. The diagnosis of WE is primarily clinical, yet the classic triad is reported in only 10% of cases. The most consistent characteristic is a change in mental status. Caine et al developed the clinical diagnostic criteria, which include dietary deficiencies, oculomotor abnormalities, cerebellar dysfunction, and altered mentation or mild memory impairment. A case series based on this criteria found that clinical features of WE vary between alcohol and non–alcohol-related etiologies. The classic triad was more common in alcoholics than in non-alcoholics. One of the main challenges is the rate of underdiagnosis, which can be due to a lack of clinical suspicion or atypical presentation. Hence, MRI is a useful test to support the diagnosis of WE with a sensitivity of 53% and specificity of 93%. MRI may demonstrate lesions with increased symmetrical signal intensity in the periaqueductal region, medullary bodies, medial thalami, and the tectum of the midbrain. Diagnosis of WE should be considered in patients with psychiatric illnesses and atypical neurologic presentation.

Effectiveness of Thiamine Supplementation Plus Optimal Medical Therapy as an Adjunct Treatment in Improving Cardiac Function Among Patients With Heart Failure With Reduced Ejection Fraction: A Meta analysis

BACKGROUND: Thiamine plays a crucial role for normal cardiac function, as severe vitamin B1 (thiamine) deficiency leads to congestive heart failure. Thus, patients undergoing diuretic treatment might have compromised heart function. Several small-scale studies were conducted with conflicting results”. OBJECTIVE: The aim of this study was to determine the effects of thiamine supplementation on cardiac function among patients with heart failure with reduced ejection fraction receiving optimal medical therapy versus optimum medical therapy alone. DESIGN: This was a meta-analysis of randomized, double-blind, placebo-controlled trials. METHODS: Studies for inclusion were searched using PubMed, Google Scholar, Cochrane, EMBASE, and other databases. Gray literature was also explored. Review Manager version 5.3 was used to analyze data. The mean difference and 95% confidence interval were estimated using random-effects model. χ2 and I2 were computed to assess heterogeneity. RESULTS: After the analysis of the combined effects of five studies with 218 subjects, the pooled results showed no significant effect on the left ventricular ejection fraction in heart failure patients when given thiamine supplementation with a P value of 0.04. CONCLUSION: Based on this limited group of studies, there is insufficient information to suggest that thiamine supplementation has a positive effect on left ventricular ejection fraction in heart failure patients. Further large-scale clinical trials are needed to determine the optimum dose, duration, and route of thiamine in patients with heart failure. KEYWORDS: thiamine supplementation, vitamin B, heart failure, HFrEF, reduced ejection fraction

1161: CANNABIS INTOXICATION: A RARE CAUSE OF LACTIC ACIDOSIS

Introduction: Lactic acidosis is common in critically ill patients and has a variety of etiologies. While sepsis, hemorrhage, and shock are the most common causes of lactic acidosis, a subset of patients have no obvious cause. Drug and medication toxicity remains a rare cause of lactic acidosis that providers often fail to recognize. Here, we present a rare case of lactic acidosis due to acute marijuana intoxication. Description: A 26-year-old male with no prior history of marijuana use was brought into the emergency department with complaints of shortness of breath and palpitations after ingesting ice cream containing cannabis. Per EMS, the patient was found screaming for help due to his symptoms but evidently with altered mentation. On arrival, the patient was febrile to 101.9 F with a heart rate of 156 bpm; he was normotensive and saturating well on room air with a normal respiratory rate. Laboratory studies were significant for an elevated lactate level of 4, a white blood cell count of 11, and a urine drug screen positive for THC. The patient was given empiric broad-spectrum antibiotics, 2 liters of lactated ringer’s, and IV naloxone with no improvement in mental status. Studies and physical examination did not reveal any source of infection. After careful monitoring, the patient’s mental status recovered and lactic acid cleared with supportive measures. The patient was later discharged safely home with appropriate follow-up. Discussion: Poisoning is one of the leading causes of injury-related casualties in the United States, and lactic acidosis is a widely used predictor to stratify patients who are at increased risk for mortality. Elevated lactate levels result from an imbalance between lactate metabolism and production. Synthetic cannabinoids have been established as rare causes of lactic acidosis. Chronic marijuana use has been associated with lactic acidosis by way of thiamine deficiency and gastrointestinal beriberi corrected promptly with vitamin administration. There are no reported cases linking acute marijuana use and lactic acidosis development in the absence of infection, hemodynamic compromise, or seizures. It is important to keep drug ingestion and intoxication in mind as important causes of lactic acidosis in the absence of other apparent etiologies.

Differential Diagnosis in the Management of CPI Immunotoxicity: Case Series of Etiologies not to Miss

Objective To present on treatable conditions arising with exposure to checkpoint inhibiting immunotherapy for malignancy. Each case was diagnostically obscured by presumed immunotoxicity. Background Neurological immune-related adverse events (n-irAEs) are rising in incidence with adoption of checkpoint inhibitors (CPIs) for many cancers. 1-3% of patients treated with CPIs experience severe n-irAEs with potential for persistent functional disability or mortality. Diagnosis can be challenging for immunologically vulnerable patients with frequently multifactorial problems from their cancer and potential infectious, metabolic, and iatrogenic complications. Design/Methods Three informative cases from a single institution were analyzed. Results 1. An 80-year old woman with metastatic melanoma and recent treatment with ipilimumab+pembrolizumab developed acute leg weakness. Given her EMG and CSF findings, she began treatment for suspected CPI-induced atypical GBS and myositis. Concomitantly she was found to have B12 and folate deficiencies, then gradually improved to baseline with vitamin repletion, steroids, and plasma exchange. 2. A 27-year old woman with metastatic melanoma and recent treatment with ipilimumab+nivolumab developed autoimmune hepatitis and intractable vomiting. Three weeks after she began dabrafenib and trametinib, she developed confusion, diplopia, and ataxia along with weakness and areflexia. She was treated for possible GBS, but was concurrently found to have thiamine deficiency with sequela of Wernicke's encephalopathy on MRI Brain. Her confusion improved with thiamine supplementation but had persistent weakness. 3. A 57-year old woman with lung adenocarcinoma who had progressed on durvalumab began pembrolizumab. Two weeks later, she developed fevers, rash, and lethargy. She was treated supportively but continued to worsen until neurological workup revealed limbic hyperintensities on MRI Brain and CSF pleocytosis with +HSV1. She had minor clinical improvement with acyclovir but remained cognitively debilitated. Conclusions Given frequently complex clinical circumstances when working up n-irAEs, a systematic approach and a broad differential must be utilized for this important intersection of cancer neurology and immunology.

Giant Cell Arteritis of the Superior Mesenteric Artery Presenting With Wernicke Encephalopathy From Thiamine Deficiency

Objective N/A. Background Giant cell arteritis (GCA) is one of the most common systemic vasculitides in adults over the age of 50 with incidence ranging from 15 to 35 per 100,000 individuals. The disorder is often included in the differential diagnosis of maladies producing atypical facial pain, headache, visual loss, amaurosis fugax, jaw pain, elevated inflammatory markers, and anemia. GCA is typically known to affect cranial arteries with physical exam findings of tenderness to palpation of the temporal arteries and cranial neuropathies. Clinical diagnosis is further supported by new headache, temporal artery abnormality, elevated ESR (= 50 mm/h), and abnormal artery biopsy. Design/Methods N/A. Results A 68-year-old female with history of primary generalized seizures presented to clinic with a 6-week history of paroxysms of acute confusional episodes, the inability to arise from a seated position due to lower extremity weakness bilaterally, alterations of consciousness without loss of consciousness, severe anorexia, and weight loss. MRI with contrast including Axial FLAIR/T2/Diffusion revealed bilateral pan-lobar cortical and subcortical atrophy with ex-vacuo ventriculomegaly and mild leukoaraiosis in the subcortical white matter tracts. PET-CT body revealed linear uptake involving the aortic root, extending into subclavian arteries bilaterally with segmental involvement of proximal common carotids, and extending inferiorly to the level of the common iliac arteries and the mesenteric arteries. Temporal artery biopsy revealed presence of granulomas with multinucleated giant cells. Serology panel revealed pan hypovitaminoses in Vitamins A, B1, B6, B12, and D. Conclusions Traditional GCA workup initially resulted inconclusive for the patient, whose condition deteriorated as the patient's altered mental status and dizziness spells continued unremittingly. This case highlights the link between large vessel vasculitis and malabsorption syndromes, with the involvement of the superior mesenteric artery, a medium sized vessel, in GCA previously unrecognized. Furthermore, this case is a superb example of multiple etiologies of treatable causes of reversible dementia.