Severe Vitamin B12 Deficiency Research Articles

Psychiatric Presentation of a Severe Vitamin B12 Deficiency Associated with Biermer’s Disease: A Case Report

Psychiatric Presentation of a Severe Vitamin B12 Deficiency Associated with Biermer’s Disease: A Case Report

A mother's deficiency, a baby's challenge: vitamin B12 deficiency-related seizures and pancytopenia in an infant

Anemia is prevalent in pediatric age and it stems from diverse factors. While iron deficiency is a common cause above six months of age, other nutritional deficits contribute to the disease burden. During pregnancy, anemia due to nutritional deficits is associated with adverse outcomes for the newborn. Precise diagnosis of dietary deficits in the pediatric population is vital to avert negative health consequences. We describe the case of a six-month-old exclusively breastfed infant with a mother having unspecified anemia under folic acid supplementation. The infant presented with neurological symptoms, including paroxysmal events and developmental regression. Laboratory analysis revealed pancytopenia and severe vitamin B12 deficiency. The patient’s mother's serum level of vitamin B12 was also low and ant parietal cell antibodies were positive, suggesting maternal autoimmune gastritis. Treatment with hydroxocobalamin led to clinical and analytical improvement. Maternal deficiency is the major cause of cobalamin deficiency in infants. It is paramount to raise awareness to this issue to prevent its avoidable repercussions.

Veganism and hypercoagulable state - hyperhomocysteinemia presenting as pulmonary thrombo-embolism in a vegetarian living at high altitude

Hyperhomocysteinemia as a hypercoagulable state has been debatable, but when associated with other high-risk factors like severe vitamin B12 and folate deficiency, smoking, high altitude, and antiphospholipid syndrome can present with thromboembolism. Vegans are at high risk of severe B12 deficiency as the primary source is animal products. Right now, the total number of vegans, vegetarians, and all related categories, is close to 14 per cent of the world population. We here present a young vegan with severe B12 deficiency presenting with sub-massive thromboembolism.

Anemia Outside the Box: Nonimmune Intramedullary Hemolytic Anemia Driven By Vitamin B12 Deficiency

Introduction: Vitamin B12 and folate deficiencies are common etiologies of macrocytic anemia, mostly encountered with chronic alcohol use, and uncommon for healthy individuals with unremarkable medical history. The pathogenesis of the resulting anemia is described by two possible mechanisms: either ineffective erythropoiesis, driven by vitamin B12 deficiency, or more rarely, via nonimmune intramedullary hemolysis. We present a very rare case of severe vitamin B12 deficiency leading to nonimmune intramedullary hemolysis and highlight the diagnostic evaluation and tailored management. Case Presentation: A 49-year-old female with history of depression, chronic alcohol use and chronic nitrous oxide inhalation, presented with lethargy, hypotension and fevers with visual hallucinations, and was subsequently admitted for acute encephalopathy. Findings on physical examination included diminished proprioception and diminished sensation to fine touch, pinprick and vibration of the lower extremities with distal hyperreflexia of the patellar and Achilles tendon reflexes bilaterally. Lab work was notable for leukopenia and macrocytic anemia with a significant drop in hemoglobin to 9.6 from a baseline of 13.2 within 5 months and MCV of 103. Extensive investigation of encephalopathy was undertaken, of which we note infectious workup, prompted by the septic presentation, which showed Staphylococcus aureus bacteremia. On the other hand, the patient's anemia was concurrently investigated. Hemolysis workup was positive (LDH 394 U/L; direct bilirubin 1.6 mg/dL; haptoglobin<8 mg/dL; reticulocyte count 6.1%); however, schistocytes were low on peripheral smear (Figures 1 and 2). As such, nonimmune intramedullary hemolysis was suspected. Further anemia workup revealed severe vitamin B12 deficiency (75 ng/L), consistent with the physical exam findings, but normal folate levels. Of note, methylmalonic acid levels and homocysteine were also elevated (respectively 4.39 nmol/mL, and 142 umol/L). The constellation of the clinical presentation and all the laboratory findings confirmed a nonimmune intramedullary hemolytic process, elicited by vitamin B12 deficiency. This deficiency was thought to be multifactorial, mainly caused by chronic alcohol abuse, in addition to persistent nitrous oxide use. It was also suggested that hemolysis could be a consequence of drug-induced carboxyhemoglobinemia (level was 9.4%), whereby carboxyhemoglobin can form during the binding and release of nitric oxide from hemoglobin. Treatment was focused on replacing vitamin B12 with 1000 mcg daily intramuscular injections for 7 days, then weekly thereafter for 4 weeks, followed by monthly injections. Improvement of hemoglobin to 11.1 with improvement of neurologic exam findings were noted prior to discharge. Conclusion: Nonimmune hemolytic anemia must be included in the differential diagnosis when evaluating patients with anemia concurrent with vitamin B12 deficiency, mostly encountered with chronic alcohol use. Vitamin B12 supplementation remains the key treatment to correct this rare, but serious outcome of vitamin B12 deficiency.

Early treatment of subacute combined degeneration of the spinal cord in pernicious anemia will improve the outcome

Vitamin B12 deficiency is probably more common than what is reported in the literature. B12 is an essential vitamin, and its deficiency can lead to neuropsychiatric manifestations such as peripheral neuropathy, myelopathy, cerebellar ataxia, dementia, delirium, even psychosis and mood disorders. We report a case of 45 year old polish male presented with symptoms and signs suggestive of SCD of the spinal cord, due to severe vitamin B12 deficiency as a result of pernicious anemia. Cervical spine MRI showed enhancement in the bilateral posterior columns of the cervical spinal cord with a classic inverted V appearance. Metabolic workup revealed severe vitamin B12 deficiency, complete blood analysis indicated megaloblastic anemia. Intramuscular injection of cobalamin was started on a timely manner with complete resolution of symptoms.

SUBACUTE COMBINED DEGENERATION OF THE SPINAL CORD SECONDARY TO NITROUS OXIDE-INDUCED B12 DEFICIENCY.

It is important to take a full history of illicit drug use, especially in young patients presenting with unusual symptoms.In cases of suspected nitrous oxide-induced neurological dysfunction with normal vitamin B12 levels, serum levels of methylmalonic acid and homocysteine can be measured to aid diagnosis.Prompt treatment of nitrous oxide-induced subacute combined degeneration of the spinal cord with B12 injections and discontinuation of nitrous oxide use allow for a gradual recovery, although in some cases patients may be left with residual symptoms.

Pancytopenia Secondary to Vitamin B12 Deficiency in Older Subjects

Vitamin B12 (cobalamin CBL) is a water-soluble vitamin required to form hematopoietic cells (red blood cells, white blood cells, and platelets). It is involved in the process of synthesizing DNA and myelin sheath. Deficiencies of vitamin B12 and/or folate can cause megaloblastic anemia (macrocytic anemia with other features due to impaired cell division). Pancytopenia is a less frequent exordium of severe vitamin B12 deficiency. Vitamin B12 deficiency can also cause neuropsychiatric findings. In addition to correcting the deficiency, an essential aspect of management is determining the underlying cause because the need for additional testing, the duration of therapy, and the route of administration may differ depending on the underlying cause. Here, we present a series of four patients hospitalized for megaloblastic anemia (MA) in pancytopenia. All patients diagnosed with MA were studied for a clinic-hematological and etiological profile. All the patients presented with pancytopenia and megaloblastic anemia. Vitamin B12 deficiency was documented in 100% of cases. There was no correlation between the severity of anemia and deficiency of the vitamin. Overt clinical neuropathy was present in none of the cases of MA, while subclinical neuropathy was seen in one case. The etiology of vitamin B12 deficiency was pernicious anemia in two cases and low food intake in the remaining cases. This case study emphasizes the role of vitamin B12 deficiency as a leading cause of pancytopenia among adults.

Clinico-Etiopathogenesis of Vitamin B12, Folic Acid and Iron Deficiency in Severe Acute Malnutrition Children: A Tertiary Care Hospital Experience from Central India.

In severe acute malnutrition, micronutrient deficiency as well as protein energy malnutrition is a major obstacle to growth & development. Iron deficiency dominates the spectrum of nutritional anemia. After taking informed consent, 211 SAM children and 211 age-and sex-matched healthy children with normal nutritional status were enrolled for the study. MUAC was used to diagnose SAM. A 5-part automated hematoanalyzer was used to measure the complete blood count and red cell indices, and the peripheral smear method to determine the red cell morphology. We measured serum ferritin, Vitamin B12, and folic acid using the ELISA method. Compared to controls, children with SAM had significantly lower red cell indices, platelet counts, and white cell counts. The most common clinical symptoms seen in SAM children were diarrhea, pneumonia, acute gastroenteritis, and acute respiratory infection. Children with SAM are more likely to suffer from iron deficiency and B12 deficiency. Severe vitamin B12 deficiency was more frequently associated with severe anemia. The severe anemia in SAM children constantly changes the body's defense mechanism, affecting the haematopoiesis. In this study, haematological indices are recommended for predicting severity of anemia, and hematopoietic changes are described, in order to improve anticipatory care and outcome in children with SAM.

Comparison between Weekly Intravenous Versus Daily Oral Vitamin B12 Supplementation in Vitamin B12 Deficiency Anemia [Courage-12]: A Randomized, Open Label, Single Centre Study

Introduction: The prevalence of symptomatic and asymptomatic Vitamin B12 deficiency is 47% in North India. The treatment for Vitamin B12 deficiency is either injectable or oral Vitamin B12 supplementation. Intramuscular VB12 is given as multiple doses of once daily or alternate day Vitamin B12 injections based on the general consensus. However, in hematology, we commonly use intravenous Vitamin B12 instead of intramuscular since most patients are thrombocytopenic. Many hematologists favor the oral route over injectable route. There are no definitive guidelines on the use of intravenous Vitamin B12 (VB12). Direct comparison of intravenous to oral VB12 has not been carried out till date. Hence, we decided to explore weekly dosing of intravenous VB12 in Vitamin B12 deficiency anemia and compare it with oral VB12 supplementation. It would be essential to seek evidence for the most effective route for the treatment of Vitamin B12 deficiency anemia. Objectives: The primary objective was to evaluate Vitamin B12 level at 5 weeks from the start of therapy and the delta change in Vitamin B12 level in both weekly intravenous and oral VB12 arms. Post-therapy improvement in signs and symptoms, Hemoglobin (Hb), MCV (in fl) response were the secondary objectives. Methodology: This was a prospective, randomized, open-label, interventional pilot study comparing daily oral versus weekly intravenous Vitamin B12 replacement at a tertiary care center between May 2020 to December 2021. Patients with anemia (for age and gender) and a pre-therapy vitamin B12 levels below 250 pg/ml were enrolled in the study. The participants were randomized using blocks of 2, 4 and 6 randomly generated by the software. The allocation concealment was done using sequentially numbered, opaque sealed envelopes (SNOSE) and monitored by the central coordinator. The participants in weekly intravenous arm received VB12 1000mcg intravenous (IV) once a week for 4 weeks whereas daily oral arm received oral VB12 1500mcg once a day for 4 weeks. All participants received 5mg Folic acid tablet orally once a day. The pre-specified baseline as well as post-therapy investigations were carried out. The statistical analysis was done as planned. Results: Overall, majority of the participants were females (64.8%) and the a median age was 32 years (Q1-Q3, 21 to 52). The most common presenting symptoms were easy fatiguability (48%), hairfall (37%), and parasthesia (19%). On comparing the two groups, the pre-therapy mean Vitamin B12 level in the oral VB12 and weekly IV VB12 group was 157 ± 66 pg/ml and 173 ± 55 pg/ml (p=0.59) respectively and post-therapy mean Vitamin B12 level was 870 ± 348 and 1273 ± 511 (p=0.02) respectively. The post therapy VB12 level was statistically significant in weekly IV VB12 group, though the delta change in vitamin B12 level was not significant among the groups. The baseline hemoglobin in oral VB12 and weekly IV VB12 groups was 10.9 ± 1.3 g/dl and 10.5 ± 2.1 g/dl (p=0.5) respectively and the post-therapy Hb was 12.1 ± 1.3 g/dl and 12.3 ± 1.1 g/dl (p=0.7) respectively. The mean change in Hb was not significant on comparison between the two groups (p=0.65). The pre-therapy MCV in the oral VB12 group and weekly IV VB12 group was 86.5 ± 9.5 fl and 88.1 ± 17.9 fl (p=0.5) whereas post-therapy MCV was 83.1 ± 9.5 fl and 83.2 ±10.7 fl (p=0.9) respectively. Conclusion: Normalization of vitamin B12 level was seen with both oral and intravenous vitamin B12, however, the weekly intravenous supplementation showed a statistically significant increase in vitamin B12 level than daily oral supplementation. Considering that the IV route provided a faster increase in vitamin B12 level, it could be a better option in patients with severe vitamin B12 deficiency anemia. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

VITAMIN B 12 DEFICIENCY MIMICKING THROMBOTIC MICROANGIOPATHY: A CASE REPORT

Vitamin B12 has an important role in DNA synthesis, erythrocyte development and neurological functions by the transfer of one-carbon methyl groups. Vitamin B 12 deficiency may mimic Thrombotic Microangiopathy (TMA) and lead to pseudo-thrombotic microangiopathy (pseudo-TMA). Early recognition of pseudo-TMA is important because treatment with vitamin B 12 replacement is quite simple and effective. A 66-year-old female patient was admitted to the emergency department with complaints of fatigue. CBC values Hb 3.8gr/dL , Hct 11.3%, MCV 115 fL , platelets 19000/mm³, WBC 6400/mm³, ind.bil.1.5 mg/dL, LDH 2111U/L . In peripheral blood smear (PBS), macroovalocytes, anisopoikilocytes, schistocytes, hypersegmented neutrophils and a normoblast with megaloblastic features (figure-1) were observed. Thrombocytopenia and the presence of schistocyte initially supported TMA. Blood was drawn from the patient for the ADAMTS-13 test. While concurrent steroid treatment with fresh frozen plasma (FFP) was started, plasmapheresis preparation was also made. The patient's vitamin B12 level was 50 pg/mLThe patient was started on vitamin B12 as 1000 mcg IM. Following clinical recovery, hemoglobin and platelets stabilized, the hemolysis panel indicated a steady improvement (graphs 1, 2, 3). Results TMA symptoms can be mimicked by severe vitamin B12 deficiency. Rapid and accurate diagnosis of pseudo-TMA and initiation of parenteral vitamin B 12 replacement can prevent unnecessary and expensive diagnostic investigations and long-term plasma exchange treatments. Our case, has demonstrated the importance of considering vitamin B12 insufficiency in cases presenting with TMA and the value of carefully examining PBS in the identification of megaloblastic anemia.

Fylkesforskjeller i utredning og behandling av vitamin B12-mangel

Severe vitamin B12 (cobalamin) deficiency is rare, but international reports show that up to 26% of the general population may have subclinical vitamin B12 deficiency. The prevalence of vitamin B12 deficiency has not been investigated in Norway. Since 2017, treatment with vitamin B12 tablets has represented an alternative to traditional treatment with intramuscular injections in Norway. When we studied the transition from injection to tablet treatment, we discovered an unexpected difference in the counties' use of vitamin B12 supplements, which we wished to investigate in more detail. Data on the dispensing of vitamin B12 supplements from pharmacies in 2020, broken down by the patients' county of residence, were retrieved from the Norwegian Prescription Database. The Norwegian Health Economics Administration (Helfo) provided figures on the number of reimbursed vitamin B12-related laboratory tests in 2020, classified by patients' municipality of residence. In 2020, the sale of vitamin B12 supplements on prescription in Norway amounted to 12 defined daily doses (DDD) per inhabitant and varied from 7 to 15 between the counties. The number of laboratory analyses that were performed varied by county from 26 to 46 per 100 inhabitants for total vitamin B12, and from 21 to 37 for folate. The number of analyses varied correspondingly from 1 to 12 per 100 inhabitants for homocysteine, from 1 to 13 for methylmalonic acid and from 0.01 to 8.13 for active vitamin B12. Our study showed large intercounty differences in the consumption of vitamin B12 supplements. These differences may have a number of explanations. Variations in the number of vitamin B12-related laboratory analyses requisitioned may indicate that doctors' assessment and diagnosis of vitamin B12 deficiency could be a contributory factor.

Sever vitamin B-12 deficiency presenting as bilateral Lower Limbs edema and Hypertension

Vitamin B-12 is a water soluble vitamin, found exclusively in products of animal origin. Vitamin B-12 deficiency presents as hematological, gastrointestinal, and neuropsychiatric disorders. Anemia is usually most common presentation of vitamin B-12 deficiency. Severe vitamin B12 deficiency at a level <12 pg/mL is uncommonly seen in the health centers setting in the emergency and laboratory setting. This is a rare case of vitamin B-12 deficiency presenting with lower limbs edema, simulating edema of cardiac origin. Patient was prescribed Vitamin B12 Supplements and antihypertensive medicines. Edema started to resolve after starting of treatment.

Sever vitamin B-12 deficiency presenting as bilateral Lower Limbs edema and Hypertension

Vitamin B-12 is a water soluble vitamin, found exclusively in products of animal origin. Vitamin B-12 deficiency presents as hematological, gastrointestinal, and neuropsychiatric disorders. Anemia is usually most common presentation of vitamin B-12 deficiency. Severe vitamin B12 deficiency at a level <12 pg/mL is uncommonly seen in the health centers setting in the emergency and laboratory setting. This is a rare case of vitamin B-12 deficiency presenting with lower limbs edema, simulating edema of cardiac origin. Patient was prescribed Vitamin B12 Supplements and antihypertensive medicines. Edema started to resolve after starting of treatment.

An Atypical Presentation of Vitamin B12 Deficiency with Hemolytic Anemia

Vitamin B12 deficiency is a common nutritional deficiency in both developed and developing countries. This water-soluble vitamin is synthesized by bacteria and archaea and plays a major role in DNA synthesis and effective hematopoiesis. Most common etiologies of B12 deficiency include pernicious anemia and dietary deficiency. Hematological manifestations including anemia, leukopenia, thrombocytopenia, and macrocytosis can commonly be seen with vitamin B12 deficiency. Vitamin B12 deficiency is a rare cause of hemolytic anemia with approximately 1.5% of cases. Hemolysis with vitamin B12 deficiency remains a rare entity that has not been well described in the literature. Here we present a case of a 49-year-old male presenting with presyncope and fatigue who was found to have hemolytic anemia secondary to severe vitamin B12 deficiency with clinical improvement after vitamin supplementation therapy and provide a brief review of literature.

Metabolism-mediated thrombotic microangiopathy and B12.

Thrombotic microangiopathies (TMAs) are a group of life-threatening conditions requiring urgent management and characterized by a clinical triad of microangiopathic hemolytic anemia, thrombocytopenia, and ischemic tissue injury. Severe vitamin B12 (Cobalamin-Cbl) deficiency or defective cobalamin metabolism, particularly defects in intracellular B12 metabolism, may lead to a TMA-like picture. The latter has been termed metabolism-mediated TMA (MM-TMA). This confusing picture is mediated partly by ineffective erythropoiesis with significant red cell fragmentation resulting in a hemolytic pattern, coupled with reduced platelet production and endothelial injury with organ damage resulting from accumulated toxic byproducts of B12 dysmetabolism. However, unlike in classic thrombotic thrombocytopenic purpura, where therapeutic plasma exchange has to be initiated promptly, cases of MM-TMA can be treated, if diagnosed properly, with adequate B12 replacement.

Megaloblastic anemia due to severe vitamin B12 deficiency.

Megaloblastic anemia due to severe vitamin B12 deficiency.

Prevalence of Vitamin B12 Deficiency In Patients With Type II Diabetes Mellitus On Metformin

Background: Diabetes Mellitus is one of the most encountered disease in our out patient department and metformin is the first drug of choice to treat Diabetes mellitus. As metformin is one of the cheapest drug, many patients use these drug for long period of time with consultation and without consultations with doctors. Patients under long term metformin use are not aware of Vitamin B12 deficiency and its associated signs and symptoms. In Nepal due to poverty, lack of education and awareness on diabetes mellitus we doctors find much difficult to explain patients on the consequences of diseases. So I decided to do this study which could be much easier to explain patients on effect of metformin of vitamin B12 levels and the consequences life style modifications and supplement of Vitamin B12 to the patients.
 Methods: This is a Cross-Sectional Study done in the patients with Type 2 diabetes were selected based on inclusion and exclusion criteria. Basic biochemical investigation were sent the lab of the National academy of medical science. Serum B12 assay were done. Vitamin B12 deficiency is defined as values <150pg/ml. Association between vitamin B12 deficiency with duration of metformin therapy, duration of diabetes, with age, sex were done.
 Results: The mean vitamin B12 level is low as the duration of metformin treatment increases. The sex, age relation with development of vitamin B12 deficiency was not significant. In my study out of 210 patients 107 patients were having severe vitamin B12 deficiency level and 63 patients had a borderline Vitamin B12 deficiency level which shows that the deficiency increases as per longer use of metformin, which shows prevalence of 50.95%.
 Conclusions: Vitamin B12 deficiency occurs in type 2 diabetes mellitus patients treated with long term metformin. The duration of metformin therapy significantly affects the development of vitamin B12 deficiency. As a treating physician we always need to explain our patients about the side effect of metformin and regular follow up and investigations must be done to early diagnosis of vitamin B12 deficiency to improve the quality of life.

Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

Vitamin B12 is an essential nutrient which plays an important role in neurological function, hematopoiesis, and DNA synthesis. Low levels usually stem from either poor intake or a malabsorptive process. Presently, the most common cause of vitamin B12 deficiency is food-bound cobalamin malabsorption, which occurs when there is impaired release of vitamin B12 from ingested food due to an outstanding factor preventing the release of the nutrient from its transport protein. Such causes include achlorhydria, gastritis, gastrectomy, or the use of PPIs or antacids. A rarer cause is autoimmune chronic atrophic gastritis, resulting in pernicious anemia. In this disease process, there is destruction of parietal cells and thus a reduction in intrinsic factor, which is essential to the absorption of vitamin B12. Deficiency will result in a variety of abnormalities including but not limited to pancytopenia, paresthesias, and neuropsychiatric symptoms. A rare manifestation of vitamin B12 deficiency is hemolytic anemia, which occurs due to intramedullary and extramedullary dysfunction. This case describes a 46-year-old male with no past medical history who presented with chest pain, fatigue, and progressive weakness, found to have hemolytic anemia, ultimately attributed to vitamin B12 deficiency. Antiparietal cell antibodies and intrinsic factor antibodies (IFA) were both negative. Still, the patient underwent an endoscopy with biopsies of the stomach; pathology was consistent with chronic metaplastic atrophic gastritis. The patient improved with intramuscular vitamin B12 supplementation. This case highlights both a rare cause and presentation of vitamin B12 deficiency. Patients with autoimmune chronic atrophic gastritis should have antiparietal cell or intrinsic factor antibodies. Still, seronegative patients have been reported, like this patient. Additionally, hemolytic anemia secondary to vitamin B12 deficiency is uncommon. The presentation will usually mirror that of a thrombotic microangiopathy (TMA), including hemolytic anemia with schistocytes on peripheral blood smear and thrombocytopenia, as it did in this patient. This clinical entity is described as pseudothrombotic microangiopathy and is crucial to identify in order to prevent the initiation of invasive treatment strategies such as plasmapheresis.

Un bambino che non mangia… e non sta seduto

The Authors describe the case of an 11-month-old infant with severe vitamin B12 deficiency consequent to a strict vegan diet followed by the mother during pregnancy and to a strictly vegan weaning. The child presented with food refusal, somatic growth arrest and seriously compromised maturational patterns. The encephalic MR showed a marked white matter atrophy. Symptoms improved after vitamin B12 supplementation.

Teaching Video NeuroImage: Choreoathetosis and Focal Dystonia in Vitamin B12 Deficiency.

An 87-year-old man presented with involuntary movements of his fingers for 3 months. Clinical examination showed dystonia with choreoathetosis of his hands and fingers (Video 1). Pinprick sensation was reduced to ankles and vibration sense was absent up to shoulders and costal margin bilaterally. Investigations revealed hemoglobin of 10.1 g/dL, mean corpuscular volume of 94.6 fL, vitamin B12 level of <92 pmol/L, and the presence of antiparietal cell antibody. He was diagnosed with pernicious anemia and treated with intramuscular cyanocobalamin (1,000 μg weekly for 4 weeks then monthly). Reassessment 2 months later showed significant clinical improvement and normalized vitamin B12 level of 534 pmol/L. Pseudoathetosis—a slow, writhing movement of the distal extremities seen in severe sensory neuropathy—was also considered. However, the patient's movements did not worsen with eye closure. Severe vitamin B12 deficiency may result in chorea, myoclonus, tremor, and dystonia.1 These manifestations, possibly a result of basal ganglia dysfunction, are rare but important to recognize as they are largely reversible with supplementation.2