Vitamin E deficiency is most commonly seen in the developed world as a result of inadequate dietary intake, whereas malabsorption syndrome after various gastrointestinal diseases or surgery may be the cause as well. Neurological deficits and hemolytic anemia are two main symptoms. Measuring vitamin E levels in blood is necessary for diagnosis, whereas supplementation is the mode of treatment.
Neurological deficits may include hyporeflexia, ataxia, strabismus, limitations in upward gaze, but also constriction of the visual field and profound muscle weakness . Dysarthria, absence of deep tendon reflexes, loss of vibratory sensations and positive Babinski reflexes may also be encountered in vitamin E deficient individuals . In most severe cases, blindness, dementia, irreversible nerve damage and cardiac arrhythmias can develop  .
A thorough neurological examination to assess the extent of symptoms is vital in the diagnostic workup , but to confirm vitamin E deficiency, serum levels of α-tocopherol should be determined and values of < 5 µg/mL (or < 11.6 µmol/L) are diagnostic for this hypovitaminosis . A lipid profile should also be obtained and a reduced α-tocopherol to lipid ration can also provide an accurate diagnosis. The search for an underlying cause should start with a thorough abdominal examination through ultrasonography or more invasive procedures (such as endoscopy) if there is valid clinical suspicion toward fat malabsorption .
Supplementation of α-tocopherol, either in oral or parenteral formulations, is the mainstay of treatment  . A dose of 15-25 mg/kg is given every day in the setting of oral supplementation, while parenteral dosages may be higher in order to overcome the inability to utilize vitamin E from the gut .
Early recognition of the disease carries a good prognosis, but profound nerve damage may be irreversible without timely identification of the underlying cause and appropriate treatment.
Various diseases have shown to induce vitamin E deficiency. Abetalipoproteinemia, chronic cholestatic liver disease, pancreatitis, short bowel syndrome, but also cystic fibrosis may cause fat malabsorption in the gut and thus impair normal vitamin E utilization from the gastrointestinal tract  .
The exact rates of vitamin E deficiency in the world are unknown, but isolated reports showed that more than 50% of individuals in Thailand suffer from this hypovitaminosis . Additionally, it is estimated that more than 90% of individuals living in the United States do not meet the recommended dietary intake of vitamin E (15 mg/day) , suggesting that the issue of insufficient ingestion of vitamin E is on a global scale.
α-tocopherol is one of the most potent free radical scavengers in the human body and it is absorbed from the gastrointestinal tract as a fat-soluble vitamin . Under physiological conditions, vitamin E is the primary defense against lipid peroxidation that can cause severe damage to cell membranes and neurons . In its absence, fragility of red blood cells and degeneration of neurons is the main cause of symptom development .
Ensuring sufficient dietary intake is an effective preventive strategy. Edible oils are abundant with vitamin E and the the richest source of this nutrient, whereas almonds, hazelnuts, peanuts, spinach, broccoli, mango and tomato are also sources of α-tocopherol .
Vitamin E is a lipid-soluble vitamin considered to be one of the most important antioxidant nutrients in the body, as it prevents cell membrane lipid peroxidation . The form which is considered to be most active, α-tocopherol, acts as a peroxyl radical scavenger in lipid environments and possesses numerous beneficiary roles in the body, including prevention of oxidative stress, but also regulation of platelet aggregation, protein kinase C activation and preservation of the cardiovascular and immune systems  . Its deficiency can stem from inadequate dietary intake, the most common cause in the developed world, or from gastric surgery and diseases that induce fat malabsorption (cystic fibrosis, abetalipoproteinemia)  . Hemolytic anemia and a myriad of neurological symptoms (due to neuronal death induced by free radicals that are not scavenged by α-tocopherol) are principal symptoms and the diagnosis can be made by determining levels of α-tocopherol in blood together with serum lipids  . Vitamin E supplementation and diet correction (when possible) are two main methods of treatment .
Vitamin E deficiency is a condition that stems either from inadequate dietary intake or due to diseases that impede its absorption from the gastrointestinal tract, such as abetalipoproteinemia, cholestatic liver disease, cystic fibrosis, short bowel syndrome or cystic fibrosis. Vitamin E, in its most biologically active form, α-tocopherol, is an essential part of defense against free radicals that can cause cell membrane damage and in its absence, the neurons and the red blood cells are most severely affected, leading to anemia and various neurological symptoms. Attenuated reflexes, visual deficits, muscle weakness, difficulties with speech and dementia are some of the most common symptoms, whereas severe deficiencies can lead to blindness and cardiac arrhythmias. To diagnose vitamin E deficiency, it is necessary to measure its concentrations in blood and to obtain a full lipid profile. Treatment comprises supplementation with vitamin E, either through tablets or injections, depending on the underlying cause. Many studies have concluded that inadequate dietary intake of vitamin E is a global issue, which is why vitamin E-rich foods - edible oils, almonds, hazelnuts, peanuts, spinach and broccoli must be taken on a regular basis.