Parenteral thiamine administration is associated with a very small risk of anaphylaxis.People who consume excessive amounts of alcohol may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses.If glucose is given, such as in people with an alcohol use disorder who are also hypoglycaemic, thiamine must be given concurrently. If this is not done, the glucose will rapidly consume the remaining thiamine reserves, exacerbating this condition.The observation of edema in MR, and also the finding of inflation and macrophages in necropsied tissues, has led to successful administration of antiinflammatories.Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease. In particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease.Other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide, zinc, phosphorus (dicalcium phosphate) and in some cases taurine, especially suitable when there cardiocirculatory impairment. Patient-guided nutrition is suggested. In patients with Wernicke-Korsakoff syndrome, even higher doses of parenteral thiamine are recommended. Concurrent toxic effects of alcohol should also be considered. Epidemiology
There are no conclusive statistical studies, all figures are based on partial studies. Wernickes lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% of people with an alcohol use disorder. This figure increases to 35% of such individuals if including cerebellar damage due to lack of thiamine.Most autopsy cases were from people with an alcohol use disorder.
Illness resulting from acute exposure is usually not fatal although some exposure may cause bronchiolitis obliterans, pulmonary edema as well as rapid asphyxiation. If the concentration of exposure is excessively high, the gas may displace oxygen resulting in fatal asphyxiation.Generally, patients and workers should be educated by medical personnel on how to identify the signs and symptoms of Nitrogen dioxide poisoning. Farmers and other farm workers should be educated on the proper way of food grain storage to prevent silo fillers disease. Biochemical effects
Chronic exposure to high level of nitrogen dioxide results in the allosteric inhibition of glutathione peroxidase and glutathione S-transferase, both of which are important enzymes found in the mucous membrane antioxidant defense system, that catalyse nucleophilic attack by reduced glutathione (GSH) on non-polar compounds that contain an electrophilic carbon and nitrogen. These inhibition mechanisms generates free radicals that causes peroxidation from the lipids in the mucous membrane leading to increased peroxidized erythrocyte lipids, a reaction that proceeds by a free radical chain reaction mechanism that result in oxidative stress. The oxidative stress on the mucous membrane causes the dissociation of the GSTp-JNK complex, oligomerization of GSTP  and induction of the JNK pathway, resulting in apoptosis or inflammation of the bronchioles and pulmonary alveolus in mild cases. On migrating to the bloodstream, nitrogen dioxide poisoning results in an irreversible inhibition of the erythrocyte membrane acetylcholinesterase which may lead to muscular paralysis, convulsions, bronchoconstriction, the narrowing of the airways in the lungs (bronchi and bronchioles) and death by asphyxiation.