Fat soluble vitamins
A recent overview published in National Geographic1 pointed to some of the dangers with excessive consumption of fat soluble vitamins, particularly D and E, as these are stored (and accumulate) in the liver and in fat. The harm associated with prescribing Vitamin K in patients on warfarin is probably a bit overstated: aphorisms from some time ago mentioned ‘prolonged’ need for bridging anticoagulation in patients given large doses of Vitamin K for a prolonged INR (>10) or active bleeding – a cohort study of 400 patients found no major differences in duration of bridging anticoagulation whether patients were given lower doses of Vitamin K, whether it was given orally or intravenously, or whether FFP was also used – broadly, the INR would settle by 48 hours with IV being a bit quicker and 2 to 5 mg dropping it as well as 10 mg. Duration of bridging anticoagulation was about a week, regardless of dose or whether FFP was given, and was needed in about 70% of patients.2
Water soluble vitamins
Less thought is sometimes given to the consequences of prescribing (normal) amounts of water soluble vitamins to vitamin deficient patients. For thiamine, there is an iatrogenic cascade: the person with poor nutritional status presents in the emergency unit with confusion, and is given a dextrose drip because his glucose is borderline low (or just because he is confused and in the emergency unit.) His confusion worsens, and for those who bother to look, there is now a 6th nerve palsy. Eventually the penny drops and he is given thiamine and seems to improve, only to deteriorate again a day or so later, while still getting lots of thiamine. Eventually the second penny drops and nicotininc acid is started for the alcohol associated pellagra encephalopathy which was possibly worsened by thiamine.3,4
Features of alcoholic pellagra encephalopathy
Pellagra classically presents with the 4Ds (diarrhoea, dermatitis and dementia, sometimes death) but the neurological manifestations may happen without the rash or GIT changes. Insomnia, nervousness, hallucinations, hypertonia, ataxia, and myoclonus are potentially due to nicotinic acid deficiency, so consider this possibility.
Vitamins B12 and folate
Then there is folate precipitating incipient B12 deficiency5 (and acute paraparesis) – an ‘acute’ subacute combined degeneration of the cord – probably not a thing, although the jury is still out, with one review of historical data suggesting that most of the described cases were simply due to progression of the underlying B12 deficiency neurology despite, rather than because of high dose folate treatment6. A better documented precipitant is nitrous oxide7 and this can occur after a single exposure. However Vitamin B12 injection itself, in the setting of severe B12 deficient anaemia, may precipitate potentially fatal hypokalaemia as the red cells start to mature and accumulate potassium.8 although another case series was unable to find any link9
https://www.nationalgeographic.com/premium/article/how-these-2-vitamin-supplements-could-do-more-harm-than-good-?cmpid=org=ngp::mc=social::src=linkedin::cmp=editorial::add=linlm20231127science-twosupplementstxt ↩
Tsu LV, Dienes JE, Dager WE. Vitamin K dosing to reverse warfarin based on INR, route of administration, and home warfarin dose in the acute/critical care setting. Ann Pharmacother. 2012 Dec;46(12):1617-26. doi: 10.1345/aph.1R497. Epub 2012 Dec 18. PMID: 23249867. ↩
Serdaru M, Hausser-Hauw C, Laplane D, et al. The clinical spectrum of alcoholic pellagra encephalopathy: a retrospective analysis of 22 cases studied pathologically. Brain 1988;111(Pt 4):829–42 ↩
Sharma B, Sannegowda RB, Jain R, et al. A rare case of alcoholic pellagra encephalopathy with startle myoclonus and marked response to niacin therapy: time for a new dictum? BMJ Case Rep. doi:10.1136/bcr-2013-008906 ↩
Hunt A, Harrington D, Robinson S. Vitamin B12 deficiency. BMJ. 2014 Sep 4;349:g5226. doi: 10.1136/bmj.g5226. PMID: 25189324. ↩
Berry RJ. Lack of historical evidence to support folic acid exacerbation of the neuropathy caused by vitamin B12 deficiency. Am J Clin Nutr. 2019 Sep 1;110(3):554-561. doi: 10.1093/ajcn/nqz089. PMID: 31187858; PMCID: PMC6785032. ↩
Marsden P, Sharma AA, Rotella J-A. Review article: Clinical manifestations and outcomes of chronic nitrous oxide misuse: A systematic review. Emergency Medicine Australasia 2022;34:492–503. doi:10.1111/1742-6723.13997 ↩
Lawson DH, Murray RM, Parker JL. Early Mortality in the Megaloblastic Anaemias, QJM: An International Journal of Medicine, Volume 41, Issue 1, January 1972, Pages 1–14, https://doi.org/10.1093/oxfordjournals.qjmed.a067290 ↩
Carmel R. Treatment of severe PA: no association with sudden death. Am J Clin Nutr. 1988;48:1443-1444 ↩