Treatment of Uncomplicated Anosmia by Vitamin A

Duncan, Robert B.; Briggs, Michael H.

doi:10.1001/archotol.1962.00740040122008

Cited by 60 publications

(25 citation statements)

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“…Another aspect that has to be considered when trying to explain the lack of benefit in this study is the dosage. Duncan and Briggs10 reported in their study on an improvement in olfactory function after administering vitamin A. Dosages in their observation varied from 50,000 to 150,000 IU per day, in some cases given intravenously, with no standardized protocol.…”

Section: Discussionmentioning

confidence: 99%

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Olfactory function in patients with postinfectious and posttraumatic smell disorders before and after treatment with vitamin A: A double‐blind, placebo‐controlled, randomized clinical trial

Reden¹,

Lill²,

Zahnert³

et al. 2012

The Laryngoscope

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Section: Discussionmentioning

confidence: 99%

“…In humans, only two studies have focused on the role of vitamin A in olfaction. Duncan and Briggs reported an improvement in olfactory function in 50 of 56 patients after treatment with vitamin A in 1962 10. Another study showed that substitution of vitamin A cured olfactory loss in patients with liver cirrhosis and vitamin A deficiency 11…”

Section: Introductionmentioning

confidence: 99%

Olfactory function in patients with postinfectious and posttraumatic smell disorders before and after treatment with vitamin A: A double‐blind, placebo‐controlled, randomized clinical trial

Reden¹,

Lill²,

Zahnert³

et al. 2012

The Laryngoscope

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“…[805] This is difficult to interpret: those seen more due to lipid therapy could have better access to cataract diagnosis leading to incorrect inferences in absence of adjustment; however, such adjustment could also extinguish a true association, through collinearity -In a US study, incidence of nuclear cataract was lower in statin users relative to nonusers controlling for age (OR 0.55; 95% CI 0.36, 0.84). [806] Confounding is a major concern in such correlational studies, and associations observed may be different in magnitude and direction from true relationships -External ophthalmoplegia has been widely described in mitochondrial disease, [808][809][810][811][812][813] and has been linked to deficiencies of fat-soluble vitamins transported by cholesterol [814] Olfaction Hyposmia [815] Lipids transport carotenoids [816] , the precursor to retinol (vitamin A), which is important in smell and has been used in treatment of anosmia [817][818][819] Hematologic and -See 'Hemorrhagic stroke' in table VII -Statin use has been observationally linked to lower bleeding, bone marrow, -Ocular hemorrhage reported as a statin AE [820] possibly as a proxy for higher cholesterol (and vitamin K?) [806] Confounding is a major concern in such correlational studies, and associations observed may be different in magnitude and direction from true relationships -External ophthalmoplegia has been widely described in mitochondrial disease, [808][809][810][811][812][813] and has been linked to deficiencies of fat-soluble vitamins transported by cholesterol [814] Olfaction Hyposmia [815] Lipids transport carotenoids [816] , the precursor to retinol (vitamin A), which is important in smell and has been used in treatment of anosmia [817][818][819] Hematologic and -See 'Hemorrhagic stroke' in table VII -Statin use has been observationally linked to lower bleeding, bone marrow, -Ocular hemorrhage reported as a statin AE [820] possibly as a proxy for higher cho...…”

Section: Continued Next Pagementioning

confidence: 99%

Statin Adverse Effects

Golomb

Evans

2008

American Journal of Cardiovascular Drugs

592

257

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HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanism, dose effect, drug interactions, and genetic predisposition is examined. We hypothesize, and provide evidence, that the demonstrated mitochondrial mechanisms for muscle AEs have implications to other nonmuscle AEs in patients treated with statins. In meta-analyses of randomized controlled trials (RCTs), muscle AEs are more frequent with statins than with placebo. A number of manifestations of muscle AEs have been reported, with rhabdomyolysis the most feared. AEs are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system. An array of additional risk factors for statin AEs are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction. Converging evidence supports a mitochondrial foundation for muscle AEs associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity.

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“…An early but poorly designed study suggested improvement in 21 patients with postviral olfactory dysfunction given intramuscular beta carotene or vitamin A [26]. A subsequent case report described improvement in one patient given retinoic acid [27].…”

Section: Therapy and Prognosismentioning

confidence: 99%