Pellagra Secondary to Medication and Alcoholism

Li, Rongrong; Yu, Kang; Wang, Qiang; Wang, Lilin; Mao, Jiangfeng; Qian, Jiaming

doi:10.1177/0884533616660991

Cited by 32 publications

(15 citation statements)

References 21 publications

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“…Whereas secondary dietary inadequacies may interrupt niacin metabolism, this also holds for certain medications including specific antituberculosis, anticonvulsant and antiproliferative drugs, as well as cyclosporine and azathioprine [32,33,34], which are common immunosuppressant drugs in RTR, although in our population those did not appear to affect N 1 -MN excretion.…”

Section: Discussionmentioning

confidence: 72%

Urinary Excretion of N1-Methylnicotinamide, as a Biomarker of Niacin Status, and Mortality in Renal Transplant Recipients

Deen

Veen

Faassen

et al. 2019

JCM

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Renal transplant recipients (RTR) commonly suffer from vitamin B6 deficiency and its functional consequences add to an association with poor long-term outcome. It is unknown whether niacin status is affected in RTR and, if so, whether this affects clinical outcomes, as vitamin B6 is a cofactor in nicotinamide biosynthesis. We compared 24-h urinary excretion of N1-methylnicotinamide (N1-MN) as a biomarker of niacin status in RTR with that in healthy controls, in relation to dietary intake of tryptophan and niacin as well as vitamin B6 status, and investigated whether niacin status is associated with the risk of premature all-cause mortality in RTR. In a prospective cohort of 660 stable RTR with a median follow-up of 5.4 (4.7–6.1) years and 275 healthy kidney donors, 24-h urinary excretion of N1-MN was measured with liquid chromatography-tandem mass spectrometry LC-MS/MS. Dietary intake was assessed by food frequency questionnaires. Prospective associations of N1-MN excretion with mortality were investigated by Cox regression analyses. Median N1-MN excretion was 22.0 (15.8–31.8) μmol/day in RTR, compared to 41.1 (31.6–57.2) μmol/day in healthy kidney donors (p < 0.001). This difference was independent of dietary intake of tryptophan (1059 ± 271 and 1089 ± 308 mg/day; p = 0.19), niacin (17.9 ± 5.2 and 19.2 ± 6.2 mg/day; p < 0.001), plasma vitamin B6 (29.0 (17.5–49.5), and 42.0 (29.8–60.3) nmol/L; p < 0.001), respectively. N1-MN excretion was inversely associated with the risk of all-cause mortality in RTR (HR 0.57; 95% CI 0.45–0.71; p < 0.001), independent of potential confounders. RTR excrete less N1-MN in 24-h urine than healthy controls, and our data suggest that this difference cannot be attributed to lower dietary intake of tryptophan and niacin, nor vitamin B6 status. Importantly, lower 24-h urinary excretion of N1-MN is independently associated with a higher risk of premature all-cause mortality in RTR.

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Section: Discussionmentioning

confidence: 72%

Urinary Excretion of N1-Methylnicotinamide, as a Biomarker of Niacin Status, and Mortality in Renal Transplant Recipients

Deen

Veen

Faassen

et al. 2019

JCM

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“…Additional support for the chromatolysis hypothesis comes from the symptoms of pellagra, a disorder characterized by central chromatolysis. Pellagra is a nutritional disorder with niacin deficiency constituting the central mechanism ( 93 , 94 ). In addition to classical symptoms of dermatitis, diarrhea, and dementia, the mental health symptoms can be mistaken for schizophrenia ( 95 ), and are similar to those in prolonged sleep loss.…”

Section: Discussionmentioning

confidence: 99%

Severe Sleep Deprivation Causes Hallucinations and a Gradual Progression Toward Psychosis With Increasing Time Awake

et al. 2018

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Background: Going without sleep for long periods of time can produce a range of experiences, including perceptual distortions and hallucinations. Many questions, however, remain unanswered regarding the types of symptoms which are most reliably elicited, the time of symptom onset, and whether symptoms worsen over time toward psychotic decompensation. Since sleep deprivation exceeding 48 h is considered unethical today, an examination of historical studies with extreme sleep-loss duration is needed to obtain information about what happens during prolonged sleep loss.Methods: A systematic-review approach was used to identify experimental and observational studies of sleep deprivation in healthy people which describe the effects of prolonged sleep loss on psychopathological symptoms, without any date restriction.Results: A total of 476 articles were identified. Of these, 21 were eligible for inclusion. Duration of sleep loss ranged between 24 h and 11 nights (total 760 participants; average 72–92 h without sleep). All studies except one reported perceptual changes, including visual distortions (i.e., metamorphopsias), illusions, somatosensory changes and, in some cases, frank hallucinations. The visual modality was the most consistently affected (in 90% of the studies), followed by the somatosensory (52%) and auditory (33%) modalities. Symptoms rapidly developed after one night without sleep, progressing in an almost fixed time-dependent way. Perceptual distortions, anxiety, irritability, depersonalization, and temporal disorientation started within 24–48 h of sleep loss, followed by complex hallucinations and disordered thinking after 48–90 h, and delusions after 72 h, after which time the clinical picture resembled that of acute psychosis or toxic delirium. By the third day without sleep, hallucinations in all three sensory modalities were reported. A period of normal sleep served to resolve psychotic symptoms in many—although not all—cases.Conclusions: Psychotic symptoms develop with increasing time awake, from simple visual/somatosensory misperceptions to hallucinations and delusions, ending in a condition resembling acute psychosis. These experiences are likely to resolve after a period of sleep, although more information is required to identify factors which can contribute to the prevention of persistent symptoms.

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“…The early clinical diagnosis in our case conferred a good prognosis, and cases reported within the past 5 years have resolved with treatment ( Table 1 ). 18 - 24 Though considered by many as a disease of the past, clinicians should still maintain a high index of suspicion for pellagra as differential diagnosis for delirium or dementia in alcoholics, which may occur with or without dermatologic or GI manifestations.…”

Section: Discussionmentioning

confidence: 99%

Chronic Diarrhea in a Drinker: A Breakthrough Case of Pellagra in the US South

Mills

Akintayo

Egbosiuba

et al. 2020

Journal of Investigative Medicine High Impact Case Reports

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The triad of diarrhea, dementia, and dermatitis constitutes the clinical diagnosis of pellagra. However, most reported cases of pellagra have occurred without all components of the triad. Pellagra was declared eradicated in the United States after an outbreak in the 1920s, and is now considered to be an exceedingly rare diagnosis in developed countries. In this article, we present a case of a 56-year-old man who presented with a significant history of alcohol use and chronic diarrhea. Pellagra was clinically diagnosed based on the triad of diarrhea, cognitive dysfunction, and dermatitis in this malnourished, alcoholic patient. The patient was treated and clinically improved with resolution of his diarrhea and cognitive dysfunction.

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Pellagra Secondary to Medication and Alcoholism

Cited by 32 publications

References 21 publications

Urinary Excretion of N1-Methylnicotinamide, as a Biomarker of Niacin Status, and Mortality in Renal Transplant Recipients

Urinary Excretion of N1-Methylnicotinamide, as a Biomarker of Niacin Status, and Mortality in Renal Transplant Recipients

Severe Sleep Deprivation Causes Hallucinations and a Gradual Progression Toward Psychosis With Increasing Time Awake

Chronic Diarrhea in a Drinker: A Breakthrough Case of Pellagra in the US South

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