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The American Journal of Medicine Jan 2022
Topics: Alcoholism; Antirheumatic Agents; Arthritis, Rheumatoid; Clobetasol; Diagnostic Errors; Glucocorticoids; Humans; Hydroxychloroquine; Male; Middle Aged; Pellagra; Psoriasis
PubMed: 34343513
DOI: 10.1016/j.amjmed.2021.06.035 -
QJM : Monthly Journal of the... Feb 2023
Topics: Humans; Pellagra
PubMed: 36106995
DOI: 10.1093/qjmed/hcac222 -
Epidemiologia (Basel, Switzerland) Apr 2022This paper argues that the public health conceptual framework of epidemiologist Geoffrey Rose, first published as "Sick Individuals and Sick Populations" in 1985,... (Review)
Review
This paper argues that the public health conceptual framework of epidemiologist Geoffrey Rose, first published as "Sick Individuals and Sick Populations" in 1985, provides a useful way to critically analyze prevention and control options for modern non-communicable diseases (NCD) and their forerunner, obesity, a pandemic now engulfing Lower-and-Middle-Income-Countries. That framework is based on the notions of primordial, primary, secondary and tertiary prevention-the full spectrum of "more upstream and more downstream" approaches, each with its pros and cons. These are illustrated using the pellagra epidemic in the southeastern USA from 1900 to the 1940s, which still has much to teach us about these same basic policy options for controlling the modern NCD pandemic. In particular, Rose's dictum, "Seek the causes of (population) incidence, not of (individual) cases", points up the compelling advantages of upstream prevention for controlling both epidemics.
PubMed: 36417251
DOI: 10.3390/epidemiologia3020015 -
Public Health Nutrition Jun 2021Pellagra is a nutritional deficiency disease associated with niacin (vitamin B3) deficiency. The history of pellagra is well documented for Europe and the USA, but less... (Review)
Review
OBJECTIVE
Pellagra is a nutritional deficiency disease associated with niacin (vitamin B3) deficiency. The history of pellagra is well documented for Europe and the USA, but less is known about the prevalence in sub-Saharan African countries. This study documents the history of pellagra in South Africa, as diagnosed based on dermatological symptoms.
DESIGN
Scoping review of information from scientific databases, library archives, other archives and record services and from Statistics South Africa.
SETTING
South Africa, 1897-2019.
PARTICIPANTS
South African.
RESULTS
Pellagra was first officially recorded in South Africa in 1906, but there are earlier indications of the disease. The prevalence of pellagra peaked after it was all but eradicated in the USA and Europe. Pellagra was never as prevalent in South Africa as in Europe, the USA and Egypt, where special hospitals for pellagrins were established. However, studies on urinary excretion of metabolites conducted in 1960s and 1970s suggested a high prevalence of subclinical (sub-pellagra) niacin deficiency, especially in previously disadvantaged Black populations. As in Europe and the USA, pellagra was associated with poverty and an overdependence on maize as staple food. Malnutrition was the main cause of the disease, but alcohol abuse might have been a contributing factor. In South Africa, reports of pellagra had declined by the late 1980s/early 1990s and hardly any cases were reported by the year 2000.
CONCLUSIONS
Although pellagra, diagnosed based on dermatological symptoms, appears to be largely eradicated in South Africa, it does not rule out the potential for subclinical niacin deficiency.
Topics: Europe; Humans; Niacin; Pellagra; Poverty; South Africa
PubMed: 33769244
DOI: 10.1017/S1368980021001336 -
Clinical Science (London, England :... Nov 2020ACE2 is a type I membrane protein with extracellular carboxypeptidase activity displaying a broad tissue distribution with highest expression levels at the brush border... (Review)
Review
ACE2 is a type I membrane protein with extracellular carboxypeptidase activity displaying a broad tissue distribution with highest expression levels at the brush border membrane (BBM) of small intestine enterocytes and a lower expression in stomach and colon. In small intestinal mucosa, ACE2 mRNA expression appears to increase with age and to display higher levels in patients taking ACE-inhibitors (ACE-I). There, ACE2 protein heterodimerizes with the neutral amino acid transporter Broad neutral Amino acid Transporter 1 (B0AT1) (SLC6A19) or the imino acid transporter Sodium-dependent Imino Transporter 1 (SIT1) (SLC6A20), associations that are required for the surface expression of these transport proteins. These heterodimers can form quaternary structures able to function as binding sites for SARS-CoV-2 spike glycoproteins. The heterodimerization of the carboxypeptidase ACE2 with B0AT1 is suggested to favor the direct supply of substrate amino acids to the transporter, but whether this association impacts the ability of ACE2 to mediate viral infection is not known. B0AT1 mutations cause Hartnup disorder, a condition characterized by neutral aminoaciduria and, in some cases, pellagra-like symptoms, such as photosensitive rash, diarrhea, and cerebellar ataxia. Correspondingly, the lack of ACE2 and the concurrent absence of B0AT1 expression in small intestine causes a decrease in l-tryptophan absorption, niacin deficiency, decreased intestinal antimicrobial peptide production, and increased susceptibility to inflammatory bowel disease (IBD) in mice. Thus, the abundant expression of ACE2 in small intestine and its association with amino acid transporters appears to play a crucial role for the digestion of peptides and the absorption of amino acids and, thereby, for the maintenance of structural and functional gut integrity.
Topics: Amino Acid Transport Systems, Neutral; Angiotensin-Converting Enzyme 2; Animals; Betacoronavirus; COVID-19; Coronavirus Infections; Host-Pathogen Interactions; Humans; Inflammatory Bowel Diseases; Intestinal Absorption; Intestinal Mucosa; Membrane Transport Proteins; Pandemics; Peptidyl-Dipeptidase A; Pneumonia, Viral; Protein Multimerization; SARS-CoV-2; Virus Internalization
PubMed: 33140827
DOI: 10.1042/CS20200477 -
Advances in Nutrition (Bethesda, Md.) Jan 2015Fortification is the process of adding nutrients or non-nutrient bioactive components to edible products (e.g., food, food constituents, or supplements). Fortification... (Review)
Review
Fortification is the process of adding nutrients or non-nutrient bioactive components to edible products (e.g., food, food constituents, or supplements). Fortification can be used to correct or prevent widespread nutrient intake shortfalls and associated deficiencies, to balance the total nutrient profile of a diet, to restore nutrients lost in processing, or to appeal to consumers looking to supplement their diet. Food fortification could be considered as a public health strategy to enhance nutrient intakes of a population. Over the past century, fortification has been effective at reducing the risk of nutrient deficiency diseases such as beriberi, goiter, pellagra, and rickets. However, the world today is very different from when fortification emerged in the 1920s. Although early fortification programs were designed to eliminate deficiency diseases, current fortification programs are based on low dietary intakes rather than a diagnosable condition. Moving forward, we must be diligent in our approach to achieving effective and responsible fortification practices and policies, including responsible marketing of fortified products. Fortification must be applied prudently, its effects monitored diligently, and the public informed effectively about its benefits through consumer education efforts. Clear lines of authority for establishing fortification guidelines should be developed and should take into account changing population demographics, changes in the food supply, and advances in technology. This article is a summary of a symposium presented at the ASN Scientific Sessions and Annual Meeting at Experimental Biology 2014 on current issues involving fortification focusing primarily on the United States and Canada and recommendations for the development of responsible fortification practices to ensure their safety and effectiveness.
Topics: Canada; Deficiency Diseases; Diet; Food, Fortified; Health; Humans; Micronutrients; United States
PubMed: 25593151
DOI: 10.3945/an.114.007443 -
Journal of Tropical Pediatrics Aug 2015Pellagra is a disorder characterized by dermatitis, diarrhea, dementia and eventually death, resulting from a deficiency of niacin or its precursor tryptophan....
Pellagra is a disorder characterized by dermatitis, diarrhea, dementia and eventually death, resulting from a deficiency of niacin or its precursor tryptophan. Ethionamide (a second-line antituberculosis agent)-induced pellagra is rarely encountered in clinical practice. Prompt diagnosis and treatment with nicotinamide can prevent life-threatening complications. To date, only three cases have been reported. We report a 13-year-old girl presenting with ethionamide-induced pellagra that resolved after the administration of niacin.
Topics: Adolescent; Antitubercular Agents; Diagnosis, Differential; Ethionamide; Female; Humans; Niacin; Pellagra; Treatment Outcome; Tuberculosis, Pulmonary
PubMed: 25828829
DOI: 10.1093/tropej/fmv021 -
International Journal of Tryptophan... 2019Good health and rapid progress depend on an optimal dose of nicotinamide. Too little meat triggers the neurodegenerative condition pellagra and tolerance of symbionts... (Review)
Review
Good health and rapid progress depend on an optimal dose of nicotinamide. Too little meat triggers the neurodegenerative condition pellagra and tolerance of symbionts such as tuberculosis (TB), risking dysbioses and impaired resistance to acute infections. Nicotinamide deficiency is an overlooked diagnosis in poor cereal-dependant economies masquerading as 'environmental enteropathy' or physical and cognitive stunting. Too much meat (and supplements) may precipitate immune intolerance and autoimmune and allergic disease, with relative infertility and longevity, via the tryptophan-nicotinamide pathway. This switch favours a dearth of regulatory T (Treg) and an excess of T helper cells. High nicotinamide intake is implicated in cancer and Parkinson's disease. Pro-fertility genes, evolved to counteract high-nicotinamide-induced infertility, may now be risk factors for degenerative disease. Moderation of the dose of nicotinamide could prevent some common diseases and personalised doses at times of stress or, depending on genetic background or age, may treat some other conditions.
PubMed: 31320805
DOI: 10.1177/1178646919855940 -
Vnitrni Lekarstvi 2021Neuroendocrine tumors (NETs, originally termed “carcinoids”) create a relatively rare group of neoplasms with an approximate incidence rate of 5 to 8 cases...
Neuroendocrine tumors (NETs, originally termed “carcinoids”) create a relatively rare group of neoplasms with an approximate incidence rate of 5 to 8 cases per 10 000 persons. NETs predominantly demonstrate indolent disease biology for many years. They become symptomatic when they are large enough or when they metastasize to the liver or the lungs, bones, or other sites. Roughly 30% to 40% of subjects with NETs develop carcinoid syndrome. Signs and symptoms of carcinoid syndrome are bronchospasm, flushing, diarrhea and cramping, cyanosis and pellagra. White plaque-like deposits on the endocardial surface of heart structures are characteristic for carcinoid heart disease. The treatment of patients with carcinoid syndrome is multi-faceted due to the necessity to manage simultaneously the systemic cancer disease as well as the signs of carcinoid syndrome and includes resection or debulking of tumor mass, biological treatment with somatostatin analogues and peptide receptor radionuclide treatment.
Topics: Carcinoid Heart Disease; Carcinoid Tumor; Humans; Neuroendocrine Tumors; Somatostatin
PubMed: 35459398
DOI: No ID Found -
Nutrients Jun 2023The oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as... (Review)
Review
The oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as well as a coenzyme for different NAD+-consuming enzymes involved in the physiological homeostasis of different organs and systems. In mammals, NAD+ is synthesized from either tryptophan or other vitamin B3 intermediates that act as NAD+ precursors. Recent research suggests that NAD+ precursors play a crucial role in maintaining the integrity of the gut barrier. Indeed, its deficiency has been associated with enhanced gut inflammation and leakage, and dysbiosis. Conversely, NAD+-increasing therapies may confer protection against intestinal inflammation in experimental conditions and human patients, with accumulating evidence indicating that such favorable effects could be, at least in part, mediated by concomitant changes in the composition of intestinal microbiota. However, the mechanisms by which NAD+-based treatments affect the microbiota are still poorly understood. In this context, we have focused specifically on the impact of NAD+ deficiency on intestinal inflammation and dysbiosis in animal and human models. We have further explored the relationship between NAD+ and improved host intestinal metabolism and immunity and the composition of microbiota in vivo. Overall, this comprehensive review aims to provide a new perspective on the effect of NAD+-increasing strategies on host intestinal physiology.
Topics: Animals; Humans; Gastrointestinal Microbiome; NAD; Dysbiosis; Niacinamide; Inflammation; Mammals
PubMed: 37447318
DOI: 10.3390/nu15132992