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The South African Journal of Psychiatry... 2023The case report depicts the complex interplay between mental and physical illness and contests the notion of mind-body dualism in medicine. It emphasises the importance...
INTRODUCTION
The case report depicts the complex interplay between mental and physical illness and contests the notion of mind-body dualism in medicine. It emphasises the importance of holistic management of patients and the misnomer of schizophrenia as a purely mental illness.
PATIENT PRESENTATION
Mr S is a 35-year-old male who presented to a South African specialist psychiatric hospital via the forensic system. He had multiple physical symptoms involving the abdominal, haematological, dermatological and neurological systems, in addition to an eight year duration of untreated psychosis with a marked decline in cognition and functioning.
MANAGEMENT AND OUTCOME
An extensive medical examination during his admission excluded conditions such as early onset dementia, Huntington's disease, pellagra, Wilson's disease, autoimmune encephalitis and substance-related complications. A definitive diagnosis of schizophrenia was made, and both physical and psychiatric symptoms responded well to the administration of an antipsychotic resulting in an eventual discharge from the hospital.
CONCLUSION
Mind-body dualism can result in a delayed diagnosis of schizophrenia and subsequent increased duration of untreated psychosis and other complications.
CONTRIBUTION
This case emphasises the flaws of mind-body dualism, and the interplay of mental and physical illness.
PubMed: 37795458
DOI: 10.4102/sajpsychiatry.v29i0.2081 -
Hellenic Journal of Nuclear Medicine 2023The carcinoid syndrome (CS) is a constellation of symptoms attributed to hypersecretion of amines, prostaglandins and polypeptides. The cardinal symptoms of CS are...
The carcinoid syndrome (CS) is a constellation of symptoms attributed to hypersecretion of amines, prostaglandins and polypeptides. The cardinal symptoms of CS are flushing, diarrhea and bronchospasm; however, CS may present with various symptoms and signs, as: Skin: cutaneous flushes, cyanosis, pellagra, Gastrointestinal: diarrhea, nausea, abdominal cramps, vomiting, Heart: tricuspid and pulmonic valve thickening causing right heart failure, edema, Respiratory: wheezing, dyspnea.
Topics: Humans; Carcinoid Heart Disease; Malignant Carcinoid Syndrome; Diarrhea; Carcinoid Tumor
PubMed: 37658565
DOI: No ID Found -
Antioxidants & Redox Signaling Dec 2023The remarkable geometry of the axon exposes it to unique challenges for survival and maintenance. Axonal degeneration is a feature of peripheral neuropathies, glaucoma,... (Review)
Review
The remarkable geometry of the axon exposes it to unique challenges for survival and maintenance. Axonal degeneration is a feature of peripheral neuropathies, glaucoma, and traumatic brain injury, and an early event in neurodegenerative diseases. Since the discovery of Wallerian degeneration (WD), a molecular program that hijacks nicotinamide adenine dinucleotide (NAD) metabolism for axonal self-destruction, the complex roles of NAD in axonal viability and disease have become research priority. The discoveries of the protective Wallerian degeneration slow (Wld) and of sterile alpha and TIR motif containing 1 (SARM1) activation as the main instructive signal for WD have shed new light on the regulatory role of NAD in axonal degeneration in a growing number of neurological diseases. SARM1 has been characterized as a NAD hydrolase and sensor of NAD metabolism. The discovery of regulators of nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) proteostasis in axons, the allosteric regulation of SARM1 by NAD and NMN, and the existence of clinically relevant windows of action of these signals has opened new opportunities for therapeutic interventions, including SARM1 inhibitors and modulators of NAD metabolism. Events upstream and downstream of SARM1 remain unclear. Furthermore, manipulating NAD metabolism, an overdetermined process crucial in cell survival, for preventing the degeneration of the injured axon may be difficult and potentially toxic. There is a need for clarification of the distinct roles of NAD metabolism in axonal maintenance as contrasted to WD. There is also a need to better understand the role of NAD metabolism in axonal endangerment in neuropathies, diseases of the white matter, and the early stages of neurodegenerative diseases of the central nervous system. 39, 1167-1184.
Topics: Humans; Wallerian Degeneration; NAD; Peripheral Nervous System Diseases; Axons; Neurodegenerative Diseases
PubMed: 37503611
DOI: 10.1089/ars.2023.0350 -
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 -
Bioscience of Microbiota, Food and... 2023Pellagra is caused by abnormal intake and/or use of nicotinic acid and is known in part to be induced by the use of medications such as isoniazid or pirfenidone. We...
Pellagra is caused by abnormal intake and/or use of nicotinic acid and is known in part to be induced by the use of medications such as isoniazid or pirfenidone. We previously investigated atypical phenotypes of pellagra, such as nausea, using a mouse model of pellagra and found that gut microbiota play an important role in the development of these phenotypes. Here, we investigated the effect of BB536 on pellagra-related nausea caused by pirfenidone in our mouse model. Our pharmacological data indicated that pirfenidone (PFD) causes modulation of the gut microbiota profile, which appeared to play an important role in the development of pellagra-related nausea. A gut microbiota-mediated protective effect of BB536 against nausea caused by PFD was also identified. Finally, the urinary ratio of nicotinamide/N-methylnicotinamide was shown to be a biomarker of pellagra-like adverse effects induced by PFD, and it may contribute to the prevention of these effects in patients with idiopathic pulmonary fibrosis.
PubMed: 37404569
DOI: 10.12938/bmfh.2022-042 -
AACE Clinical Case Reports 2023Micronutrient deficiencies such as pellagra are rarely seen after bariatric surgery and can be challenging to diagnose and manage. Alcohol use can precipitate...
BACKGROUND/OBJECTIVE
Micronutrient deficiencies such as pellagra are rarely seen after bariatric surgery and can be challenging to diagnose and manage. Alcohol use can precipitate nutritional deficiencies.
CASE REPORT
A 51-year-old woman with a history of Roux-en-Y gastric bypass surgery who later developed an alcohol-use disorder after her diagnosis of breast cancer. She experienced a subacute decline in her physical and cognitive function along with a rash after radiation treatment for breast cancer, lower extremity pain and weakness, anemia, and diarrhea with severe hypokalemia. Workup showed undetectable niacin levels. She initially did not respond to an oral niacin replacement, necessitating intramuscular injections. Alcohol cessation and parenteral B complex replacement led to the resolution of her symptoms and biochemical derangements.
DISCUSSION
Bariatric surgery with concomitant alcohol use can precipitate niacin deficiency-induced liver dysfunction. In the correct clinical setting, screening for alcohol use and checking niacin levels may help avoid extensive testing and can help make the correct diagnosis. Parenteral replacement may be necessary in this setting.
CONCLUSION
Niacin deficiency needs to be considered in patients with bariatric surgery with a history of alcoholism in the correct clinical setting.
PubMed: 37251973
DOI: 10.1016/j.aace.2023.04.002