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Homocystinuria
Published in Charles Theisler, Adjuvant Medical Care, 2023
Cysteine: Vitamin B6 nonresponders may benefit from supplementation with cysteine.7 Treatment for B6 nonresponders is multifaceted, also including supplementation with pyridoxine (vitamin B6), vitamin B12, folate, and betaine.5,6
Asthma and COPD
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Balamugesh Thangakunam, Devasahayam J Christopher
Cysteinyl leukotriene antagonists have a well-established role in the management of asthma, which is uncontrolled on inhaled corticosteroids. Its role in management of COPD is less well defined, although there is some evidence to support its use (Rubinstein et al. 2004). Theophyllines are recommended in both conditions, when the symptoms are not controlled with inhaled medications. The Center for Disease Control and Prevention has recommended seasonal influenza vaccination and pneumococcal vaccination in both COPD and asthma (COPDGold 2019, Magnussen et al. 1998, CDC 2012).
Hereditary and Metabolic Diseases of the Central Nervous System in Adults
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Amino acid analysis: Elevated plasma and urine homocysteine and methionine levels.Decreased levels of cysteine.
Expression of urinary exosomal miRNA-615-3p and miRNA-3147 in diabetic kidney disease and their association with inflammation and fibrosis
Published in Renal Failure, 2023
Jiaxin Wang, Yiying Tao, Fan Zhao, Tong Liu, Xiahong Shen, Ling Zhou
As a traditional inflammatory indicator, Cystatin C not only reflects the degree of renal damage but is also one of the important indicators of the micro-inflammatory state in DKD patients [46]. Cystatin C is a low molecular weight protein (13KD) produced by all nucleated human cells and is primarily catabolized by proximal tubular cells [47]. As an endogenous inhibitor of cysteine protein, it is not affected by age, gender, muscle mass, or protein intake [48]. However, studies [46] have shown that serum Cystatin C is positively correlated with the micro-inflammatory state of DKD and related inflammatory factors. Cystatin C is not only correlated with eGFR and other indicators of renal function damage but also in evaluating the degree and progression of inflammatory response in the course of DKD. The present study provided evidence that the expression level of urinary exosomal miRNA-615-3p correlated with serum Cystatin C, so urinary exosomal miRNA-615-3p might be useful as a marker of the inflammatory response and the progression of kidney damage in DKD.
A review of alternative intravenous acetylcysteine regimens for acetaminophen overdose
Published in Expert Review of Clinical Pharmacology, 2021
Kevin Burnham, Tianrui Yang, Haleigh Smith, Steven Knight
Patients who have overdosed on acetaminophen are at risk of developing severe hepatotoxicity, acute liver failure, and may potentially require liver transplantation [6]. Hepatic injury is related to N-acetyl-para-benzoquinone imine (NAPQI), a toxic intermediate of acetaminophen metabolism. NAPQI is usually neutralized by glutathione conjugation, but hepatic stores of glutathione may become depleted [7]. In the case of acetaminophen poisoning, NAC may serve several hepatoprotective roles. One of these roles is the provision of cysteine for glutathione production [8]. Acetylcysteine is the most effective at preventing hepatotoxicity when given within 8–10 hours of acute acetaminophen ingestions [9,10]. Historically, intravenous NAC has been administered as a standard three-bag regimen over 20.25–21 hours. This standard approach is complex, prone to error, and has also been associated with high rates of cutaneous and systemic anaphylactoid reactions [11–13]. Alternatively, novel intravenous regimens have been produced in an attempt to solve some of these shortcomings.
The development and hepatotoxicity of acetaminophen: reviewing over a century of progress
Published in Drug Metabolism Reviews, 2020
Mitchell R. McGill, Jack A. Hinson
Finally, the fourth manuscript reported the importance of glutathione (GSH) in preventing the APAP-induced hepatotoxicity (Mitchell et al. 1973). A dose of 375 mg/kg of APAP produced approximately a 50% incidence of hepatotoxicity. Pretreatment with the nontoxic compound diethylmaleate to deplete hepatic GSH increased the incidence to 100%. Pretreatment with cysteine decreased the incidence of hepatotoxicity in a dose dependent manner. Hepatic GSH was depleted following a toxic dose of APAP in a time and dose dependent manner. By two hours following a very hepatotoxic dose of APAP (400 mg/kg), total hepatic GSH was depleted by more than 80%. Pretreatments that altered drug metabolism and toxicity (increased or decreased) similarly altered hepatic GSH depletion. Importantly, GSH depletion preceded covalent binding and, as discussed above, covalent binding preceded the development of hepatotoxicity (Jollow et al. 1973). These data indicated that GSH is important to prevent covalent binding and development of hepatotoxicity.