Decreased muscle strength and contents of Mg and Na,K‐pumps in chronic alcoholics occur independently of liver cirrhosis

Aagaard, Niels Kristian; Andersen, Henning; Vilstrup, Hendrik; Clausen, Torben; Jakobsen, Johannes; Dørup, I

doi:10.1046/j.1365-2796.2003.01100.x

Cited by 16 publications

(13 citation statements)

References 34 publications

(49 reference statements)

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“…[19][20][21] Magnesium deficiency occurs because of malabsorption of magnesium in the small intestine and is exacerbated by diuretic use. Magnesium deficiency is associated with reduced cognitive performance as well as reduced muscle strength in adults with cirrhosis [22][23][24] and with increased bone resorption in children with cholestatic liver disease. 25 Impaired Nutrient Uptake Impaired nutrient uptake is multifactorial, resulting from malabsorption, maldigestion, and altered macronutrient metabolism.…”

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confidence: 99%

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

et al. 2021

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This is the first American Association for the Study of Liver Diseases (AASLD) Practice Guidance on the management of malnutrition, frailty, and sarcopenia in patients with cirrhosis. This guidance represents the consensus of a panel of experts after a thorough review and vigorous debate of the literature published to date, incorporating clinical experience and common sense to fill in the gaps when appropriate. Our goal was to offer clinicians pragmatic recommendations that could be implemented immediately in clinical practice to target malnutrition, frailty, and sarcopenia in this population. This AASLD Guidance document differs from AASLD Guidelines, which are supported by systematic reviews of the literature, formal rating of the quality of the evidence and strength of the recommendations, and, if appropriate, meta-analysis of results using the Grading of Recommendations Assessment Development and Evaluation system. In contrast, this Guidance was developed by consensus of an expert panel and provides guidance statements based on formal review and analysis of the literature on the topics, with oversight Accepted ArticleThis article is protected by copyright. All rights reserved provided by the AASLD Practice Guidelines Committee at all stages of Guidance development. The AASLD Practice Guidelines Committee chose to perform a Guidance on this topic because a sufficient number of randomized controlled trials (RCTs) were not available to support the development of a Guideline. Definitions of Malnutrition, Frailty, and Sarcopenia and Their Relationship in Patients With CirrhosisCirrhosis is a major predisposing condition for the development of malnutrition, frailty, and sarcopenia.Multiple, yet complementary, definitions of these conditions exist in the published domain outside of the field of hepatology, but consensus definitions have not yet been established by the AASLD for patients with cirrhosis. Furthermore, there has been ambiguity related to operationalization of these constructs in clinical practice. To address this, we offer definitions of the theoretical constructs of malnutrition, frailty, and sarcopenia as commonly represented in all populations, partnered with operational definitions, developed by consensus, to facilitate pragmatic implementation of these constructs in clinical practice as applied to patients with cirrhosis (Table 1). Malnutrition is a clinical syndrome that results from "an imbalance (deficiency or excess) of nutrients that causes measurable adverse effects on tissue/body form (body shape, size, composition) or function, and/or clinical outcome." 1 Key to this definition is the recognition that malnutrition represents a spectrum of nutritional disorders across the entire range of body mass index (BMI)from underweight to obese. By this definition, malnutrition leads to adverse physical effects, which, in patients with cirrhosis, are commonly manifested phenotypically as frailty or sarcopenia. Frailty has most commonly been defined as a clinical state of decreased physiologic reserve...

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Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

et al. 2021

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“…In a group of 76 patients, who had received diuretics for 1-17 yr, oral administration of Mg 2ϩ for 26 wk restored the contents of K ϩ , Mg 2ϩ , and [ 3 H]ouabain binding sites in the vastus lateralis toward the normal levels (117). Mg 2ϩ and K ϩ deficiency developing in alcoholics is associated with a minor, but significant, downregulation of [ 3 H]ouabain binding sites (8 -14%) in vastus lateralis (1).…”

Section: K ϩ Deficiencymentioning

confidence: 99%

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Clausen

2003

Physiological Reviews

514

673

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In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.

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“…A rising blood alcohol level has been associated with magnesuria and is a factor contributing to Mg deficiency in chronic alcoholism [83]. Magnesium depletion occurs independently of the development of cirrhosis [84]. Even moderate alcohol consumption on a chronic basis has been associated with increased urine Mg excretion [85].…”

Section: Renal Causesmentioning

confidence: 99%

Magnesium Deficiency in Critical Illness

Tong

Rude

2005

J Intensive Care Med

241

176

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Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma. Magnesium regulates hundreds of enzyme systems. By regulating enzymes controlling intracellular calcium, Mg affects smooth muscle vasoconstriction, important to the underlying pathophysiology of several critical illnesses. The principle causes of Mg deficiency are gastrointestinal and renal losses; however, the diagnosis is difficult to make because of the limitations of serum Mg levels, the most common assessment of Mg status. Magnesium tolerance testing and ionized Mg2+ are alternative laboratory assessments; however, each has its own difficulties in the ICU setting. The use of Mg therapy is supported by clinical trials in the treatment of symptomatic hypomagnesemia and preeclampsia and is recommended for torsade de pointes. Magnesium therapy is not supported in the treatment of acute myocardial infarction and is presently undergoing evaluation for the treatment of severe asthma exacerbation, for the prevention of post-coronary bypass grafting dysrhythmias, and as a neuroprotective agent in acute cerebral ischemia.

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Decreased muscle strength and contents of Mg and Na,K‐pumps in chronic alcoholics occur independently of liver cirrhosis

Abstract: Abstract. Aagaard NK,

Cited by 16 publications

References 34 publications

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Magnesium Deficiency in Critical Illness

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Decreased muscle strength and contents of Mg and Na,K‐pumps in chronic alcoholics occur independently of liver cirrhosis

Abstract: Abstract. Aagaard NK,

Cited by 16 publications

References 34 publications

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases

Na+-K+Pump Regulation and Skeletal Muscle Contractility

Magnesium Deficiency in Critical Illness

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Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility