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ORIGINAL ARTICLE
Year : 2021  |  Volume : 34  |  Issue : 1  |  Page : 148-153

Assessment of serum magnesium level in patients with liver cirrhosis


1 Department of Tropical Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Tropical Medicine, Damanhur Fever Hospital, Damanhour, Egypt

Date of Submission16-Aug-2019
Date of Decision23-Sep-2019
Date of Acceptance29-Sep-2019
Date of Web Publication27-Mar-2021

Correspondence Address:
Ayman A Elgamal
Damnhour, Behira
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_233_19

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  Abstract 


Objective
The aim was to assess serum magnesium level in patients with liver cirrhosis.
Background
Cirrhosis is a chronic disease of the liver in which diffuse destruction and regeneration of hepatic parenchymal cells and diffuse increase in connective tissue result in disorganization of the lobular architecture. Micronutrients play a significant role in liver diseases.
Patients and methods
A case–control study was conducted on 60 patients with liver cirrhosis who were classified into the following groups. Group I included 60 patients with liver cirrhosis. They were classified according to the Child-Pugh class into: group Ia which included 20 Child-Pugh A cirrhotic patients; group Ib included 20 Child-Pugh B cirrhotic patients; and group Ic included 20 Child-Pugh C cirrhotic patients. Group II included 20 healthy participants as a control group. Patients and controls were selected from the inpatient and outpatient clinic of the Hepatology Department Damanhur Fever Hospital and Tropical Department of Menoufia University. Routine investigations, magnesium, potassium, and sodium levels were investigated.
Results
Sodium, potassium, and magnesium levels were decreased than the normal range among cirrhotic patients and the lowest mean value was 122.950 ± 2.502, 4.165 ± 0.503, and 1.277 ± 0.202, respectively, among cirrhotic patients (Child class C).
Conclusion
Trace element abnormalities may reflect the condition of liver dysfunction. Liver dysfunction may alter the metabolism of trace elements. Does correction of these metabolic abnormalities of trace elements delay or prevent complication of cirrhosis should be evaluated in upcoming studies.

Keywords: liver cirrhosis, magnesium, micronutrients, potassium, sodium


How to cite this article:
Ali AA, Elgamal AA, Enab AM. Assessment of serum magnesium level in patients with liver cirrhosis. Menoufia Med J 2021;34:148-53

How to cite this URL:
Ali AA, Elgamal AA, Enab AM. Assessment of serum magnesium level in patients with liver cirrhosis. Menoufia Med J [serial online] 2021 [cited 2021 Oct 23];34:148-53. Available from: http://www.mmj.eg.net/text.asp?2021/34/1/148/312023




  Introduction Top


Cirrhosis of the liver is a growing health problem and death from this condition is increasing rapidly among both men and women. Cirrhosis is a chronic disease of the liver in which diffuse destruction and regeneration of hepatic parenchymal cells and diffuse increase in connective tissue result in disorganization of the lobular architecture. Micronutrients play a significant role in liver diseases. In hepatic cirrhosis, the presence of any one or more of jaundice, ascites, portal hypertensive gastrointestinal bleeding, and/or encephalopathy is considered as decompensation. Decompensation is a significant risk for mortality. One-year mortality in compensated cirrhosis is 1–3.4% but in decompensation it is elevated to 20–57% [1]. The role of trace elements in the pathogenesis of liver cirrhosis and its sequelae is still not clearly understood. The evaluation of functions that trace elements play in health and disease becomes more difficult when it is recognized that there were not only nutritional but also metabolic interactions among different trace elements. Several authors have pointed out that levels of a few trace elements like iron and magnesium are altered in diseases like cirrhosis of the liver, but the alteration is not uniform and not always they are. Similarly, copper and zinc are essential trace elements for several metabolic processes and overload, or deficiencies of these elements have been found to lead to metabolic disorders and some other diseases. Decompensation followed by death is the most serious outcome in patients suffering from cirrhosis of the liver. Alteration of trace elements may play a vital role in the process of decompensation [2]. Low serum magnesium level was found which is common in chronic liver disease. It has been demonstrated that alcohol impairs magnesium transport and homeostasis in the brain, skeletal muscle, heart, and the liver [3]. Magnesium deficiency is also associated with peripheral insulin resistance which is common in alcoholic liver disease [4]. In a randomized clinical trial magnesium treatment was reported to improve hepatic enzyme levels [5]. Low magnesium is typically due to decreased absorption of magnesium in the gut or increased excretion of magnesium in the urine. Low magnesium levels in otherwise healthy people are uncommon. This is because magnesium levels are largely controlled by the kidneys. The kidneys increase or decrease excretion (waste) of magnesium based on what the body needs. Continually low dietary intake of magnesium, excessive loss of magnesium, or the presence of other chronic conditions can lead to hypomagnesemia. Hypomagnesemia is also more common in people who are hospitalized. This may be due to their illness, having certain surgeries, or taking certain types of medication. Very low magnesium levels have been linked to poorer outcomes for severely ill, hospitalized patients. Conditions that increase the risk of magnesium deficiency include gastrointestinal diseases, advanced age, type 2 diabetes, use of loop diuretics (such as Lasix), treatment with certain chemotherapies, and alcohol dependence [6]. This study aims to assess the serum magnesium level in patients with liver cirrhosis.


  Patients and methods Top


A case–control study was conducted on 60 patients with liver cirrhosis and 20 healthy participants without evidence of any liver disease as controls. Patients and controls were selected from the inpatient and outpatient clinics of Hepatology Department Damanhur Fever Hospital and Tropical Department of Menoufia University. Patients and controls were classified into group I: included 60 patients with liver cirrhosis. They were classified according the Child-Pugh class into group Ia: included 20 Child-Pugh A cirrhotic patients; group Ib: included 20 Child-Pugh B cirrhotic patients; group Ic: included 20 Child-Pugh C cirrhotic patients. Group II included 20 healthy participants as a control group. Informed consents were obtained from all patients included in the study which is approved by the Local Ethics Committee of Tropical Medicine Department of Faculty of Medicine, Menoufia University. Inclusion criteria included patients with liver cirrhosis due to any cause. Patients and controls were subjected to careful medical history, full clinical examination. laboratory investigations such as: complete blood picture included Hb or Hgb hemoglobin and platelets. Liver function tests included aspartate transferase, alanine transferase, serum albumin, prothrombin time, total and direct bilirubin. Kidney function tests included blood urea, nitrogen, and serum creatinine. Serum electrolytes included Na, K, and Mg. Serological tests for viral markers included HBsAg, HCVAb by enzyme-linked immunosorbent assay (ELISA). Radiological evaluation in the form of pelvi-abdominal US (Diagnostic Ultrasound Systems of Toshiba Medical Systems Corporation “Canon, Tokyo, Japan;) to show the features of liver cirrhosis.

Statistical analysis

The results were tabulated and statistically analyzed by using a personal computer using Microsoft Excel 2016 and SPSS v. 21 (SPSS Inc., Chicago, Illinois, USA). Statistical analysis was done using descriptive, for example, percentage (%), mean and SD. Analytical that includes χ2, t-tests, analysis of variance, F–test, and receiver-operating characteristic curve. A value of P less than 0.05 was considered statistically significant.


  Results Top


In this study, there was no statistically significant differences between cirrhotic patients regarding age (P = 0.394), sex (P = 0.6056) and causes of cirrhosis (P = 0.837). On the other hand, highly statistically significant differences were recorded among cirrhotic patients regarding physical examination. Shrunken liver was the most common finding by palpation of the liver (P = 0.001) and enlarged was the most palpation finding by the spleen. Regarding, percussion ascites was presented only among cirrhotic patients' class C and statistically there was a significant difference (P = 0.001) [Table 1].
Table 1: Distribution of studied groups regarding age, sex, causes, and physical examination of cirrhotic patients

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In this study, there was no statistically significant differences between cirrhotic patients regarding pulse rate (P = 0.326) and total leukocyte count (P = 0.294). On the other hand, highly statistically significant differences were recorded among cirrhotic patients regarding respiratory rate hemoglobin, platelet, liver enzymes (alanine transaminase, aspartate transaminase, albumin, bilirubin) and renal function (urea and creatinine) [Table 2].
Table 2: Comparison between the studied groups regarding pulse, respiration rate, complete blood picture, liver enzymes, and kidney function test

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In this study there was a significant difference between the studied groups regarding sodium, potassium, and magnesium. The level of sodium, potassium, and magnesium were decreased than normal range among cirrhotic patients and the lowest mean value was 122.950 ± 2.502, 4.165 ± 0.503, and 1.277 ± 0.202, respectively, among cirrhotic patients (Child class C) [Table 3].
Table 3: Comparison between the studied groups regarding sodium, potassium, and magnesium levels

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Also, the area under the curve between cases and controls to predict the common macronutrients decreased among cirrhotic patients which has revealed that the element sodium has the highest area under the curve of 0.987, which shows that there is excellent element decrease among cirrhotic patients followed by element Mg with the second highest area under the curve of 0.806, which shows a very good element decrease among cirrhotic patients. On the other hand, the element potassium had the third highest area under the curve of 0.525 which shows poor element decrease among cirrhotic patients [Table 4] and [Figure 1].
Table 4: Area under the curve between cases and controls to predict the common macronutrients decreased among cirrhotic patients

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Figure 1: Receiver operating characteristic curve between cases and control to predict the common macronutrients decreased among cirrhotic patients.

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  Discussion Top


Micronutrients such as sodium, magnesium, and potassium have played a significant role in liver diseases, and in relation to sodium element there was a decrease among cirrhotic patients due to portal hypertension and this leads to systemic vasodilation which in turn activates sodium-retaining and water-retaining systems such as the renin-angiotensin-aldosterone system and arginine vasopressin. Arginine vasopressin increases solute-free water retention by acting on the V2 receptors of the kidney-collecting tubes. Hyponatremia in cirrhosis is defined as a serum sodium level of less than 130 meq/l [7]. So, in present work it was revealed that sodium was decreased than the normal range among cirrhotic patients and the lowest mean value was 122.950 ± 2.502 among cirrhotic patients (Child class C). In agreement with the present study Robert and Gianotti [8] found that hyponatremia is a common complication of advanced cirrhosis related to impairment in the renal capacity for eliminating solute-free water causing retention of water that was disproportionate to the retention of sodium, thus leading to a reduction in serum sodium concentration and hyposmolality. Also, it was reported that hyponatremia in cirrhosis is associated with increased morbidity and mortality [8]. Similar to the present study Bernardi et al. [9] studied hyponatremia in patients with cirrhosis of the liver and revealed that hyponatremia is common in cirrhosis. It mostly occurs in an advanced stage of the disease and was associated with complications and increased mortality. Either hypovolemic or, more commonly, hypervolemic hyponatremia can be seen in cirrhosis. Impaired renal sodium handling due to renal hypoperfusion and increased arginine–vasopressin secretion secondary to reduced effective volemia due to peripheral arterial vasodilation represent the main mechanisms leading to dilutional hyponatremia in this setting. Patients with cirrhosis usually develop slowly progressing hyponatremia. In different clinical contexts, it is associated with neurological manifestations due to increased brain water content, where the intensity is often magnified by concomitant hyperammonemia leading to hepatic encephalopathy [9]. In relation to magnesium element in this study it was reported that the magnesium was decreased than the normal range among cirrhotic patients and the lowest mean value was 1.277 ± 0.202 among cirrhotic patients (Child class C). In the same direction Bémeur and Butterworth [10] reported that the low serum magnesium level was common in chronic liver disease and liver cirrhosis, so magnesium treatment was reported to improve hepatic enzyme levels [10] Also, Ahad et al. [4] found that the low serum magnesium level was due to decreased nutritional intake of the metal and increased excretion of magnesium due to decreased plasma level of albumin, administration of magnesiuric diuretics (furosemide), poor absorption of magnesium in the distal jejunum, and indirect effect of alcohol on renal tubules [4]. In agreement to the present study, Saxena et al. [11] studied serum zinc and magnesium levels in patients of liver cirrhosis and found that serum magnesium level was significantly (P < 0.001) decreased in liver cirrhosis patients where its mean was 46.38 ± 8.59 mg/dl at a range of 30.08–57.13 mg/dl [11]. In contrast to the present study Amit et al. [12] studied the correlation of trace elements in patients of chronic liver disease with respect to Child–Turcotte–Pugh scoring system and found that the serum levels of magnesium were significantly higher in patients with Child-Turcotte-Pugh (CTP) C class (5.22 ± 7.32) in comparison to patients with CTP A and B class (1.57 ± 1.99 and 2.09 ± 1.19, respectively) and also reported that magnesium showed significant positive correlation with CTP score (r = 0.271; P = 0.019). The concentrations of magnesium did not differ significantly between CTP class with the mean level difference being not statistically significant [12]. Higher serum levels of magnesium were found in the Krieger et al. [13] study as well as in the study by Layrargues et al. [14]. After all, it seems that serum levels of magnesium are higher in patients with CLD than in healthy people. Magnesium is a secreted in the bile so the concentration of magnesium increases in cholestatic liver disease, which could be one of the possible explanations why magnesium accumulation is common in CLD. Rahelic et al. [15] also concluded the same findings in his study. It seems that magnesium concentrations are higher in patients with severe liver disease possibly due to the advanced intrahepatic and portosystemic shunting [15]. As regards potassium in the present study it was found that potassium was decreased than the normal range among cirrhotic patients and the lowest mean value was 4.165 ± 0.503 among cirrhotic patients (Child C). Similar to the present study Kristina et al. [16] found low potassium linked with liver disease patients with nonalcoholic fatty liver disease also had low potassium levels. Researchers in China found that patients with nonalcoholic fatty liver disease also had low potassium levels and patients with nonalcoholic fatty liver disease had significantly lower serum potassium levels than those who did not have the liver condition (4.09 vs 4.14 mmol/l, P < 0.0001) [16].


  Conclusion Top


Trace element abnormalities may reflect the condition of liver dysfunction. Liver dysfunction may alter the metabolism of trace elements. Does correction of these metabolic abnormalities of trace elements delay or prevent complication of cirrhosis should be investigated.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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2.
Kaushik K, Anindya M, Vijaya B, Sudhakar K. Alteration of micronutrient status in compensated and decompensated liver cirrhosis. Indian J Clin Biochem 2014; 29:232–237.  Back to cited text no. 2
    
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Ahad E, Saman N, Bita G, Seyed A. Serum magnesium concentration is independently associated with non-alcoholic fatty liver and non-alcoholic steatohepatitis. United European Gastroenterol J 2018; 6:97–103.  Back to cited text no. 4
    
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Zohreh A, Ghazaleh E, Mousa S, Sareh K. A randomized controlled trial of the effects of an almond-enriched, hypocaloric diet on liver function tests in overweight/obese women. Iran Red Crescent Med J 2016; 18:23628.  Back to cited text no. 5
    
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Robert J, Gianotti A. Hyponatraemia and cirrhosis. Gastroenterology 2014; 2:1–6.  Back to cited text no. 8
    
9.
Bernardi M, Ricci CS, Santi L. Hyponatremia in patients with cirrhosis of the liver. J Clin Med 2015; 4:85–101.  Back to cited text no. 9
    
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Bémeur C, Butterworth RF. Nutrition in the management of cirrhosis and its neurological complications. J Clin Exp Hepatol 2014; 4:141–150.  Back to cited text no. 10
    
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Saxena T, Agarwal BK, Makwane HS, Kare P. Study of serum zinc and magnesium levels in patients of liver cirrhosis. Biomed Pharmacol J 2012; 5:327–331.  Back to cited text no. 11
    
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Amit A, Lario M, Alvarez-Mon M. Cirrhosis-associated immune dysfunction: distinctive features and clinical relevance. J Hepatol 2017; 61:1385–1396.  Back to cited text no. 12
    
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Krieger D, Krieger S, Jansen O, Gass P, Theilmann L, Lichtnecker H. Magnissium and chronic hepatic encephalopathy. Lancet 2015; 346:270–274.  Back to cited text no. 13
    
14.
Layrargues GP, Rose C, Spahr L, Zayed J, Normandin L, Butterworth RF. Role of magnissium in the pathogenesis of portal-systemic encephalopathy. Metab Brain Dis 2018; 13:311–317.  Back to cited text no. 14
    
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Rahelic D, Kujundzić M, Romić Z, Brkić K, Petrovecki M. Serum concentration of zinc, copper, magnissium, magnesium in patients with liver cirrhosis. Coll Antropol 2016; 30:523–528.  Back to cited text no. 15
    
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Kristina D, Krieger S, Jansen O, Gass P, Theilmann L, Lichtnecker H. Magnissium and chronic hepatic encephalopathy. Lancet 2013; 346:270–274.  Back to cited text no. 16
    


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  [Table 1], [Table 2], [Table 3], [Table 4]



 

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