Evaluation of magnesium deficiency
小结
Magnesium deficiency is a state of decreased total body magnesium content. The human body contains 21-28 g of magnesium, the majority of which is localized in bone (>53%) and nonmuscular tissue (approximately 19%). Hypomagnesemia (low serum magnesium concentration) is generally defined as serum magnesium <1.5 mEq/L.[1]
Serum magnesium level is a poor indicator of the total magnesium content and availability in the body, because only 1% of magnesium is found in the extracellular fluid. There is no simple, rapid, and accurate laboratory test to determine total body magnesium status in humans.[2]
Evaluating a combination of serum, urinary, and dietary magnesium may be the most appropriate method to determine total body magnesium status.[3][4] Determination of a single 24-hour urinary magnesium level provides an indirect assessment of whole body magnesium content; it should be interpreted in combination with serum magnesium levels.[3] Multiple determinations of 24-hour urinary magnesium have been used in epidemiologic studies to assess reproducibility, but are not practical for routine measurement of magnesium status.[3][5][6]
Magnesium deficiency is usually detected because of the resultant hypomagnesemia. However, it may also be revealed by the development of clinical symptoms or associated hypokalemia or hypocalcemia.
Calcium competes with magnesium for uptake in the loop of Henle, and an increase in the filtered calcium load can impair magnesium reabsorption. Hypomagnesemia, in turn, leads to parathyroid hormone (PTH) resistance and a decrease in PTH secretion, both of which lead to hypocalcemia.
Hypokalemia is commonly seen in patients with hypomagnesemia, partly because the associated underlying disorders can produce both these disturbances. However, there is also evidence that hypomagnesemia can lead to increased renal potassium wasting.
Patients with abnormalities of magnesium homeostasis typically fall into one of three groups:
Patients with magnesium deficiency (low total body magnesium content) and a resultant hypomagnesemia (low serum magnesium concentration)
Patients with hypomagnesemia (low serum magnesium concentration) in the absence of magnesium deficiency (i.e., a normal total body magnesium content)
Patients with magnesium deficiency (low total body magnesium content) but no evidence of hypomagnesemia (i.e., a normal serum magnesium concentration).
Magnesium homeostasis
About 60% of magnesium in the serum is free, whereas approximately 33% is bound to proteins, and <7% is bound to citrate, bicarbonate, ATP, and phosphate.[7]
Magnesium status is regulated by the intestines, which control absorption; the kidneys, which control excretion; and bone, which is the major storage site. Absorption and excretion are mediated by the selective magnesium channel TRPM6, whereas magnesium uptake and release from tissues outside the intestines and kidneys is controlled by TRPM7, which has an approximately 60% homology to TRPM6.[8][9]
Absorption: magnesium absorption is a saturable process that occurs throughout the small and large intestines, with most of the absorption taking place in the colon. The average daily intake of magnesium is approximately 320 mg in men and 240 mg in women; approximately two-thirds of this amount is eliminated with the feces, while one third is absorbed and passed into the circulation.[10] Magnesium regulates the expression of TRPM6; a sustained fall in magnesium level results in increased expression, and increased magnesium absorption.[11][12]
Excretion and reabsorption: the major site of reabsorption is the loop of Henle, although additional reabsorption takes place in the distal convoluted tubule.[13] Approximately 2400 mg/day of magnesium passes through the kidneys, <5% of which is eventually excreted. Because magnesium regulates the expression of TRPM6, a sustained fall in magnesium level results in increased magnesium reabsorption.[11]
Although there is no direct hormonal control of magnesium absorption, excretion, and reabsorption, TRPM6 expression appears to be under estrogen modulation.
There is normally very little exchange between intracellular and extracellular magnesium. In the acute phase of a fall in magnesium content, intestinal absorption and renal reabsorption both increase. Hormones such as glucagon, catecholamines, and PTH can mobilize magnesium from bone and other tissues.[14] Magnesium, in turn, exhibits negative feedback on catecholamine release. Conversely, hormones such as insulin, antidiuretic hormone (ADH), and thyroid hormone promote magnesium uptake and storage.[14]
Cellular functions of magnesium
Magnesium is a predominantly intracellular ion and is distributed between the nucleus, endoplasmic or sarcoplasmic reticulum, mitochondria, and cytoplasm.[15] Approximately 200 enzymes involved in cellular metabolism and the cell cycle require magnesium as a cofactor, including adenyl cyclase and ATPases. Magnesium is also an important cofactor for potassium and calcium channels, and therefore plays a role in regulating action potentials in cardiac and neural tissues, as well as calcium signaling in a wide range of tissues.[16]
Recommended dietary allowance for magnesium
The recommended dietary allowance for magnesium varies according to age and sex as follows:[1]
[Figure caption and citation for the preceding image starts]: Recommended Dietary Allowances (RDAs) for MagnesiumTable used with permission from the U.S. Department of Health and Human Services, National Institutes of Health. Original source for figures: Institute of Medicine (IOM). Food and Nutrition Board. Dietary reference intakes: calcium, phosphorus, magnesium, vitamin D and fluoride. Washington, DC: National Academy Press, 1997. [Citation ends].
鉴别诊断
常见
- Malnutrition
- Isolated dietary magnesium deficiency
- Drug-induced
- Alcohol misuse
- Laxative abuse
- Crohn disease
- Gastroenteritis
- Ulcerative colitis
- Celiac disease
- Short gut syndrome
- Diabetic ketoacidosis
不常见
- Excess of intravenous fluids
- Acute pancreatitis
- Chronic pancreatitis
- Whipple disease
- Cirrhosis
- Hyperaldosteronism
- Hypoparathyroidism
- Hyperthyroidism
- Hungry bone syndrome
- Recovery phase of acute tubular necrosis
- Renal tubular acidosis
- Postobstructive diuresis
- Primary renal magnesium wasting
- Preeclampsia
- Pregnancy
撰稿人
作者
Andrea Romani, MD
Associate Professor
Department of Physiology and Biophysics
School of Medicine
Case Western Reserve University
Cleveland
OH
利益声明
AR is the author of several studies referenced in this topic.
同行评议者
Rhian Touyz, MD, PhD
Professor
Institute of Cardiovascular and Medical Science
BHF Glasgow Cardiovascular Research Centre
Glasgow
UK
利益声明
Not disclosed.
Paul Dargan, MB, BS, FRCPE, FACMT
Consultant Physician and Clinical Director
Clinical Toxicology Service
Guy's and St Thomas' NHS Foundation Trust
London
UK
利益声明
PD is the author of one case report referenced in this topic.
Peer reviewer acknowledgements
BMJ Best Practice topics are updated on a rolling basis in line with developments in evidence and guidance. The peer reviewers listed here have reviewed the content at least once during the history of the topic.
Disclosures
Peer reviewer affiliations and disclosures pertain to the time of the review.
参考文献
关键文献
Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. 2005 Jan-Feb;20(1):3-17. 摘要
参考文献
A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.
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