Hypomagnesemia overview

Jump to navigation Jump to search

Hypomagnesemia Microchapters

Home

Patient Information

Overview

Pathophysiology

Causes

Differentiating Hypomagnesemia from other Diseases

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hypomagnesemia overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hypomagnesemia overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hypomagnesemia overview

CDC on Hypomagnesemia overview

Hypomagnesemia overview in the news

Blogs on Hypomagnesemia overview

Directions to Hospitals Treating Hypomagnesemia

Risk calculators and risk factors for Hypomagnesemia overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.

Overview

The prefix hypo- means low (contrast with hyper-, meaning high). The middle magnes refers to magnesium. The end portion of the word, -emia, means 'in the blood' (note, however, that hypomagnesemia is usually indicative of a systemic magnesium deficit). Thus, Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood. Usually a serum level less than 0.7 mmol/l is used as reference. It must be noted that hypomagnesemia is not equal to magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa.

It may result from a number of conditions including inadequate intake of magnesium, chronic diarrhea, malabsorption, alcoholism, chronic stress, diuretic use and other disorders.

Homeostasis

The body contains 21-28 grams of magnesium (1 mmol=2mEq=24.6 mg). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium. Most of the serum magnesium is bound to chelators, (i.e. ATP, ADP, proteins and citrate). Roughly 33% is bound to proteins, and 5-10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7-2.3 mg/dl (0.69-0.94 mmol/l). Of this 60% is free, 33% is bound to proteins, and less than 7% is bound to citrate, bicarbonate and phosphate.

Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll, coca-derivatives, nuts, wheat, seafood, and meat. It is resorbed through the small intestine, and to a lesser degree in the colon. The rectum and sigmoid colon can absorb magnesium. Hypermagnesemia has been reported after enemas containing magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.

The kidneys regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys, of which 5% (120 mg) is excreted through urine. The loop of Henle is the major site for Mg-homeostasis and 60% is resorbed.

Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.

Metabolism

Magnesium is a cofactor in more than 300 enzyme regulated reactions. Most importantly forming and using ATP, i.e. kinase. There is a direct effect on sodium- (Na), potassium- (K) and calcium (Ca)channels. It has several effects:

  • Potassium channels are inhibited by magnesium. Hypomagnesemia results in increased efflux of intracellular Mg. The cell loses potassium which then is excreted by the kidneys, resulting in hypokalemia.
  • Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's calcium inhibitor." Lack of magnesium inhibits the release of parathyroid hormone, which can also result in hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
  • Through relaxation of bronchial smooth muscle it causes bronchodilation.
  • The neurological effects are:
    • reducing electrical excitation
    • blocking release of acetylcholine
    • blocking N-methyl-D-aspartate, an excitatory neurotransmitter of the central nervous system

References