hypomagnesemia

Hypomagnesemia is present in many but not all cases.

Prolonged use can cause significant hypomagnesemia in some patients.

Hypomagnesemia is identified by a loss of balance due to muscle weakness.

Hypomagnesemia can be present without magnesium deficiency and vice versa.

A number of genetically attributable hypomagnesemia disorders have also been identified in humans.

Hypomagnesemia in type II diabetes: effect of a 3-month replacement therapy.

Note, however, that hypomagnesemia is usually indicative of a systemic magnesium deficit.

Thus hypomagnesemia results in an increased intracellular calcium level.

Severe hypomagnesemia during long-term treatment with a proton pump inhibitor.

Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia.

Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects.

Hypomagnesemia in chronic obstructive lung disease: effect of therapy.

Approximately 50% of patients may experience long-lasting hypomagnesemia.

Mutations in this gene are associated with renal hypomagnesemia.

For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia.

It is used in severe hypomagnesemia and eclampsia.

Hypomagnesemia after small bowel resection: treatment with 1-alpha-hydroxylated vitamin D metabolites.

Less desirable side-effects of its chronic usage include hypokalemia and hypomagnesemia.

Hypomagnesemia therefore also makes spontaneous depolarization more likely.

Loop and thiazide diuretic use (the most common cause of hypomagnesemia)

Toxicity of cardiac glycosides is increased due to hypokalemia and hypomagnesemia.

Some conserved forages are also low in magnesium and may be conducive to hypomagnesemia.

A case series of proton pump inhibitor-induced hypomagnesemia.

Long-term use is associated with hypomagnesemia.

Common causes for torsades de pointes include diarrhea, hypomagnesemia and hypokalemia.