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Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, [7] basal ganglia ...
Major causes of hypomagnesemia are from gastrointestinal losses such as vomiting and diarrhea. Another major cause is from kidney losses from diuretics, alcohol use, hypercalcemia, and genetic disorders. Low dietary intake can also contribute to magnesium deficiency. [citation needed]
Normal magnesium levels are between 0.6 and 1.1 mmol/L (1.46–2.68 mg/dL) with levels less than 0.6 mmol/L (1.46 mg/dL) defining hypomagnesemia. [21] Specific electrocardiogram (ECG) changes may be seen. [21] Causes include low dietary intake, alcoholism, diarrhea, increased urinary loss, poor absorption from the intestines, and diabetes mellitus.
[8] [9] Acute deficiency (see hypomagnesemia) is rare, and is more common as a drug side-effect (such as chronic alcohol or diuretic use) than from low food intake per se, but it can occur in people fed intravenously for extended periods of time. [citation needed] The most common symptom of excess oral magnesium intake is diarrhea.
Levels of serum glucose may rise, and B 1 vitamin may fall. Abnormal heart rhythms are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure. [citation needed]
Bartter syndrome (BS) is a rare inherited disease characterised by a defect in the thick ascending limb of the loop of Henle, which results in low potassium levels (hypokalemia), [2] increased blood pH (), and normal to low blood pressure.
Gitelman syndrome; Other names: Primary renal tubular hypokalemic hypomagnesemia with hypocalciuria: A model of transport mechanisms in the distal convoluted tubule.Sodium chloride (NaCl) enters the cell via the apical thiazide-sensitive NCC and leaves the cell through the basolateral Cl − channel (ClC-Kb), and the Na + /K +-ATPase.
For infants who are infected by their mothers before birth, two potential adverse scenarios exist: Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice).