Normal Magnesium Concentrations Research Articles

Hypomagnesemia Is Associated with the Skull CT Black Hole Sign in Patients with Spontaneous Intracerebral Hemorrhage

ObjectivesThe evaluation of hypomagnesemia's significance in predicting the presence of the black hole sign in patients with intracranial hemorrhage (ICH) is currently under investigation. MethodsThe study included 261 patients with cerebral hemorrhage who underwent initial skull computed tomography (CT) within 24 hours of admission.Sixty-nine patients (26.4%) exhibited hypomagnesemia in the initial laboratory examinations. The black hole sign was observed in 123 patients (referred to as the black hole sign group, which includes patients with and without hypomagnesemia), while the remaining 138 patients (non-black hole sign group) did not exhibit this feature. The values of hypomagnesemia were assessed through multivariable logistic regression analyses. ResultsThe black hole sign occurred in 45 of the 69 (65.2%) patients with hypomagnesemia, and in 78 of the 192 (40.6%) patients without hypomagnesemia.In the black hole sign group, hypomagnesemia was observed in 45 patients (36.6%). However, only 24 patients (19.5%) from the normal magnesium concentration group exhibited hypomagnesemia.The sensitivity, specificity, and positive and negative predictive values of hypomagnesemia for predicting the black hole sign were 69.9%, 82.5%, 36.6%, and 82.8% respectively.The odds ratios for hypomagnesemia, smoking history, and hypokalemia in predicting the presence of the black hole sign were 2.74, 1.971, and 1.629 correspondingly. ConclusionsThe presence of hypomagnesemia may serve as a predictive factor for the black hole sign and rebleeding in patients with intracerebral hemorrhage (ICH), thereby providing valuable guidance for clinical treatment.

Do we need to measure vitamin B12 and magnesium in morbidly obese patients with type 2 diabetes mellitus?

ObjectiveWe aimed to investigate the prevalence of B12 deficiency in metformin-treated, morbidly obese, type 2 diabetes mellitus (T2DM) patients, compared to morbidly obese controls, as well as to evaluate the magnesium status.DesignRetrospective cross-sectional analysis of plasma vitamin B12, plasma magnesium, glucometabolic status and clinical measurements in all consecutive morbidly obese patients was conducted during 1 year.SettingOutpatient Clinic of Obesity Care.SubjectsOne hundred forty-seven patients were evaluated: 107 morbidly obese controls and 40 metformin-treated, morbidly obese patients with T2DM.Main outcome measuresCirculating plasma concentrations of vitamin B12 (cobalamin), magnesium, clinical measurements and metformin medication.ResultsThere were differences between the two groups regarding age, sagittal diameter, glucose parameters and magnesium concentrations. Longer diabetes duration was associated with lower magnesium. Metformin-treated T2DM patients had lower magnesium (0.76±0.07 mmol/L) than controls (0.82±0.07 mmol/L). A subgroup analysis of 26 non-metformin-treated T2DM patients showed a normal magnesium concentration compared to controls, that is, 0.81±0.06 mmol/L. We found no statistical difference in B12 concentrations between the two groups.ConclusionTo fully benefit from metformin medication, routine testing of B12 as well as magnesium in metformin-treated, morbidly obese patients should be performed, with consideration of substitution to avoid low levels.

Effect of magnesium on vascular reactivity in NOS inhibition-induced hypertension

This study investigated the effect of magnesium on the vascular reactivity of conduit and resistance arteries in a nitric oxide synthase inhibition-induced hypertension model. The aorta and third-order branches of the mesenteric artery were dissected from normotensive control and hypertensive rats, and their constriction and dilation responses in physiological saline solution containing normal (1.2 mM) or high (4.8 mM) magnesium concentrations were examined. The responses of the vessels were evaluated using potassium chloride (KCl) and phenylephrine (Phe), acetylcholine (ACh) and sodium nitroprusside. The Phe-induced constriction response of the aortic rings increased, whereas the ACh-induced dilation response decreased, in the hypertensive group compared to controls, in the presence of a normal magnesium concentration. High magnesium did not alter these responses in either group. Both the KCl- and Phe-induced constriction responses of the mesenteric arteries increased, and the ACh-induced dilation response decreased in the hypertensive group compared to controls, in the presence of a normal magnesium concentration. High magnesium significantly decreased the KCl and Phe-induced constriction and increased the ACh-induced dilation response of the mesenteric arteries in the hypertensive group, while it did not alter these responses in controls. This study suggests that high magnesium improves vascular reactivity of resistance-, but not conduit-type arteries in the nitric oxide synthase inhibition-induced hypertension model.

Contemporary view of the clinical relevance of magnesium homeostasis

Magnesium is one of the most abundant cations in the body and is essential for a wide variety of metabolically important reactions. Serum magnesium concentration is regulated by the balance between intestinal absorption and renal excretion. Hypomagnesaemia is relatively common, with an estimated prevalence in the general population ranging from 2.5 to 15%. It may result from inadequate magnesium intake, increased gastrointestinal or renal loss or redistribution from extracellular to intracellular space. Drug-induced hypomagnesaemia, particularly related to proton-pump inhibitor (PPI) therapy, is being increasingly recognized. Although most patients with hypomagnesaemia are asymptomatic, manifestations may include neuromuscular, cardiovascular and metabolic features. Due to the kidney's ability to increase fractional excretion to nearly 100% when the renal magnesium threshold is exceeded, clinically significant hypermagnesaemia is uncommon, generally occurring only in the setting of renal insufficiency and excessive magnesium intake. Symptoms include hypotension, nausea, facial flushing, ileus and flaccid muscle paralysis. In most cases, simply withdrawing exogenous magnesium is sufficient to restore normal magnesium concentrations, although occasionally administration of intravenous calcium or even dialysis may be required.

Analysis of Glutamatergic and Gabaergic Receptor Dynamics in Coupled Oscillator Neural Model

The hippocampus plays a crucial role in information storage and is associated with long-term episodic and semantic memories. It is frequently used as a test bed for the development and evaluation of neural prosthetic devices for cognitive function restoration. Here, a modification of the mapped clock oscillator (MCO) model representation of the hippocampal CA3 region was developed. We addressed several limitations with the experimental design of the existing MCO model. It was modified to include kinetics of N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and γ-aminobutyric acid (GABAA) receptors, capable of generating activity in close agreement with experimental results. The model response showed that lower than normal magnesium concentrations will increase the network excitability in the absence of AMPA and GABAA receptors. In a network of reciprocally connected MCOs, effective synaptic excitation will increase the excitability of the network, while effective synaptic inhibition would push the network towards less excitable states. The new glutamatergic and GABAergic receptor pathways were also designed to be adaptive, making them more suitable for the future integration with a hippocampal system for cognitive neural prosthesis.

Serum and Cerebrospinal Fluid Magnesium in Severe Traumatic Brain Injury Outcome

Serum magnesium concentration has a neuroprotective effect in experimental models of traumatic brain injury (TBI). This study was designed to assess the relationship between initial serum magnesium, cerebrospinal fluid (CSF) magnesium, neurological outcome and the efficacy of magnesium replacement therapy (MgSO4). A retrospective analysis was performed on a prospectively collected dataset from 216 patients admitted during 1996-2006 to the University of Pittsburgh Medical Center with severe TBI. Admission serum and CSF magnesium were dichotomized into low and normal magnesium concentration groups for serum and normal and high concentration groups for CSF. A logistic-regression analysis was performed with 6-month Glasgow Outcome Scale (GOS) scores as outcome variable. The outcome of a subset of 31 patients who presented with low serum magnesium and who were rapidly corrected within 24 h of admission was also analyzed. Low initial serum magnesium was measured in 56.67% of all patients. Patients with an initial serum magnesium of <1.3 mEq/L were 2.37 times more likely to have a poor outcome (CI: 1.18-4.78, p = 0.016). The prognostic significance of depressed serum magnesium remained, even in patients whose serum magnesium levels were corrected within 24 h (OR = 11.03, CI: 1.87-68.14, p = 0.008). Patients with an initial high CSF magnesium were 7.63 more likely to have a poor outcome (p = 0.05). Elevated CSF magnesium correlated with depressed serum magnesium only in patients with poor outcome (p = 0.013). Patients with low serum magnesium and high CSF magnesium are most likely to have poor outcome after severe TBI. Rapid correction of serum magnesium levels does not reverse the prognostic value of these markers.

Magnesium deficiency induces joint cartilage lesions in juvenile rats which are identical to quinolone-induced arthropathy

Quinolones accumulate in cartilage, and because they form chelate complexes with divalent cations, they possess the potential to induce a deficiency of functionally available magnesium. To test the hypothesis that quinolone-induced arthropathy is caused (or aggravated) by magnesium deficiency in cartilage, we induced magnesium deficiency by feeding juvenile rats a magnesium-deficient diet for 9 days and treated the rats with single oral doses of ofloxacin (0, 100, 300, 600, or 1,200 mg/kg of body weight) during this period. Additional groups of juvenile rats on a normal diet were treated with ofloxacin correspondingly. Typical cartilage lesions (e.g., swollen matrix, cleft formation) were found in knee joints of all magnesium-deficient rats, including those without ofloxacin treatment. Lesions in these groups were not distinguishable from lesions induced by a single dose of 600 mg of ofloxacin per kg of body weight or higher in rats on a normal diet. Ofloxacin levels in plasma after 600 mg/kg of body weight were approximately 10-fold higher than those in humans during therapy with this quinolone. Lesions in rats treated with ofloxacin plus magnesium deficiency were more pronounced than those in rats with normal magnesium concentrations. After intake of a magnesium-deficient diet for 9 days, the magnesium concentration in serum (mean +/- standard deviation) was 0.18 +/- 0.05 mmol/liter (control on normal diet, 0.82 +/- 0.10 mmol/liter). Magnesium concentrations in bone (femur) and cartilage (processus xiphoideus) samples were 64.7 +/- 10.5 and 14.3 +/- 3.9 mmol/kg of dry weight, respectively, which corresponded to approximately 50% of the concentrations measured in controls on a normal diet. It was concluded that quinolone-induced arthropathy is probably caused by a deficit of available magnesium in joint cartilage due to the formation of quinolone-magnesium chelate complexes. If juvenile patients must be treated with quinolones for serious infections, it seems prudent to ensure that these patients do not have a disturbed magnesium balance.

Prognostic importance of the serum magnesium concentration in patients with congestive heart failure

Magnesium abnormalities are common in patients with congestive heart failure but the clinical and prognostic significance of an abnormal serum magnesium concentration in this disorder has not been investigated. Therefore, the relation between serum magnesium concentration and the clinical characteristics and long-term outcome of 199 patients with chronic heart failure was evaluated. The serum magnesium concentration was less than 1.6 mEq/liter in 38 patients (19%), within the normal range in 134 patients (67%) and greater than 2.1 mEq/liter in 27 patients (14%). Patients with hypomagnesemia had more frequent ventricular premature complexes and episodes of ventricular tachycardia than did patients with a normal serum magnesium concentration (p less than 0.05). Even though the two groups were similar with respect to severity of heart failure and neurohormonal variables, patients with a low serum magnesium concentration had a significantly worse prognosis during long-term follow-up (45% versus 71% 1 year survival, p less than 0.05). Patients with hypermagnesemia had more severe symptoms, greater neurohormonal activation and worse renal function than did patients with a normal serum magnesium concentration but tended to have fewer ventricular arrhythmias. Hypermagnesemic patients had a worse prognosis than did those with a normal magnesium concentration (37% versus 71% 1 year survival, p less than 0.05). In conclusion, the measurement of serum magnesium concentration provides important clinical and prognostic information in patients with chronic heart failure.

Responses to the lowering of magnesium and calcium concentrations in the cerebrospinal fluid of unanesthetized sheep.

A technique for ventriculolumbar perfusion of the cerebrospinal fluid space has been used to study the neuromuscular effects of low concentrations of magnesium and calcium in the cerebrospinal fluid of conscious sheep. Perfusion with synthetic cerebrospinal fluid solutions containing less than 0-6 mg magnesium/100 ml produced episodes of tetany which were abolished by perfusion with a solution of normal magnesium concentration. This suggests that the low cerebrospinal fluid magnesium concentrations reported in cases of hypomagneseamic tetany may result in changes within the central nervous system that could produce the nervous signs. Perfusates with a calcium concentration below 2-0 mg/100 ml caused hyperpnoea and continuous muscle tremors. Magnesium (0-6 mg/100 ml) and calcium (2-0 mg/100 ml) perfused simultaneously acted synergistically to produce signs characteristic of low levels of each of the ions.