Fatal Hypermagnesemia Due to Laxative Use

We report a case of fatal hypermagnesemia in a 53-year-old woman admitted for acute exacerbation of chronic obstructive pulmonary disease and with a history of chronic constipation treated regularly with magnesium-containing laxatives. On admission, her magnesium level was 2.0 mg/dL, which rose to a peak of 10.8 mg/dL despite hydration and diuresis in the presence of a normal kidney function. Continuous renal replacement therapy was promptly initiated, which reduced her serum magnesium levels, but her condition continued to deteriorate precipitously progressing to shock leading to oligoanuric renal failure, and she died 2 days later. A review of the literature shows that though rare and often unsuspected, severe hypermagnesemia frequently results in death even in individuals with normal renal function despite renal replacement therapy. In patients with constipation, retention of magnesium-based laxative in the gut apparently serves as a reservoir for continuous magnesium absorption and contributes to mortality     

Fatal hypermagnesemia induced by preoperative colon preparation in an elderly woman: report of a case

An 85-year-old woman with rectal carcinoma was referred to our hospital for surgical treatment. She had a history of constipation treated with oral magnesium oxide. She received 34 g of magnesium citrate (Magcolol P^®) orally for 2 days as a mechanical bowel preparation prior to the operation. Just before the operation, she suddenly developed nausea, vomiting, and cyanosis and went into cardiac arrest. Despite support by mechanical ventilation, dopamine, dobutamine, and norepinephrine, she exhibited repeated bradycardia that was nearly fatal and required temporary pacing. The following day, her laboratory tests revealed marked hypermagnesemia (14.3 mg/dL). After a hemodialysis session, she recovered dramatically and all vasopressors were withdrawn. We conclude that preoperative mechanical bowel preparation with magnesium-containing cathartics can cause fatal hypermagnesemia in elderly patients even if their renal function is normal.     

Assessment of magnesium status in patients with bronchial asthma.

To elucidate the contribution of magnesium to bronchial hyperreactivity in patients with stable bronchial asthma, magnesium concentrations in serum (S-Mg), erythrocytes (R-Mg), and lymphocytes (L-Mg) were measured in 25 patients with bronchial asthma (BA group) and 9 age-matched healthy subjects (control group). A parenteral magnesium loading test, a continuous low-dose magnesium infusion of 0.2 mEq/kg over 4 hr, was performed in 10 of 25 asthmatic patients and in the control group. R-Mg was significantly lower in the BA group than in the control group (4.96 +/- 0.47, 6.13 +/- 0.62 mEq/L, p < 0.001, respectively), although S-Mg (2.4 +/- 0.1, 2.4 +/- 0.2 mg/dL) and L-Mg (1.28 +/- 0.26, 1.15 +/- 0.13 microg/mg/protein) were not significantly different between the two groups. Magnesium deficiency in total body stores was revealed in 40% of patients (4/10 patients) and 11% of control subjects (1/9 subjects) by parenteral magnesium loading test. The ratio of magnesium retention to urinary excretion through the parenteral magnesium loading test showed a significant inverse correlation with R-Mg (r = -0.78, p < 0.01). Bronchial reactivity to inhaled methacholine had a significant inverse correlation with R-Mg (r = -0.42, p < 0.05). We conclude that 40% of asthmatic patients demonstrated magnesium deficiency, and that the low magnesium concentration in erythrocytes reflects decreased magnesium stores in patients with bronchial asthma.     

Correlation of serum magnesium levels and cardiac digitalis intoxication

A prospective study was undertaken to compare the prevalence of hypomagnesemia and hypermagnesemia in patients with cardiac digitalis toxicity and in digitalized patients without toxicity. During an 8 month period on a general medical service, there were 38 patients with “definite” or “possible” digitalis toxicity, by serial electrocardiographic studies, among 120 digitalized patients whose serum magnesium levels were obtained. Serum magnesium concentrations were measured by atomic absorption spectrometry.Hypomagnesemia was present in 21 percent of patients with and 10 percent of those without digitalis toxicity. Hypomagnesemia was not more prevalent in patients with toxicity but relatively lower serum levels of digoxin or digitoxin. The presence of hypermagnesemia was significantly greater in patients with toxicity (18 percent) than in those without toxicity (5 percent), and appeared to be related to a significantly greater prevalence of abnormal renal function in the former group. The potential value of magnesium administration in hypomagnesemic patients with cardiac digitalis toxicity warrants investigation. Caution should be exercised in the administration of magnesium sulfate to digitalis-toxic, azotemic patients who may already be hypermagnesemic.     

Evaluation of Paraoxonase,Malondialdehyde, and Lipoprotein Levels in Patients with Asymptomatic Cholelithiasis

Background/Aim:

To compare lipoprotein and malondialdehyde levels and paraoxonase-1 activity between subjects with asymptomatic cholelithiasis and controls.

Patients and Methods:

Eighty subjects with asymptomatic cholelithiasis (55 women, 25 men, mean age: 51, SD 14 years) and 40 control subjects without cholelithiasis (25 women, 25 men, mean age: 51, SD 12 years) were enrolled to the study. Serum paraoxonase activity, lipoproteins, and malondialdehyde were measured.

Results:

In the cholelithiasis group, serum total cholesterol, low-density lipoprotein cholesterol, and malondialdehyde were significantly higher and high-density lipoprotein cholesterol (HDL-C) and paraoxonase-1 were significantly lower than the controls. In cholelithiasis patients with serum glucose level > 100 mg/dL, body mass index, serum total cholesterol, triglyceride (TG), and malondialdehyde levels were significantly higher than cholelithiasis patients with serum glucose level < 100 mg/dL. Paraoxonase-1 activity was significantly lower in patients with serum glucose level > 100 mg/dL. In cholelithiasis patients with TG > 150 mg/dL, mean age, body mass index, glucose, total cholesterol, and malondialdehyde were significantly higher than in cholelithiasis patients with TG < 150 mg/dL. In cholelithiasis subgroup with TG > 150 mg/dL, HDL-C level and paraoxonase-1 activity were lower than in the cholelithiasis subgroup with TG < 150 mg/dL. All of the above comparisons were statistically significant (P < 0.05).

Conclusions:

Patients with asymptomatic cholelithiasis have evidence of increased lipid peroxidation and decreased antioxidant capacity. Patients with asymptomatic cholelithiasis with components of the metabolic syndrome have more lipid peroxidation and less antioxidant capacity than patients with asymptomatic cholelithiasis but without the components of the metabolic syndrome.     

Correction of hypomagnesemia by dapagliflozin in patients with type 2 diabetes: A post hoc analysis of 10 randomized,placebo-controlled trials

AimsHypomagnesemia (serum magnesium [Mg] <0.74 mmol/L [<1.8 mg/dL]) is commonly observed in patients with type 2 diabetes (T2D). This study investigated the effect of treatment with dapagliflozin 10 mg on Mg concentrations in patients with T2D.MethodsIn this post hoc analysis, we used pooled data from 10 placebo-controlled studies of dapagliflozin over 24 weeks of treatment in patients with T2D. We evaluated the change in Mg in patients receiving dapagliflozin vs. placebo overall, and in subgroups with baseline hypomagnesemia and normal/hypermagnesemia (≥0.74 mmol/L [≥1.8 mg/dL]). We determined the proportion of patients with baseline hypomagnesemia who achieved Mg ≥0.74 mmol/L (≥1.8 mg/dL).ResultsA total of 4398 patients with T2D were included. The mean change from baseline to week 24 in Mg was significantly larger with dapagliflozin vs. placebo; difference, 0.06 mmol/L (95% confidence interval [CI]: 0.05, 0.06). The proportion of patients with Mg within the population reference range after 24 weeks of treatment was significantly higher with dapagliflozin vs. placebo; difference, 47.8% (95% CI: 41.4, 53.9). The proportion of patients displaying hypermagnesemia did not increase with dapagliflozin treatment.ConclusionsTreatment with dapagliflozin 10 mg resulted in correction of Mg concentrations in patients with T2D and hypomagnesemia.     

The effect of losartan and losartan/hydrochlorothiazide fixed-combination on magnesium, zinc, and nitric oxide metabolism in hypertensive patients: a prospective open-label study

BACKGROUND: Thiazide diuretics and angiotensin-converting enzyme inhibitors can cause excessive urinary zinc (Zn) loss and Zn depletion. Thiazides may also induce magnesium (Mg) deficiency, which may exacerbate hypertension. Data on the effects of angiotensin receptor blockers on Zn and Mg homeostasis are scarce. METHODS: Seventeen hypertensive patients were studied (ten men and seven women, age 50 +/- 3 years, blood pressure 158 +/- 5 / 95 +/- 3 mm Hg). Patients were treated with losartan 50 mg/day for 4 weeks followed by a fixed combination of 50 mg losartan and 12.5 mg hydrochlorothiazide for 4 weeks more. Blood and 24-h urine were collected at baseline and after each study period. Zinc and Mg levels were measured in serum, urine, and peripheral blood mononuclear cells. Nitric oxide metabolites were measured in urine. RESULTS: Treatment with losartan resulted in a significant increase in the urinary Zn/creatinine ratio (from 0.020 +/- 0.004 microg/mg to 0.034 +/- 0.005 microg/mg, P = .02), which was further increased by the losartan/hydrochlorothiazide combination (from 0.034 +/- 0.005 microg/mg to 0.053 +/- 0.008 microg/mg, P = .03). Serum Zn levels were significantly decreased after losartan/hydrochlorothiazide (from 80.0 +/- 4.0 microg/dL at baseline to 74.0 +/- 3.0 microg/dL, P = .007). Peripheral blood mononuclear Zn concentrations were decreased also, but this was not statistically significant. Serum, urinary, and peripheral blood mononuclear Mg levels were not significantly affected by treatment. Nitric oxide urinary metabolites were unchanged throughout the study. CONCLUSIONS: Treatment with losartan causes an increase in urinary Zn excretion and induces Zn deficiency in patients with hypertension. The addition of hydrochlorothiazide has an additive effect. Magnesium and nitric oxide metabolism are not affected by either treatment.     

Hypermagnesemia predicts mortality in elderly with congestive heart disease: relationship with laxative and antacid use

The aim of this study was to evaluate the role of magnesium levels on 3-year survival in the elderly with congestive heart failure (CHF) admitted to the Rehabilitative Cardiology Unit of S. Maugeri Foundation Scientific Institute of Telese/Campoli. All elderly patients > or = 65 years old with a diagnosis of CHF underwent clinical and instrumental examination, and their demographics, co-morbidity, and in-hospital and 3-year mortality rates were recorded. Hypomagnesemia was found in 4.8%, normomagnesemia in 67.5%, and hypermagnesemia in 27.8% of subjects. The hypomagnesemic group was excluded for numerical exiguity; the analysis was performed on a total of 199 elderly patients. Hypermagnesemia was found in 29.1% and normomagnesemia in 70.9%. At the univariate analysis no differences were found in hypermagnesemia in respect to normomagnesemia group, except for slightly higher levels of creatininemia (1.35 +/- 0.61 vs. 1.13 +/- 0.55 mg/dL, respectively; p < 0.02), greater disability (lost ADL, 2.69 +/- 1.57 vs. 2.15 +/- 1.56, respectively; p < 0.05), more mortality for CHF (32.6 vs. 48.3%; p < 0.05), and higher antacid and laxative use (82.7 vs. 24.8%, respectively; p < 0.0001). Patients with higher magnesium showed less probability to survive at a 3-year follow-up than did patients with lower levels (17.32 +/- 15.93 vs. 22.46 +/- 16.16 months; p < 0.05), and this finding remained significant in the multivariate analysis after adjusting for some confounders. Finally hypermagnesemia should also be considered in the absence of pre-existing renal failure clinical evidence because of its negative prognostic value, especially in elderly patients with CHF. The shown relationship between hypermagnesemia and laxative/antacid use should induce physicians to pay more attention to abuse of these drugs.     

Effect of oral magnesium supplementation on blood pressure, platelet aggregation and calcium handling in deoxycorticosterone acetate induced hypertension in rats

OBJECTIVE: To study the effect of oral magnesium supplementation on blood pressure, platelet aggregation and platelet calcium handling in deoxycorticosterone acetate (DOCA)-induced hypertension in rats. DESIGN AND METHODS: Rats were divided into four groups of 20 each. Drug treatments were given for a 6-week period. Control rats were vehicle treated. In the second group, DOCA, 15 mg/kg, was injected subcutaneously twice weekly with 1% NaCl used instead of drinking water. The third group was given magnesium oxide (MgO), 1 g/kg daily, orally by gavage. The fourth group was given MgO along with DOCA and 1% NaCl. Blood pressure and heart rate were measured weekly. Platelet aggregation, intracellular calcium, calcium uptake and calcium efflux studies were performed at the end of sixth week. Serum magnesium concentration, plasma levels of reactive nitrogen intermediates (RNI) and citrulline were also measured RESULTS: There was a significant rise in blood pressure in the DOCA-treated rats. Magnesium prevented the gradual rise in blood pressure when given along with DOCA, but had no effect in normotensive rats. Heart rate did not show any significant change. Platelet aggregation was significantly reduced in all the treatment groups compared to the control group. DOCA treatment produced a significant increase in the intracellular calcium concentration as well as the calcium uptake compared to the control group. Magnesium supplementation inhibited the increased intracellular calcium concentration and calcium uptake in DOCA-treated rats. RNI and citrulline levels were elevated in all the treatment groups. Serum magnesium levels were significantly higher in the magnesium-treated and DOCA plus magnesium-treated rats. CONCLUSIONS: Magnesium supplementation prevents blood pressure elevation in DOCA hypertensive rats. These effects are associated with inhibition of platelet calcium uptake and decreased intracellular free calcium concentration.     

Cystatin C is a biomarker for predicting acute kidney injury in patients with acute-on-chronic liver failure

AIM:To investigate serum cystatin C level as an early biomarker for predicting acute kidney injury(AKI)in patients with acute-on-chronic liver failure(ACLF).METHODS:Fifty-six consecutive patients with hepatitis B virus-related ACLF who had normal serum creatinine(Cr)level(<1.2 mg/dL in men,or<1.1 mg/dL in women)were enrolled in the Liver Failure Treatment and Research Center of Beijing 302 Hospital between August 2011 and October 2012.Thirty patients with chronic hepatitis B(CHB)and 30 healthy controls in the same study period were also included.Measurement of serum cystatin C(CysC)was performed by a particle-enhanced immunonephelometry assay using the BN Prospec nephelometer system.The ACLF patients were followed during their hospitalization period.RESULTS:In the ACLF group,serum level of CysC was 1.1±0.4 mg/L,which was significantly higher(P<0.01)than those in the healthy controls(0.6±0.3mg/L)and CHB patients(0.7±0.2 mg/L).During the hospitalization period,eight ACLF patients developed AKI.Logistic regression analysis indicated that CysC level was an independent risk factor for AKI development(odds ratio=1.8;95%CI:1.4-2.3,P=0.021).The cutoff value of serum CysC for prediction of AKI in ACLF patients was 1.21 mg/L.The baseline CysC-based estimated glomerular filtration rate(eGFR CysC)was significantly lower than the creatinine-based eGFR(eGFR CG and eGFR MDRD)in ACLF patients with AKI,suggesting that baseline eGFR CysC represented early renal function in ACLF patients while the Cr levels were still within the normal ranges.CONCLUSION:Serum CysC provides early prediction of renal dysfunction in ACLF patients with a normal serum Cr level.     

Comparison of serum copper, magnesium, zinc and calcium levels between G6PD deficient and normal Chinese adults

Minerals are important for normal hematopoiesis and may play a role in acute hemolytic anemia induced by G6PD deficiency. To compare serum magnesium, copper, zinc and calcium levels between G6PD deficiency and normal control adults, we investigated 69 G6PD deficient (28 male, 41 female) and 61 age- matched G6PD normal adults (26 male, 35 female). Serum magnesium, copper, zinc and calcium levels were determined by atomic absorbance spectrometry. Our results revealed that male adults with G6PD deficiency had significantly higher serum copper and magnesium levels than those of the control group (P < 0.01, < 0.05, respectively). In G6PD normal adults, serum copper levels were significantly lower in males than in females (P < 0.01). In the group of G6PD deficiency adults, serum copper levels in males (103.0 +/- 10.4 ug/dL) were significantly lower than those in females (139.0 +/- 34.3 ug/dL) (P < 0.01). Serum magnesium values and zinc values in males (2.42 +/- 0.38 mEq/L and 102.2 +/- 26.5 ug/dL) were significantly higher than those in females (2.07 +/- 0.20 mEq/L and 87.0 +/- 14.9 ug/dL) (P all < 0.01). Female adults with G6PD deficiency had significantly higher serum calcium levels and lower magnesium levels than those of the control group (P all < 0.01). The significantly higher levels of serum copper and magnesium in G6PD deficient male adults may play some role concerning red blood cells in resistance to plasmodium falciparum.     

Efficacy of tolvaptan in patients with refractory ascites in a clinical setting

AIM: To elucidate the efficacies of tolvaptan (TLV) as a treatment for refractory ascites compared with conventional treatment.METHODS: We retrospectively enrolled 120 refractory ascites patients between January 1, 2009 and September 31, 2014. Sixty patients were treated with oral TLV at a starting dose of 3.75 mg/d in addition to sodium restriction (> 7 g/d), albumin infusion (10-20 g/wk), and standard diuretic therapy (20-60 mg/d furosemide and 25-50 mg/d spironolactone) and 60 patients with large volume paracentesis in addition to sodium restriction (less than 7 g/d), albumin infusion (10-20 g/wk), and standard diuretic therapy (20-120 mg/d furosemide and 25-150 mg/d spironolactone). Patient demographics and laboratory data, including liver function, were not matched due to the small number of patients. Continuous variables were analyzed by unpaired t-test or paired t-test. Fisher’s exact test was applied in cases comparing two nominal variables. We analyzed factors affecting clinical outcomes using receiver operating characteristic curves and multivariate regression analysis. We also used multivariate Cox’s proportional hazard regression analysis to elucidate the risk factors that contributed to the increased incidence of ascites.RESULTS: TLV was effective in 38 (63.3%) patients. The best cut-off values for urine output and reduced urine osmolality as measures of refractory ascites improvement were > 1800 mL within the first 24 h and > 30%, respectively. Multivariate regression analysis indicated that > 25% reduced urine osmolality [odds ratio (OR) = 20.7; P < 0.01] and positive hepatitis C viral antibodies (OR = 5.93; P = 0.05) were positively correlated with an improvement of refractory ascites, while the total bilirubin level per 1.0 mg/dL (OR = 0.57; P = 0.02) was negatively correlated with improvement. In comparing the TLV group and controls, only the serum sodium level was significantly lower in the TLV group (133 mEq/L vs 136 mEq/L; P = 0.02). However, there were no significant differences in the other parameters between the two groups. The cumulative incidence rate was significantly higher in the control group with a median incidence time of 30 d in the TLV group and 20 d in the control group (P = 0.01). Cox hazard proportional multivariate analysis indicated that the use of TLV (OR = 0.58; P < 0.01), uncontrolled liver neoplasms (OR = 1.92; P < 0.01), total bilirubin level per 1.0 mg/dL (OR = 1.10; P < 0.01), and higher sodium level per 1.0 mEq/L (OR = 0.94; P < 0.01) were independent factors that contributed to incidence.CONCLUSION: Administration of TLV results in better control of refractory ascites and reduced the incidence of additional invasive procedures or hospitalization compared with conventional ascites treatments.     

The relationship between serum trace element levels and clinical parameters in patients with fibromyalgia

We examined the association between serum trace elements and clinical findings such as number of sensitive tender points, severity of fatigue and functional status in patients with fibromyalgia (FM). Thirty-two patients diagnosed as having FM according to the ACR 1990 criteria and 32 normal healthy controls (NHC) were included in this study. The demographic data, disease duration, number of tender points and accompanying symptoms (fatigue, sleep disorders, headache, paresthesia, irritable bowel syndrome, sicca symptoms, Raynaud's phenomena) of the patients were noted. Visual analog scale (10 cm) was implemented to estimate daily severity of pain and fatigue. Fibromyalgia impact questionnaire was used for functional assessment. Serum selenium (mug/dL) and serum zinc (mug/dL) levels were measured by atomic absorption spectrometer. Serum magnesium (mmol/L) level was measured by the original kits of Abbott Aeroset auto-analyzer. The mean age of patients in FM group and NHC were calculated as 42.9 (SD = 7.7) years and 41.3 (SD = 9.7) years, respectively. Serum levels of zinc (P = 0.001) and magnesium (P = 0.002) were significantly decreased by FM groups, whereas there was no considerable difference with selenium levels of both groups (P > 0.05). Association between serum zinc level and number of tender points (P = 0.008) and that between fatigue and magnesium level (P = 0.003) was found as meaningful. According to the results of this study, it was asserted that serum magnesium and zinc levels may play an important role in the pathophysiology of FM.     

Hypermagnesemia associated with catharsis in a salicylate-intoxicated patient with anorexia nervosa

While clinicians have raised concerns about giving multiple doses of a cathartic as a part of therapy for acute poisoning, fears of excessive magnesium absorption or fluid or electrolyte imbalances have been largely unrealized. We present the case of a 19-year-old woman with anorexia nervosa and long-term laxative abuse who, despite a normal baseline serum magnesium concentration, developed hypermagnesemia during treatment with multiple doses of activated charcoal-magnesium citrate for acute salicylate intoxication. The peak serum magnesium concentration, after two doses of magnesium citrate, reached 9.8 mg/dL (4.0 mmol/L). It fell to normal levels when sorbitol was substituted as a cathartic and after the patient had been hemodialyzed for symptoms of salicylate toxicity that continued despite conventional therapy. While disordered magnesium metabolism in one patient with a severe underlying medical condition should not interdict the use of repetitive doses of magnesium citrate as a cathartic, patients requiring such therapy should have serum magnesium concentrations measured serially to monitor for signs of magnesium loading.     

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.     

Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease

BACKGROUND: Although reduced intracellular levels of magnesium have been described in patients with acute myocardial infarction, its significance as a regulator of thrombosis remains unknown. METHODS AND RESULTS: To determine whether reduced intracellular levels of magnesium enhance platelet-dependent thrombosis, we evaluated 42 patients with coronary artery disease (CAD) by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 minutes by using an ex vivo perfusion (Badimon) chamber. Baseline analysis demonstrated significant associations between intracellular levels of magnesium, platelet-dependent thrombosis (P =.02), and platelet P-selectin (CD62P) expression (P <.05). Patients were divided into 2 groups: below (n = 22) and above (n = 20) the median intracellular levels of magnesium (1.12 microg/mg protein). There were no significant differences in age, body mass index, serum lipids, fibrinogen, platelet count, or serum magnesium levels between the two groups. Platelet-dependent thrombosis was significantly higher in patients with intracellular levels of magnesium below compared with above median (150 +/- 128 vs 45 +/- 28 microm(2)/mm, P <.004). Neither platelet aggregation nor CD62P expression was significantly different between the two groups. CONCLUSIONS: Platelet-dependent thrombosis was significantly increased in patients with stable CAD with low intracellular levels of magnesium, suggesting a potential role for magnesium supplementation in CAD.     

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.     

Comparison of CGM-Derived Measures of Glycemic Variability Between Pancreatogenic Diabetes and Type 2 Diabetes Mellitus

Background:To compare glycemic variability (GV) indices between patients with fibrocalculous pancreatic diabetes (FCPD) and type 2 diabetes mellitus (T2D) using continuous glucose monitoring (CGM).Methods:We measured GV indices using CGM (iPro™2 Professional CGM, Medtronic, USA) data in 61 patients each with FCPD and T2D who were matched for glycated hemoglobin A1c (HbA1c) and duration of diabetes. GlyCulator2 software was used to estimate the CGM-derived measures of GV (SD, mean amplitude of glycemic excursion [MAGE], continuous overall net glycemic action [CONGA], absolute means of daily differences [MODD], M value, and coefficient of variance [%CV]), hypoglycemia (time spent below 70 mg/dL, AUC below 70 mg/dL, glycemic risk assessment diabetes equation hypoglycemia, Low Blood Glucose Index), and hyperglycemia (time spent above 180 mg/dL at night [TSA > 180], AUC above 180 mg/dL [AUC > 180], glycemic risk assessment diabetes equation hyperglycemia, High Blood Glucose Index [HBGI], and J index). The correlation of GV indices with HbA1c, duration of diabetes, and demographic and biochemical parameters were also assessed.Results:All the CGM-derived measures of GV (SD, MAGE, CONGA, MODD, and %CV), except M value, were significantly higher in the FCPD group than in the T2D group (P < 0.05). Measures of hyperglycemia (TSA >180, AUC >180, HBGI, and J index) were significantly higher in the FCPD group than in the T2D group (P < 0.05). The measures of hypoglycemia were not significantly different between the two groups. All the hyperglycemia indices showed a positive correlation with HbA1c in both groups.Conclusions:FCPD is associated with higher GV than is T2D. The findings of higher postprandial glycemic excursions in patients with FCPD could have potential therapeutic implications.     

Hyperphosphatemia after sodium phosphate laxatives in low risk patients： Prospective study

AIM: To establish the frequency of hyperphosphatemia following the administration of sodium phosphate laxatives in low-risk patients.METHODS: One hundred consecutive ASA I-II individuals aged 35-74 years, who were undergoing colonic cleansing with oral sodium phosphate (OSP) before colonoscopy were recruited for this prospective study. Exclusion criteria: congestive heart failure, chronic kidney disease, diabetes, liver cirrhosis, intestinal obstruction, decreased bowel motility, increased bowel permeability, and hyperparathyroidism. The day before colonoscopy, all the participants entered a 24-h period of diet that consisted of 4 L of clear fluids with sugar or honey and 90 mL (60 g) of OSP in two 45-mL doses, 5 h apart. Serum phosphate was measured before and after the administration of the laxative.RESULTS: The main demographic data (mean ± SD) were: age, 58.9 ± 8.4 years; height, 163.8 ± 8.6 cm; weight, 71 ± 13 kg; body mass index, 26 ± 4; women, 66%. Serum phosphate increased from 3.74 ± 0.56 to 5.58 ± 1.1 mg/dL, which surpassed the normal value (2.5-4.5 mg/dL) in 87% of the patients. The highest serum phosphate was 9.6 mg/dL. Urea and creatinine remained within normal limits. Post-treatment OSP serum phosphate concentration correlated inversely with glomerular filtration rate (P < 0.007, R² = 0.0755), total body water (P < 0.001, R² = 0.156) and weight (P < 0.013, R² = 0.0635).CONCLUSION: In low-risk, well-hydrated patients, the standard dose of OSP-laxative-induced hyperphosphatemia is related to body weight.