McMahon, Molly

Abstract Magnesium (Mg) is an essential element involved in cellular metabolism. We demonstrated that in patients with diffuse large B-cell lymphoma (DLBCL) undergoing autologous stem cell transplant (SCT), those with a serum Mg < 2.0 mg/dL at the time of transplant had worse outcomes. In this study, we aimed to learn the prognostic value of low serum Mg in patients with untreated DLBCL. We analyzed serum from 408 patients and tested 2 Mg cutpoints—low (<1.7 mg/dL) and low normal (<2.0 mg/dL), a range we found associated with lower survival in the SCT group. We found 3% of patients with low levels and 23% with low normal levels. Low normal serum Mg levels were associated with a higher stage at diagnosis, more extranodal involvement, higher international prognostic index score, lower overall survival (OS), and event-free survival. These data warrant testing Mg replacement to a target of >2.0 mg/dL to learn if survival can be improved.

e20048 Background: No literature exists regarding whether hypomagnesemia at the time of diagnosis in Burkitt Lymphoma (BL) is associated with inferior survival. Methods: Patients with new diagnosis of BL who were seen at Mayo Clinic, MN from 2000-2019 with a serum magnesium level available prior to chemotherapy were included. Patients were allocated to two groups; Abnormal Magnesium Group (AMG), defined as a magnesium level < 1.7 mg/dL and Normal Magnesium Group (NMG), defined as ≥ 1.7 – 2.3mg/dL. Two-sided Wilcoxon rank sum test and Chi square/Fischer’s exact test were used to compare the continuous and categorical variables, respectively. Kaplan-Meier and log-rank tests were used to perform all time to event analysis which were done from time of treatment. Hazard ratios (HR) with confidence intervals (CI) were calculated using Cox-proportional hazards. Results: Of 90 patients with a diagnosis of BL, 42 patients had a magnesium level at or before time of diagnosis. The Table lists the baseline characteristics and significant findings of the AMG/NMG groups. The median follow-up was 30 months. Hypomagnesemia was predictive for inferior EFS at 30 months - 34.3% (95% CI: 8.7–74.0) for AMG and 79.3% (95% CI: 60.8-90.4) for NMG (p = 0.038). OS at 30 months for AMG was 42.9% (95% CI: 14.4-77.0) and for NMG was 93.7% (95% CI: 78.1-98.4%) (p = 0.002). Other parameters significant on univariate analysis included the Charlson Comorbidity Index (p = 0.034), creatinine (p = 0.009), and number of treatments (p = 0.048). In the multivariate analysis, creatinine (p = 0.005) and number of treatments (p = 0.004) were significant. Likelihood ratio testing of predictors associated with inferior OS were significant for hypomagnesemia (likelihood ratio 3.99, p = 0.046). Conclusions: Patients with hypomagnesemia at the time of BL diagnosis have inferior outcomes compared to BL patients with a normal magnesium level. Prospective studies are needed to confirm this finding and test Mg replacement strategies to mitigate the effects of hypomagnesemia. [Table: see text]

As part of its Healthy Aging & Independent Living (HAIL) initiative, Mayo Clinic Center for Innovation (CFI) examined the patient experience regarding the decision to receive a ventricular assistive device (VAD) implant, and patients’ quality of life after the surgery. As health care technology continues to develop, more people will be living longer, fuller lives with the assistance of wearable/implantable medical devices such as the VAD. This case study examined and made recommendations on ways for the Mayo Clinic VAD Committee to improve the program.

Basal insulin supplementation has been used as a therapy for patients with non-insulin-dependent diabetes mellitus (NIDDM) who require insulin. To determine whether basal insulin supplementation in addition to lowering postabsorptive plasma glucose concentration also improves the postprandial pattern of glucose disposition, glucose metabolism after ingestion of a solid mixed meal was assessed in obese patients with NIDDM before and after treatment with ultralente and compared with glucose metabolism observed in nondiabetic subjects. Splanchnic uptake of ingested glucose clearance was assessed by including [2-3H]glucose (a tracer that only minimally cycles through glycogen) in a solid mixed meal. Postprandial gluconeogenesis was estimated by measuring the rate of incorporation of carbon dioxide into glucose. Net glucose and lipid oxidation were measured by indirect calorimetry. Both splanchnic uptake of ingested glucose (27 ± 1 vs. 14 ± 2 g) and postprandial hepatic glucose release (51 ± 5 vs. 24 ± 3 g) were greater (P &lt; .001) in diabetic than in nondiabetic subjects. Although the percentage of postprandial hepatic glucose release accounted for by glucose synthesis from bicarbonate was similar in the two groups (25 ± 2 vs. 35 ± 5%), the absolute rate was greater in the diabetic patients (13 ± 1 vs. 8 ± 1 g; P &lt; .05). Postprandial glucose oxidation and glucose disposal (measured either isotopically or by the forearm-catheterization technique) were similar in both groups. However, total lipid oxidation was increased in the diabetic patients. (P &lt; .05). Two weeks of basal insulin supplementation lowered fasting glucose concentrations (from 219 ± 22 to 144 ± 21 mg/dl; P &lt; .01) and integrated postprandial glycemic response (from 814 ± 68 to 621 ± 72 min · mg· ml−1) but not to normal. Although circulating insulin concentrations were two- to threefold greater (P &lt; .02) after 3 mo of basal insulin supplementation, the postprandial pattern of glucose metabolism remained essentially the same. Basal insulin supplementation decreased (P &lt; .05) both splanchnic uptake of ingested glucose and hepatic glucose release. The addition of a preprandial injection of soluble insulin to basal insulin supplementation further suppressed (P &lt; .05) postprandial hepatic glucose release, thereby further improving postprandial glucose tolerance. These studies indicate that initial splanchnic glucose clearance, hepatic glucose release, and new glucose synthesis, as well as extrahepatic substrate metabolism, are altered in NIDDM after ingestion of a mixed meal. Basal insulin supplementation improves but does not normalize postprandial glucose metabolism.