To evaluate the safety and efficacy of GlucoStabilizer software intravenous insulin (IV) dosing in comparison to American Diabetes Association protocol-directed provider-guided insulin dose ...adjustment (PGIA).
GlucoStabilizer calculates the dose of IV insulin required to reach a prescribed target glucose range. GlucoStabilizer has not been fully studied in DKA. This retrospective study compared outcomes in patients with DKA before and after the implementation of GlucoStabilizer. Insulin doses were administered based on GlucoStabilizer calculations or PGIA. The analysis evaluated before-after changes in the amount of insulin used, time to target, hypoglycemia or hypokalemia events, and the time to DKA resolution.
We studied 77 patients with insulin doses calculated by GlucoStabilizer and 69 patients with PGIA dosing. GlucoStabilizer was superior to PGIA. Patients treated with GlucoStabilizer-calculated doses did not experience hypoglycemia (N = 0 versus N = 10;
<.001). The 10 unique PGIA patients had a total of 18 episodes with 17 between 55 to 69 mg/dL; 1 <54 mg/dL, and no episodes <40 mg/dL. The GlucoStabilizer group required less insulin to reach DKA resolution (59.2 versus 101.2 units;
<.001). Time to glycemic target and DKA resolution were similar (6.7 versus 4.6 hours;
= .132) and (9.8 versus 9.9 hours;
= .803), respectively. No difference in the incidence of hypokalemia was seen (N = 9 versus N = 11;
= .48).
This study demonstrates the Gluco Stabilizer settings that can be successfully used in the management of DKA with the avoidance of hypoglycemia. Patients treated with GlucoStabilizer-calculated doses experienced no hypoglycemia and required less insulin as compared to those managed with PGIA.
= American Diabetes Association;
= diabetic ketoacidosis;
= emergency department;
= electronic glycemic management systems;
= intensive care unit;
= intravenous;
= protocol-directed provider-guided insulin dose adjustment.
To report a rare case of ectopic parathyroid hormone (PTH) secretion from poorly-differentiated adenocarcinoma and the lessons learned in management.
A 54-year-old woman presented with fatigue, hip ...pain, and confusion. Workup revealed calcium of 16.9 mg/dl (N: 8.5–10.3 mg/dl), PTH of 981 pg/ml (N: 15–65 pg/ml), and parathyroid hormone-related peptide (PTHrP) of 20 pmol/L (N: 14–27 pmol/L). Parathyroid four-dimensional computed tomography was unrevealing. Magnetic resonance cholangiopancreatography demonstrated innumerable hepatic lesions. Biopsy of the liver and pubic ramus revealed poorly differentiated adenocarcinoma of unknown origin with acinar cell differentiation and focal PTH positivity.
Initial treatment with intravenous bisphosphonates and cinacalcet showed a poor response. Calcitonin had a short-lived response. Although chemotherapy significantly improved calcium levels, she was unable to tolerate chemotherapy. Despite a rise in PTH from 196 to 674 pg/ml, denosumab improved calcium levels from 13 to 9.7 mg/dl. She expired due to a cardiac arrest.
PTH secretion from tumors with acinar cell differentiation outside of the pancreas has not been described. Cinacalcet was ineffective and it is doubtful that the malignant cells had calcium-sensing receptors. Calcitonin was effective initially, but she eventually developed tachyphylaxis. Use of denosumab later in the treatment course has resulted in significant improvement in calcium despite worsening PTH levels.
Denosumab is effective in the treatment of paraneoplastic PTH-mediated hypercalcemia and should be considered in patients who have resistance to bisphosphonate therapy.
•A rare case of Hypercalcemia of Malignancy due to paraneoplastic PTH secretion.•PTH production from an extra-pancreatic tumor with acinar cell differentiation.•Bisphosphonate resistance in ectopic PTH induced Hypercalcemia of Malignancy.•A review of medications used for treating hypercalcemia in our patient.
Abstract
Disclosure: A. Poloju: None. P. Majety: None. A.Y. Groysman: None.
Background/Objective: Sodium glucose cotransporter 2 (SGLT2) inhibitors are increasingly being used in the treatment of ...type 2diabetes mellitus (T2DM). With the recent FDA approval of these medications for treatment of heart failure, their use is expected to increase further. Common adverse events associated with SGLT2 inhibitors are genitourinary infections, hypotension, acute kidney injury and euglycemic diabetic ketoacidosis. Recently, SGLT2 inhibitors are increasingly associated with drug induced acute pancreatitis (DIAP). We present a case of empagliflozin associated DIAP, with the intent to add to the limited data on this possible adverse effect. Clinical Case: A 57-year-old woman with a history of T2DM presented to the hospital with severe abdominal pain. She had no recent alcohol use or prior episodes of pancreatitis. There was no history of trauma. Home medications include metformin, glipizide, empagliflozin, and lisinopril. Exam showed epigastric tenderness to palpation without guarding or rebound tenderness. Labs were notable for elevated white blood cell count, normal lipase, calcium, triglycerides, and liver function tests. CT abdomen showed induration of the peri-pancreatic fat, suggestive of pancreatitis. After ruling out common causes of pancreatitis, DIAP and idiopathic pancreatitis were considered possible etiologies. Obtaining further history revealed that patient was started on empagliflozin two weeks prior to this presentation. The only other medication that is known to cause pancreatitis is lisinopril but our patient was on this medication for several years. The Naranjo probability scale for empagliflozin showed a possible association between the drug and side effect. Empagliflozin was discontinued and the patient was discharged on metformin and glipizide. Conclusions: Pancreatitis is a common diagnosis requiring hospital admission and is associated with significant costs to the healthcare system. Although pancreatitis is a known side-effect with other medications used in treatment of T2DM, such as GLP1RAs and DPP-4inhibitors, it has not been well described with SGLT2 inhibitors. The prevalence of DIAP is difficult to assess since most of the existing data comes from individual case reports. Our patient had no known risk factors for pancreatitis. It is yet to be studied if genetic predisposition has a role in the development of pancreatitis with SGLT-2 inhibitors. With the increasing use of these medications in the treatment of type 2diabetes mellitus and heart failure, more cases of DIAP are being reported. It is important for physicians to consider SGLT2 inhibitors as a cause of pancreatitis after excluding other common etiologies. This may reduce episodes of recurrent pancreatitis and the burden of extensive workup for idiopathic pancreatitis.
Presentation: Thursday, June 15, 2023
A search for the decay of the tau lepton to seven charged pions and one or zero pizero mesons was performed using the BaBar detector at the PEP-II asymmetric-energy e+e- collider. The analysis uses ...232.2 fb-1 of data at center-of-mass energies on or near the Y(4S) resonance. We observe 24 events with an expected background of 21.6+-1.3 events. Without evidence for a signal, we calculate an upper limit of BR(tau- --> 4pi- 3pi+ (pizero) nu_tau) < 3.0*10^-7 at 90 % confidence level. This is an improvement by nearly an order of magnitude over the previously established limit. In addition, we set upper limits for the exclusive decays tau- --> 4pi- 3pi+ nu_tau and tau- --> 4pi- 3pi+ pizero nu_tau.
We present a measurement of the time-dependent CP-violating asymmetries in $B^0 \to K^{*0}\gamma (K^{*0}\to K_S^0 \pi^0)$ decays based on 124 million $\Upsilon(4S)\to B^0\bar{B}^0$ decays collected ...with the BaBar detector at the PEP-II asymmetric-energy $B$ Factory at the Stanford Linear Accelerator Center. In a sample containing $105\pm 14$ signal decays, we measure $S_{K^{*0}} = 0.25 \pm 0.63 \pm 0.14$ and $S_{K^{*0}} = -0.57 \pm 0.32 \pm 0.09$, where the first error is statistical and the second systematic.
We present results from an analysis of B(0)B(0)--> rho(+)rho(-) using 232 x 10(6) Gamma (4S) --> BB decays collected with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. We ...measure the longitudinal polarization fraction f(L) = 0.978 +/- 0.014(stat) + 0.021 / -0.029(syst) and the CP-violating parameters S(L)= -0.33 +/- 0.24(stat) + 0.08 / -0.14(syst) and C(L)= -0.03 +/- 0.18(stat) +/- 0.09(syst). Using an isospin analysis of B --> rhorho decays, we determine the unitarity triangle parameter alpha. The solution compatible with the standard model is alpha = (100 +/- 13) degrees.
We present an updated measurement of time-dependent \CP asymmetries and the \CP-odd fraction in the decay $B^0 \to D^{*+}D^{*-}$ using $232 \times 10^{6} \BB$ pairs collected by the \babar detector ...at the PEP-II $B$ factory. We determine the \CP-odd fraction to be $0.125 \pm 0.044\stat \pm 0.007\syst$. The time-dependent \CP asymmetry parameters $C_+$ and $S_+$ are determined to be $0.06\pm 0.17\stat \pm 0.03\syst$ and $-0.75 \pm 0.25\stat \pm 0.03\syst$, respectively. The Standard Model predicts these parameters to be 0 and $-\stwob$, respectively, in the absence of penguin amplitude contributions.
We present updated measurements of the CP-violating parameters S_pipi and C_pipi in B0 -> pi+pi- decays. Using a sample of 227 million Y(4S) -> BBbar decays collected with the BaBar detector at the ...PEP-II asymmetric-energy e+e- collider at SLAC, we observe 467 +- 33 signal decays and measure S_pipi = -0.30 +- 0.17 (stat) +- 0.03 (syst), and C_pipi = -0.09 +- 0.15 (stat) +- 0.04 (syst).
PDF
