New onset nonischemic cardiomyopathy post liver transplantation

Abstract Background:The frequency of new-onset diabetes after transplant(NODAT) is 5-30% in liver transplant recipients. Aims: We aimed to analyze the frequency and predictors of NODAT in the patients undergoing liver transplantation(LTx) due to acute liver failure(ALF), and to investigate whether pretransplant hypoglycemia had any effect on NODAT. Methods:Adult patients undergoing LTx due to ALF were analyzed retrospectively. The patients with chronic liver failure or diabetes were excluded. We measured pretransplant random blood glucose(RBG) and posttransplant fasting blood glucose(FBG). NODAT was diagnosed according to principally 1 st month FBG (group 1:<100, group 2:100-125, group 3:>125 mg/dL). The participants were subgrouped according to age, gender, BM, etiology, antiviral medication, thyroid function, pretransplant RBG, donor type, immunosuppressive drug, common infection, and surgical complication. Results:A total of 91 patients were analyzed; mean age was 33.48(±13.35), and 52.7%(n=48) of them was female. The etiology was Budd-Chiari syndrome in 3(3.29%), acute viral hepatitis in 38(41.75%), drug or toxin-related in 21(23.07%), and other/unknown causes in 29(31.86%) patients. The ratio of NODAT was 26.98% on the 1 st month. NODAT group had a higher pretransplant RBG than the others. Pretransplant hypoglycemia did not have any effect on NODAT; however, pretransplant hyperglycemia increased the risk of NODAT by 4.065 times(p=0.018). Conclusions:We showed that pretransplant hyperglycemia increased the risk of NODAT by 4 times, but hypoglycemia did not affect. The frequency of NODAT decreased progressively during follow-up. We recommend perioperative glycemic control should be maintained as early as possible to manage NODAT; however, it might be complicated in such a clinical condition.

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Genetic or Autoimmune: POLG-Related Epilepsy Initially Treated as an Autoimmune Encephalitis, a Case Report

The Neurohospitalist ◽

10.1177/1941874420952263 ◽

2020 ◽

Vol 11 (1) ◽

pp. 80-83

Author(s):

Suma Shah ◽

Abigail Berezoski ◽

Shareena Rahman ◽

Christopher Eckstein ◽

Matthew Luedke

Keyword(s):

Valproic Acid ◽

Liver Transplantation ◽

Autoimmune Encephalitis ◽

Healthy Person ◽

Autoimmune Epilepsy ◽

Number Of Patients ◽

Autoimmune Processes ◽

Refractory Seizures ◽

New Onset

Hospital neurologists participate at the forefront of managing fulminant acute and subacute onset epilepsy, frequently attributed to autoimmune encephalitis (AE). As the recognition of antibody-mediated AE grows, there is a growing number of patients who are treated as antibody-negative AE. While antibody-negative autoimmune processes should be considered in the setting of acute and subacute onset of fulminant epilepsy, other causes must be considered before subjecting patients to long-term immunomodulatory treatments and other potential therapeutic toxicities. We present the case of a previously healthy young man who presented with new-onset refractory seizures treated with escalating doses of anti-epileptic drugs as well as immunosuppression for presumed autoimmune epilepsy. He developed valproic acid induced hepatotoxicity requiring liver transplantation and was later found to have a POLG mutation. We discuss the presentation of POLG mutations as well as the diagnosis of seronegative autoimmune encephalitis. We highlight the need for a broad differential when evaluating new onset refractory seizures in an otherwise healthy person.

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