ABSTRACT
A patient receiving daptomycin developed asymptomatic transaminitis and hyperbilirubinemia without concurrent multiorgan dysfunction or elevation of his creatinine kinase level. After ruling out other etiologies, the liver injury was attributed to daptomycin and was subsequently resolved. A single-center retrospective cohort analysis of baseline and follow-up liver function panels (n = 614) from all admissions from 2008 to 2013 during which daptomycin was administered did not reveal any other cases of probable or definite drug-induced liver injury associated with daptomycin.
Subject(s)
Anti-Bacterial Agents/adverse effects , Chemical and Drug Induced Liver Injury/etiology , Daptomycin/adverse effects , Adult , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/rehabilitation , Hospitalization , Humans , Liver/drug effects , Liver/enzymology , Liver/pathology , Liver Function Tests , Male , Methicillin-Resistant Staphylococcus aureus/pathogenicity , Methicillin-Resistant Staphylococcus aureus/physiology , Recovery of Function , Retrospective Studies , Staphylococcal Infections/drug therapy , Staphylococcal Infections/microbiologyABSTRACT
INTRODUCTION: Markers of systemic inflammation have been shown to be elevated in patients with gastroparesis (Gp). We hypothesized the presence of elevated markers of inflammation and/or coagulation can predict death in gastroparesis. METHODS: Retrospective evaluation of 396 patients with symptoms of gastroparesis with baseline measures of inflammation and coagulation, using a database of patients from 2001 through 2011 followed for an additional 5 plus years. Patients were divided into two groups; diabetic (DM; n=137) and non-diabetic (non-DM; n=259). Inflammation, evaluated by C-reactive protein (CRP), and coagulation by fibrinogen by factor VIII assays, was compared to patient mortality, reported as death during the follow-up period. RESULTS: Six DM and 13 non-DM patients died during the study period. DM patients had higher fibrinogen, CRP, and factor VIII levels of 454.0±135.2, 4.0±6.3, and 168±63.5, versus non-DM whose levels were 410.4±127.9, 2.6±4.9, 140.4±127.9, p=0.03, 0.001, and <0.001 respectively. Hypercoagulability risk differed by DM status (37% Vs. 29%, p=0.08). Compared to living non-DM, deceased non-DM/idiopathic patients had lower factor VIII (142.3±51.2 vs 117.7±40.3, p=0.07). The majority of deceased non-DM patients had abnormal fibrinogen (62%) but CRP and factor VIII were normal (80% and 85% respectively). CONCLUSIONS: In this sample of 396 patients with symptoms of gastroparesis, systemic inflammation and coagulopathy appear related to diabetes mellitus. Patients who died had markers of inflammation and coagulation that differed from those still alive. Further analysis may suggest a link between inflammation, hypercoagulability, and the mechanism for mortality in gastroparesis or as a marker of disease severity.