The incidence, risk factors, and outcomes of acute kidney injury in patients with pyogenic liver abscesses.

BACKGROUND: Acute kidney injury (AKI) can occur in various infectious conditions. Liver abscess is relatively rare, but can lead to sepsis and/or other severe complications. Few studies of AKI in patients with a liver abscess have been conducted. Therefore, we analyzed the clinical and laboratory data of AKI in patients with a liver abscess. METHODS: We retrospectively reviewed the medical records of patients who were diagnosed with a liver abscess from January 2000 to March 2013. The study included 404 patients with a liver abscess confirmed by clinical presentation and computed tomography. RESULTS: AKI occurred in 137 patients (34 %). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (35.8 %), renal injury (47.4 %), and renal failure (16.5 %). AKI occurred more frequently in males and patients with liver cirrhosis (P < 0.001 and P = 0.005). Patients with AKI had lower serum albumin and higher AST and ALT levels than did patients without AKI. Bacteria were frequently isolated in AKI patients from blood culture and liver abscess aspirates (P < 0.001 and P = 0.007). The occurrence of septic shock was positively correlated with AKI (P = 0.002) and AKI was more frequent in patients with chronic kidney disease (P = 0.04). Higher mortality was observed in CKD patients accompanied by AKI (P < 0.001). Three patients with AKI underwent hemodialysis; two patients who had initially normal renal function completely recovered whereas one CKD patient progressed to ESRD, requiring maintenance hemodialysis. CONCLUSION: AKI is relatively common in patients with liver abscess. Physicians should therefore attempt to prevent, detect, and manage AKI early in patients with liver abscess.

Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace.

A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8 mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3 = 130.40 ng/dL, TSH = 0.06 mIU/L, and free T4 = 1.73 ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4 mmol/L by intravenous infusion of only 40 mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient's thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea.

The concordance and correlation of measurements by multiple electrode and light transmittance aggregometries based on the pre-defined cutoffs of high and low on-treatment platelet reactivity.

The consensus document suggested the definition of high on-treatment platelet reactivity (HPR) and future directions. Although multiple platelet function assays have developed based on different mechanisms, inter-assay concordance of HPR identification may be an important pressing need. This study was performed to correlate between the cutoffs of HPR suggested by multiple electrode (MEA) and light transmittance aggregometries (LTA). We enrolled 246 consecutive patients undergoing non-emergent percutaneous coronary intervention after dual antiplatelet therapy. On the basis of consensus document, the cutoffs of HPR to adenosine diphosphate (ADP) were defined as ADPtest ≥ 47 U, and 5 and 20 µM ADP-induced maximal platelet aggregation (MPA) ≥ 46% and 59%, respectively. In addition, the cutoff of low PR (LPR) for major bleeding was selected as ADPtest ≤ 19 U. ADPtest showed moderate correlations with ADP-based LTA data (0.663 ≤ r ≤ 0.710). In the receiver-operating characteristics (ROC) curve analysis, ADPtest ≥ 47 U was corresponded to 5 and 20 µM ADP-induced MPAs ≥ 46.4% and ≥ 56.8%, respectively. Good agreements were observed between ADPtest ≥ 47 U, and 5 µM ADP-induced MPA ≥ 46% (κ=0.537, 80.5% of concordance rate) and 20 µM ADP-induced MPA ≥ 59% (κ=0.564, 81.7% of concordance rate). In the ROC curve analysis for the cutoff of LPR (ADPtest ≤ 19 U), 5 and 20 µM ADP-induced MPAs ≤ 26.6% and ≤ 35.3%, respectively, were suggested as the hypothetical threshold for major bleeding. On the basis of consensus document, the cutoffs of MEA- and LTA-based HPR are well matched. However, the agreement of HPR between assays is moderate, which may implicate the limitation of risk stratification by platelet function testing.

Platelet inhibition by adjunctive cilostazol versus high maintenance-dose clopidogrel in patients with acute myocardial infarction according to cytochrome P450 2C19 genotype.

OBJECTIVES: The aim of this study was to assess the degree of platelet inhibition by adjunctive cilostazol in patients with acute myocardial infarction (AMI) according to hepatic cytochrome P450 2C19 (CYP2C19) genotype. BACKGROUND: Although adjunctive cilostazol intensifies platelet inhibition in AMI patients, it is not established whether this regimen can be free from the effect of CYP2C19 loss-of-function variants (*2/*3). METHODS: We randomly assigned 126 AMI patients with available CYP2C19 genotyping to receive adjunctive cilostazol (triple group; n = 64) or high maintenance-dose (MD) clopidogrel of 150 mg/day (high-MD group; n = 62). Using conventional aggregometry and VerifyNow (Accumetrics Inc., San Diego, California), platelet reactivity was measured at pre-discharge and 30-day follow-up. Primary endpoint was change in maximal platelet aggregation (ΔAgg(max)) between pre-discharge and 30-day follow-up. High on-treatment platelet reactivity (HPR) was defined as 20 µmol/l adenosine diphosphate-induced maximal platelet aggregation (Agg(max)) >59%. RESULTS: In noncarriers, despite numerically greater inhibition by adjunctive cilostazol, changes in platelet measures and the rate of HPR did not significantly differ between the 2 groups. In carriers, ΔAgg(max) after 5 and 20 µmol/l adenosine diphosphate stimuli was significantly higher in the triple (n = 39) versus high-MD group (n = 38) (21.8 ± 13.9% vs. 9.0 ± 13.3%, p < 0.001, and 24.2 ± 17.2% vs. 7.7 ± 15.5%, p < 0.001, respectively). Likewise, changes in late platelet aggregation and P2Y12 reaction unit were consistently greater in the triple versus high-MD group. Fewer patients in the triple group met the criteria of HPR at 30-day follow-up than in the high-MD group (15.4% vs. 44.7%, p = 0.005). CONCLUSIONS: Compared with high-MD clopidogrel, adjunctive cilostazol significantly enhances platelet inhibition and reduces the rate of HPR, especially in AMI patients with CYP2C19 loss-of-function variants. (Adjunctive Cilostazol Versus High Maintenance-Dose Clopidogrel in Acute Myocardial Infarction (AMI) Patients According to CYP2C19 Polymorphism [ACCELAMI2C19]; NCT00915733).