A Case of Fenofibrate-Induced Immune Thrombocytopenia: First Report.

Fenofibrate is widely prescribed as a hypolipidemic drug and is well tolerated by most patients. We present the case of a 40-year-old woman who developed severe immune thrombocytopenia while on fenofibrate treatment. Clinical features included spontaneous bruising on the feet and hands, a purpuric rash, and menorrhagia. All the laboratory results were normal except for the finding of isolated thrombocytopenia. The subsequent evolution was favorable after fenofibrate removal and with the administration of immunoglobulin G (IgG) plus corticosteroids. Drug-induced thrombocytopenia is briefly reviewed, and a possible mechanism responsible for causing this side effect of fenofibrate is suggested. This is the first reported case of fenofibrate-induced immune thrombocytopenia.

Coagulation and inflammation biomarkers may help predict the severity of community-acquired pneumonia.

BACKGROUND AND OBJECTIVE: There are limited data on the relationship between the severity of community-acquired pneumonia (CAP) and biomarkers of inflammation and coagulation. The aim of this study was to evaluate the association between the severity of CAP and serum levels of antithrombin III (AT-III), protein C (P-C), D-dimers (D-D) and CRP, at hospital admission. METHODS: This was a prospective observational study in 77 adults (62.3% men), who were hospitalized for CAP. The severity of CAP was assessed using the confusion, uraemia, respiratory rate >or=30 breaths/min, low blood pressure, age >or=65 years (CURB-65) score. RESULTS: Forty patients (52%) had severe CAP (CURB-65 score 3-5). Serum levels of AT-III were lower and levels of D-D and CRP were higher in patients with severe CAP than in patients with mild CAP (CURB-65 score 0-2) (P < 0.001 for all comparisons). Levels of P-C were lower in patients with severe CAP compared with those with mild CAP, but the difference was not significant (P = 0.459). At a cut-off point of 85%, AT-III showed a sensitivity of 80% and a specificity of 75%, as a determinant of the need for hospitalization. At a cut-off point of 600 ng/mL, D-D showed a sensitivity of 90% and a specificity of 75% and at a cut-off point of 110 mg/L, CRP showed a sensitivity of 83% and a specificity of 79%, as determinants of the need for hospitalization. CONCLUSIONS: Serum levels of AT-III, D-D and CRP at admission appear to be useful biomarkers for assessing the severity of CAP.

The Role of Mean Platelet Volume in Chronic Obstructive Pulmonary Disease Exacerbation.

BACKGROUND: Studies have supported the correlation between mean platelet volume and COPD. However, there are limited data on the relationship between COPD exacerbation and mean platelet volume. We aimed to evaluate the mean platelet volume trend in patients with COPD exacerbation. METHODS: A total of 81 subjects, 62 men and 19 women, who were admitted to the hospital because of exacerbation of COPD during 9 months, were enrolled in this prospective observational study. The levels of mean platelet volume, C-reactive protein, complete blood count, and percent-of-predicted FEV1 were measured in subjects at admission (exacerbation period) and after 3 months (stable period). Thirty-seven age- and sex-matched healthy individuals constituted the control group. RESULTS: Subjects in the exacerbation period had significantly higher levels of C-reactive protein (P = .001), white blood cell count (P = .01), and percentage of neutrophils (P = .01) and lower percent-of-predicted FEV1 than in the stable period (P = .02). Mean platelet volume levels were significantly decreased in the exacerbation period (P = .001). Considering a cut-off point of mean platelet volume levels <8.2 fL for indicating COPD exacerbation showed a sensitivity of 80% and a specificity of 76%. Also, mean platelet volume levels correlated significantly with increase of C-reactive protein level, white blood cell count, and neutrophil percentage in the exacerbation period (P = .01, P = .01, and P = .02, respectively). CONCLUSIONS: Mean platelet volume may be an inflammatory marker in exacerbation of COPD, and the measurement of mean platelet volume values may be useful for identifying patients who are at increased risk for exacerbations of illness.