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A Case of Statin-Induced Interstitial Pneumonitis due to Rosuvastatin.

Kim SY, Kim SJ, Yoon D, Hong SW, Park S, Ock CY - Tuberc Respir Dis (Seoul) (2015)

Bottom Line: We suspected rosuvastatin-induced lung injury, discontinued rosuvastatin and initiated prednisolone 1 mg/kg tapered over 2weeks.After initiating steroid therapy, his symptoms and radiologic findings significantly improved.We suggest that clinicians should be aware of the potential for rosuvastatin-induced lung injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, The Armed Forces Medical Hospital, Seongnam, Korea.

ABSTRACT
Statins lower the hyperlipidemia and reduce the incidence of cardiovascular events and related mortality. A 60-year-old man who was diagnosed with a transient ischemic attack was started on acetyl-L-carnitine, cilostazol, and rosuvastatin. After rosuvastatin treatment for 4 weeks, the patient presented with sudden onset fever, cough, and dyspnea. His symptoms were aggravated despite empirical antibiotic treatment. All infectious pathogens were excluded based on results of culture and polymerase chain reaction of the bronchoscopic wash specimens. Chest radiography showed diffuse ground-glass opacities in both lungs, along with several subpleural ground-glass opacity nodules; and a foamy alveolar macrophage appearance was confirmed on bronchoalveolar lavage. We suspected rosuvastatin-induced lung injury, discontinued rosuvastatin and initiated prednisolone 1 mg/kg tapered over 2weeks. After initiating steroid therapy, his symptoms and radiologic findings significantly improved. We suggest that clinicians should be aware of the potential for rosuvastatin-induced lung injury.

No MeSH data available.


Related in: MedlinePlus

(A-E) Chest radiography showed subtle diffuse ground glass opacity in both lower lobe field and subsegmental atelectasis in left lower lobe field on admission. A computed tomography scan of the chest showed diffuse ill-defined ground glass opacity with septal line thickening in bilateral lung fields combined with several subpleural ground glass opacity nodules on admission.
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Figure 1: (A-E) Chest radiography showed subtle diffuse ground glass opacity in both lower lobe field and subsegmental atelectasis in left lower lobe field on admission. A computed tomography scan of the chest showed diffuse ill-defined ground glass opacity with septal line thickening in bilateral lung fields combined with several subpleural ground glass opacity nodules on admission.

Mentions: Upon admission, the patient's vital signs were as follows: blood pressure, 116/77 mm Hg; pulse, 114 beats per minute; respiratory rate, 26 breaths per minute; and body temperature, 36.9℃. On physical examination, a coarse breath sound with fine crackles but without wheezing was heard upon auscultation of both lungs. The patient's laboratory test results were as follows: hemoglobin, 14.1 g/dL; white blood cell count, 8,770 cells/µL (neutrophils, 62.6%; lymphocytes, 26.0%; monocytes, 7.2%; eosinophils, 3.9%; and basophils, 0.3%); and platelet count, 391,000 cells/µL. The patient's serum biochemistry test results revealed the following: aspartate aminotransferase, 35 IU/L; alanine aminotransferase, 35 IU/L; total bilirubin, 0.4 mg/dL; alkaline phosphatase, 311 IU/L; total protein, 7.6 g/dL; albumin, 4.0 g/dL; blood urea nitrogen, 26.0 mg/dL; creatinine, 0.84 mg/dL; total cholesterol, 106 mg/dL; C-reactive protein, 1.06 mg/dL; and LDL cholesterol, 56 mg/dL. His coagulation profile was within normal limits. A urinalysis with microscopy was clear. An arterial blood gas analysis of the fraction of inspired oxygen (FiO2) was conducted with the patient breathing room air and revealed the following: pH, 7.46; partial pressure of oxygen (PaO2), 54.6 mm Hg; partial pressure of carbon dioxide (PaCO2), 37.4 mm Hg; bicarbonate (HCO3-), 26.0 mEq/L; and saturation level of oxygen (SaO2), 85.9%. A chest radiograph showed a subtle, diffuse ground-glass opacity in both lower lung fields and subsegmental atelectasis in the left lower lobe. A chest computed tomography scan revealed diffuse ill-defined ground-glass opacities with septal line thickening bilaterally, combined with several subpleural ground-glass opacity nodules (Figure 1). A pulmonary function test revealed the following: forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio, 102; FEV1, 2.8 L (94%); FVC, 3.47 L (92%); and diffuse capacity for carbon monoxide (DLCO), 57%. Based on his past medical history, clinical symptoms, and laboratory findings, a diagnosis of DILD was suspected. Consequently, bronchoscopy with bronchoalveolar lavage (BAL) was performed. There were no endobronchial lesions revealed with bronchoscopy. The BAL fluid results were as follows: white blood cell count, 480 cells/µL (neutrophils, 9%; lymphocytes, 30%; macrophages, 57%; eosinophils, 4%; and basophils, 0%); and red blood cell count, 30 cells/µL. Microbiological culture and polymerase chain reaction of the bronchoscopic wash specimens were negative for Mycobacterium tuberculosis, pneumococcus and respiratory virus. The real-time polymerase chain reaction of bronchial washing specimens was performed as following: Mycoplasma, Chlamydia, Legionella, Bordetella, Haemophilus pneumonia, adenovirus, rhinovirus, coronavirus, influenza virus A and B, parainfluenza virus, respiratory syncytial virus A and B, bocavirus, metapneumovirus. The results were all negative. Additionally, the urine antigen and immunologic study were performed to exclude others pathogen. The results revealed the following: streptococcal pneumonia and Legionella urinary antigen, negative; Mycoplasma pneumoniae IgG/IgM, negative; and Chlamydia pneumoniae IgG (17.65, positive; normal range, <9 index), IgM (4.62, negative; normal range, <9 index). According to the cytology, the majority of the alveolar macrophages had a foamy appearance (Figure 2). To make a differential diagnosis of connective disease or allergic disease, immunologic studies and multiple allergosorbent test system (MAST) were performed as follow: all allergens of MAST, class 0 (0.00-0.34 IU/mL); rheumatoid factor, negative; C3 complement, 135.00 mg/dL (normal range, 90-180 mg/dL); C4 complement, 42.20 mg/dL (normal range, 10-40 mg/dL); anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies, negative.


A Case of Statin-Induced Interstitial Pneumonitis due to Rosuvastatin.

Kim SY, Kim SJ, Yoon D, Hong SW, Park S, Ock CY - Tuberc Respir Dis (Seoul) (2015)

(A-E) Chest radiography showed subtle diffuse ground glass opacity in both lower lobe field and subsegmental atelectasis in left lower lobe field on admission. A computed tomography scan of the chest showed diffuse ill-defined ground glass opacity with septal line thickening in bilateral lung fields combined with several subpleural ground glass opacity nodules on admission.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4499600&req=5

Figure 1: (A-E) Chest radiography showed subtle diffuse ground glass opacity in both lower lobe field and subsegmental atelectasis in left lower lobe field on admission. A computed tomography scan of the chest showed diffuse ill-defined ground glass opacity with septal line thickening in bilateral lung fields combined with several subpleural ground glass opacity nodules on admission.
Mentions: Upon admission, the patient's vital signs were as follows: blood pressure, 116/77 mm Hg; pulse, 114 beats per minute; respiratory rate, 26 breaths per minute; and body temperature, 36.9℃. On physical examination, a coarse breath sound with fine crackles but without wheezing was heard upon auscultation of both lungs. The patient's laboratory test results were as follows: hemoglobin, 14.1 g/dL; white blood cell count, 8,770 cells/µL (neutrophils, 62.6%; lymphocytes, 26.0%; monocytes, 7.2%; eosinophils, 3.9%; and basophils, 0.3%); and platelet count, 391,000 cells/µL. The patient's serum biochemistry test results revealed the following: aspartate aminotransferase, 35 IU/L; alanine aminotransferase, 35 IU/L; total bilirubin, 0.4 mg/dL; alkaline phosphatase, 311 IU/L; total protein, 7.6 g/dL; albumin, 4.0 g/dL; blood urea nitrogen, 26.0 mg/dL; creatinine, 0.84 mg/dL; total cholesterol, 106 mg/dL; C-reactive protein, 1.06 mg/dL; and LDL cholesterol, 56 mg/dL. His coagulation profile was within normal limits. A urinalysis with microscopy was clear. An arterial blood gas analysis of the fraction of inspired oxygen (FiO2) was conducted with the patient breathing room air and revealed the following: pH, 7.46; partial pressure of oxygen (PaO2), 54.6 mm Hg; partial pressure of carbon dioxide (PaCO2), 37.4 mm Hg; bicarbonate (HCO3-), 26.0 mEq/L; and saturation level of oxygen (SaO2), 85.9%. A chest radiograph showed a subtle, diffuse ground-glass opacity in both lower lung fields and subsegmental atelectasis in the left lower lobe. A chest computed tomography scan revealed diffuse ill-defined ground-glass opacities with septal line thickening bilaterally, combined with several subpleural ground-glass opacity nodules (Figure 1). A pulmonary function test revealed the following: forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio, 102; FEV1, 2.8 L (94%); FVC, 3.47 L (92%); and diffuse capacity for carbon monoxide (DLCO), 57%. Based on his past medical history, clinical symptoms, and laboratory findings, a diagnosis of DILD was suspected. Consequently, bronchoscopy with bronchoalveolar lavage (BAL) was performed. There were no endobronchial lesions revealed with bronchoscopy. The BAL fluid results were as follows: white blood cell count, 480 cells/µL (neutrophils, 9%; lymphocytes, 30%; macrophages, 57%; eosinophils, 4%; and basophils, 0%); and red blood cell count, 30 cells/µL. Microbiological culture and polymerase chain reaction of the bronchoscopic wash specimens were negative for Mycobacterium tuberculosis, pneumococcus and respiratory virus. The real-time polymerase chain reaction of bronchial washing specimens was performed as following: Mycoplasma, Chlamydia, Legionella, Bordetella, Haemophilus pneumonia, adenovirus, rhinovirus, coronavirus, influenza virus A and B, parainfluenza virus, respiratory syncytial virus A and B, bocavirus, metapneumovirus. The results were all negative. Additionally, the urine antigen and immunologic study were performed to exclude others pathogen. The results revealed the following: streptococcal pneumonia and Legionella urinary antigen, negative; Mycoplasma pneumoniae IgG/IgM, negative; and Chlamydia pneumoniae IgG (17.65, positive; normal range, <9 index), IgM (4.62, negative; normal range, <9 index). According to the cytology, the majority of the alveolar macrophages had a foamy appearance (Figure 2). To make a differential diagnosis of connective disease or allergic disease, immunologic studies and multiple allergosorbent test system (MAST) were performed as follow: all allergens of MAST, class 0 (0.00-0.34 IU/mL); rheumatoid factor, negative; C3 complement, 135.00 mg/dL (normal range, 90-180 mg/dL); C4 complement, 42.20 mg/dL (normal range, 10-40 mg/dL); anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies, negative.

Bottom Line: We suspected rosuvastatin-induced lung injury, discontinued rosuvastatin and initiated prednisolone 1 mg/kg tapered over 2weeks.After initiating steroid therapy, his symptoms and radiologic findings significantly improved.We suggest that clinicians should be aware of the potential for rosuvastatin-induced lung injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, The Armed Forces Medical Hospital, Seongnam, Korea.

ABSTRACT
Statins lower the hyperlipidemia and reduce the incidence of cardiovascular events and related mortality. A 60-year-old man who was diagnosed with a transient ischemic attack was started on acetyl-L-carnitine, cilostazol, and rosuvastatin. After rosuvastatin treatment for 4 weeks, the patient presented with sudden onset fever, cough, and dyspnea. His symptoms were aggravated despite empirical antibiotic treatment. All infectious pathogens were excluded based on results of culture and polymerase chain reaction of the bronchoscopic wash specimens. Chest radiography showed diffuse ground-glass opacities in both lungs, along with several subpleural ground-glass opacity nodules; and a foamy alveolar macrophage appearance was confirmed on bronchoalveolar lavage. We suspected rosuvastatin-induced lung injury, discontinued rosuvastatin and initiated prednisolone 1 mg/kg tapered over 2weeks. After initiating steroid therapy, his symptoms and radiologic findings significantly improved. We suggest that clinicians should be aware of the potential for rosuvastatin-induced lung injury.

No MeSH data available.


Related in: MedlinePlus