Objective The purpose of this study was to perform clinicopathological evaluations of patients with pure influenza A virus pneumonia. Methods We performed clinicopathological analyses of four cases of pure influenza A virus pneumonia. Patients Among the four cases, three were caused by the pandemic (H1N1) 2009 virus. Three patients were analyzed during autopsy, and one underwent transbronchial lung biopsy. Results We suggest that the interval between influenza virus A pneumonia onset and our analysis affected the pathological findings. Diffuse alveolar damage was observed during the acute phase. After ten days, organizing pneumonia and marked proliferation of premature type II alveolar epithelium were observed. Clinically, intra-alveolar hemorrhage was observed in two patients. Pathologically, hyaline membrane formation and intra-alveolar hemorrhage were observed in all cases. Conclusion Severe epithelial damage was determined as the main mechanism of respiratory failure caused by influenza A virus pneumonia.
Primary biliary cirrhosis is often associated with autoimmune diseases. However, an association between primary biliary cirrhosis and pernicious anemia has rarely been reported. We report a patient with primary biliary cirrhosis associated with pernicious anemia and autoimmune gastritis. The patient was a 64-year-old Japanese woman who had been diagnosed as having primary biliary cirrhosis 5 years previously. She was readmitted with jaundice and macrocytic anemia. The diagnosis of pernicious anemia was confirmed by the low level of serum vitamin B12 and the presence of anti-parietal cell antibody and anti-intrinsic factor antibody. Pernicious anemia should be regarded as a possible complication of primary biliary cirrhosis.
A 24-year-old female presented with fever and dry cough. Influenza A virus infection was suspected and the patient was treated with neuraminidase inhibitors. Five days after diagnosis, the patient developed persistent fever and dyspnea, and was diagnosed with severe pneumonia. Despite intensive treatment, the pneumonia worsened and the patient died 14 days after admission. At autopsy, a diffuse alveolar damage (DAD) pattern was observed. Immunohistochemical evaluation indicated severe epithelial damage, resulting in successive regeneration of alveolar type II cells followed by marked proliferation of smooth muscle cells and an increase of collagen fibers at the tip of alveolar orifices.
We present a case of a 78-year-old woman who visited our hospital for chronic atrial fibrillation. She consulted an orthopedic surgeon for lumbar pain in August 2009 and has been followed up for osteoporosis. However, her lumbar pain became exacerbated. In December 2009, clinical examination revealed that the pain was caused by tuberculous spondylitis and iliopsoas abscess. Diffuse miliary shadow, which was undetected earlier, was noted on chest roentgenogram; she was diagnosed with miliary tuberculosis. Lumbar pain is common in elderly individuals and should be regarded as one of the tuberculosis symptoms, considering its atypical course in elderly patients.
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