A case of tuberculosis pleuritis developing contralateral pleural effusion during anti-tuberculosis chemotherapy,falling into chronic respiratory failure

The patient was a 74 year-old male presenting right pleural effusion with mild fever. His temperature was 37.0 degrees C. Culture of a pleural biopsy specimen revealed Mycobacterium tuberculosis, although culture of sputum and pleural effusion were negative. Therapy was begun with 300 mg of isoniazid (INH) per day, 600 mg of rifampicin (RFP) per day, and 1200 mg of pyrazinamide (PZA) per day. His temperature improved temporarily. One week after beginning of the therapy he had a fever over 38.0 degrees C. On the 17th day after starting chemotherapy, a chest radiological examination showed left pleural effusion in which numerous lymphocytes were found but Mycobacterium tuberculosis was negative. We assumed that the left pleural effusion was due to a paradoxical reaction to the anti-tuberculosis chemotherapy. After 3 days' discontinuation, the same regimen was resumed with an addition of prednisolone, but bilateral pleural effusion remained and the case finally fell into chronic respiratory failure.     

A case of CD56 positive T-cell lymphoma originating from mediastinal lymph nodes]

The patient, a 63-year-old man was admitted to our hospital with complaints of high-grade fever and left chest pain. The chest X-ray film taken on admission showed the presence of pleural effusion. The chest CT scan revealed left mediastinal enlargement. Examination of the pleural effusion showed a high concentration of adenosine deaminase (ADA) and the cytological examination showed no malignancy. We diagnosed pleuritis tuberculosa. His general condition worsened in spite of anti-tuberculosis therapy and soluble interleukin-2 receptor (sIL-2R) was elevated. The video-assisted thoracoscopic biopsy was negative. Soon after that the lymph nodes from the left supraclavicular region to the mediastinum became swollen. The diagnosis of peripheral T-cell lymphoma, unspecified (WHO classification) with CD56 expression, was established based on the results of lymph node biopsy and pleural effusion cytology. He was treated with cyclophosphamide/doxorubicin/vincristine/prednisolone (CHOP) chemotherapy. Since two courses of chemotherapy were not effective we changed to carboplatin/ifosfamide/ etoposide/dexamethasone (DeVIC) chemotherapy. His condition improved and a complete response was obtained. In conclusion, the presence of a high level of ADA in the pleural effusion and resistance to anti-tuberculosis therapy should suggest a malignant lymphoma.     

A case of anaphylactoid purpura associated with tuberculous pleuritis

A 46-year-old man was admitted to Shin-Kokura Hospital because of fever and right chest pain. Laboratory studies showed mild leukocytosis, an increased erythrocyte sediment rate, positive C-reactive protein, and abnormal liver function. The tuberculin skin test was positive. A chest X-ray showed massive right pleural effusion, and exudative pleural effusion fluid was obtained by thoracocentesis. The pleural fluid revealed an increased adenosine deaminase concentration and cultures were negative for mycobacteria. A polymerase chain reaction test of the pleural effusion for Mycobacterium tuberculosis was positive. The patient was diagnosed with tuberculous pleuritis, and antitubercular therapy was started. The fever and chest pain was improved, but rashes appeared on the lower extremities. A biopsy of the skin lesion showed anaphylactoid purpura. Steroid ointment improved the skin lesion. Anaphylactoid purpura associated with tuberculosis is rare. The immunological response to mycobacteria may heve been related to the mechanism of the anaphylactoid purpura in this case.     

A case of post-traumatic bilateral eosinophilic pleural effusion]

A 58-year-old man was admitted to our hospital with chest pain caused by chest trauma. After admission, his chest pain decreased and he was discharged. Later, he was admitted again with a high fever and dyspnea. Laboratory findings on second admission showed a leukocyte count of 7,900/microliter (9% eosinophils) and a C-reactive protein of 17.0 mg/dl. Chest radiography and chest CT scanning on second admission showed moderate bilateral pleural effusion. Close examination showed an increase of eosinophils in the pleural effusion (14% of total cell counts on the right and 27% of total cell counts on the left) that was exudate. Post-traumatic bilateral eosinophilic pleural effusion was diagnosed. The patient was treated with antibiotic therapy and his condition improved. A chest CT scan afterwards showed improvement of the bilateral pleural effusion. The eosinophil count in the peripheral blood was 1% at chest trauma, 15% in the hospital to the max and decreased to 3% with the decrease of pleural effusion. Post-traumatic eosinophilic pleural effusion may be accompanied with inflammatory findings, and the mechanism is guessed by immunological reaction.     

Pulmonary dirofilariasis with cavity formation and pleural effusion]

A 61-year-old man visited a community hospital because of hemosputum. A solitary nodule in the left lower lung field was pointed out on a chest roentgenogram. The patient was treated with antibiotics, but the solitary nodule increased in size. He was referred to our hospital because of high fever and observations of cavity formation and pleural effusion on a chest roentgenogram. The pleural effusion showed no cytologic evidence of malignancy, and cultures were also negative for bacteria. An increased percentage of lymphocytes was detected in the pleural effusion, but slight eosinophilia was found in blood samples. Dot enzyme-linked immunosorbent assay and Ouchterlony's double-diffusion test yielded a diagnosis of pulmonary dirofilariasis. After drainage of the pleural effusion by thoracentesis, spontaneous regression was observed. Cavity formation, pleural effusion, and spontaneous regression are in general rare in patients with pulmonary dirofilariasis.     

A case of tuberculous pleurisy developing contralateral effusion during anti-tuberculosis chemotherapy

A 55-year-old woman was admitted to our hospital because of chest pain, fever, and right pleural effusion that was exudative and lymphocyte-dominant with a high level of adenosine deaminase (ADA). Since her blood QuantiFERON-TB 3G test (QFT) was positive, she was diagnosed with tuberculous pleurisy. After initiation of anti-tuberculosis chemotherapy with isoniazid, rifampicin, ethambutol, and pyrazinamide, her symptoms improved. Later, liquid culture of the pleural effusion turned positive for Mycobacterium tuberculosis. On the 18th day of treatment, her chest X-ray and computed tomography exhibited pleural effusion in a moderate amount in the left thorax, with subsiding pleural effusion in the right thorax. Thoracocentesis demonstrated that the left thorax effusion was also exudative and lymphocyte-dominant, with elevated QFT response and high ADA concentration, suggesting tuberculous pleurisy. Mycobacterium tuberculosis was detected in the culture of a left pleural biopsy specimen obtained by thoracoscopy. We assumed that the left pleural effusion was due to paradoxical worsening because (1) on admission no effusion or lung parenchymal lesion was detected in the left hemithorax, (2) on the 14th day of treatment she was afebrile without pleural effusion on both sides, and (3) the bacilli were sensitive to the drugs she had been taking regularly. We performed drainage of the left effusion and continued the same anti-tuberculosis drugs, which led to the elimination of all her symptoms and of the pleural effusion on both sides. In conclusion, paradoxical worsening should be included in the differential diagnosis when contralateral pleural effusion is detected during the treatment of tuberculosis.     

Myeloid Sarcoma: An Unusual Case of Mediastinal Mass and Malignant Pleural Effusion with Review of Literature

Myeloid sarcoma is an extramedullary tumor seen most commonly in patients with acute myeloid leukemia and less frequently in chronic myeloid leukemia, myelodysplastic syndrome and rarely, in an isolated form without any other underlying malignancy. Malignant pleural effusion in hematological malignancies is rare when compared with solid tumors. We present an unusual case of myeloid sarcoma in which a mediastinal mass with pleural effusion was the initial presentation. A 27 year old gentleman presented with complaints of fever, chest pain and swelling in the anterior chest wall for 6 months. Examination revealed a lump measuring 5 × 5 cm on the left side of the chest wall. Hematological evaluation showed hemoglobin-14.2 g/dL, platelet count-233 × 10⁹/L, TLC-117 × 10⁶/L with normal differential counts. Contrast enhanced computerised tomography (CECT) confirmed the presence of a soft tissue mass in the superior mediastinum abutting against the chest wall. Core biopsy was suggestive of myeloid sarcoma and immunohistochemistry was positive for myeloperoxidase and negative for CD3, CD 20 and CD 23. Pleural fluid analysis showed the presence of malignant cells. Bone marrow examination did not show an excess of blasts. A final diagnosis of extramedullary myeloid sarcoma with malignant pleural effusion was made. The patient was given induction chemotherapy (3 + 7 regimen) with daunorubicin and cytosine arabinoside. Repeat CECT done on day 28 showed complete resolution of pleural effusion and significant reduction in the size of mediastinal mass. The patient has successfully completed three cycles of consolidation therapy following which there has been complete resolution of the mass. He remains asymptomatic on close follow up.     

A case of intrathoracic extension of retroperitoneal fibrosis]

A 70-year-old man was diagnosed as having retroperitoneal fibrosis 12 years ago. The patient was admitted to our hospital with complaints of fever and left chest pain. On admission, chest radiography revealed left pleural effusion and left pleural thickening. Percutaneous pleural biopsy was performed, and the pleural tissue gave a chronic inflammatory reaction characterized by proliferation of collagen fibers and chronic inflammatory cellular infiltration. Since the retroperitoneal fibrosis had been diagnosed in similar tissue, it was considered that this condition had extended to the pleura. On administration of prednisolone, the intrathoracic lesions and clinical symptoms were improved, but the patient later died of pneumonia. Autopsy showed fibrous pleuritis and chronic fibrosing lung disease. This was an extremely rare case. Prednisolone appears to be useful in the treatment of intrathoracic extension of retroperitoneal fibrosis.     

急性嗜酸粒细胞性肺炎1例并文献复习

目的 探讨急性嗜酸性粒细胞肺炎的临床表现、诊断、治疗方法及预后.方法 结合我院收治的1例急性嗜酸粒细胞性肺炎的临床资料及国内外文献报道的病例进行综合分析.结果 患者18岁,青年男性,咳嗽、咯痰10余天,胸闷、胸痛8 d,加重伴发热4 d入院.胸部CT示双肺炎,双侧胸腔积液,抗感染治疗无效,病情进行性加重,胸水中找到嗜酸...     

Childhood Ki-1 lymphoma complicated with multiple bone destruction

A 4-year-old girl was admitted because of fever, swelling of left chest wall and left axillary lymphadenopathy. Chest XP revealed left pleural effusion. Ga-scintigram showed multiple accumulation in skull, left ribs and iliac bone. A diagnosis of childhood Ki-1 lymphoma was made from the pathological findings of tumor in the skull. Immunopathological study revealed that the neoplastic cells were CD8 positive (suppressor phenotype).     

Primary amyloidosis with pulmonary involvement which presented exudative pleural effusion and high fever

We describe here an extremely rare case of primary amyloidosis which presented moderate pleural effusion and high fever. A 71-year-old man was admitted to our hospital because of exertional dyspnea, fatigue and fever. A chest X-ray showed right-sided moderate pleural effusion. A thoracocentesis revealed an exudative pleural effusion. Cytology and cultures of the effusion were negative. External drainage failed to control the effusion. To determine the etiology of the effusion and fever, bronchoscopy was performed. Biopsies of the tracheal wall showed amyloid deposition. The pleural effusion might have been due to the inflammation and the disturbed lymphatic drainage caused by the amyloid deposition. Treatment with melphalan (6 mg) and prednisolone (35 mg) for 4 days every 6 weeks decreased the fever and alleviated his symptoms.     

Painless left hemorrhagic pleural effusion: an unusual presentation of leaking saccular aortic arch aneurysm

Most thoracic aortic aneurysms are asymptomatic and are detected by chance on routine chest imaging for some other reasons. Only rarely it is symptomatic due to leak and dissection which is a potentially life threatening event that commonly presents with severe pain. In this report, we present the case of a 67-year-old man who presented with shortness of breath, intermittent cough, fever, and left sided painless hemorrhagic pleural effusion. Further investigation by plain radiography, computed tomography and magnetic resonance imaging revealed a saccular aneurysm arising from the lateral aspect of the mid-transverse arch of the aorta, along with a dissecting descending aortic aneurysm with false lumen communicating with left pleural space. The patient refused any surgical procedure and was treated conservatively with blood transfusions and anti hypertensive medication. On the 8th day patient finally succumb to a fatal episode of shock. We suggest dissecting thoracic aneurysm be included in the differential diagnosis of non-traumatic hemorrhagic pleural effusion in an elderly patient presenting with dysnea, cough and fever, which otherwise suggest the clinical diagnosis of bronchogenic carcinoma. Computed tomography of the chest should be immediately performed as the diagnostic procedure of choice.     

Churg-Strauss Syndrome with pleural involvement

A 51-year-old Japanese man with Churg-Strauss Syndrome (CSS) diagnosed by pleural biopsy is described. He was hospitalized because of high fever and bilateral knee, elbow and shoulder joint pain. Chest roentgenogram and chest computed tomography (CT) scan revealed bilateral massive pleural effusion. Pleural biopsy revealed eosinophilic infiltration and necrotizing granulomas. He was treated with oral prednisolone and his symptoms improved. This is the first report of CSS diagnosed by pleural biopsy.     

A case of limited Wegener granulomatosis with hypereosinophilia]

A 51-year-old female was admitted to Nagano Matsushiro General Hospital because of fever, cough and dyspnea on exertion. Her laboratory data revealed leukocytosis with hypereosinophilia, a high erythrocyte sedimentation rate and c-reactive protein. Chest radiography revealed an infiltration shadow with a cavity in the right upper lobe. A lung abscess was diagnosed and antibiotics were administered. Laboratory results showed improvement, but chest radiography continued to show cavities. She was admitted to our hospital because of fever, left pleural effusion and progression of cavities on chest radiographs. She showed no abnormalities of the upper airway or kidney, and was negative for c-antineutrophil cytoplasmic antibody (c-ANCA). Because a positive c-ANCA was seen on day 8 of hospitalization, L-type limited Wegener granulomatosis (WG) was diagnosed according to Gross et al. Prednisolone (PSL) was administered, which improved the anemia, eosinophilia and the cavities. On day 7 of PSL administration, of the left pneumothorax occurred as a complication caused by perforation of the left chest cavity, but her clinical course was good after a cavernectomy was performed. Some studies have reported that limited WG shows a negative c-ANCA, and that antibiotic therapy improves inflammation. The L-type of limited WG revealed a low-grade positive ratio and titer of c-ANCA. Moreover, L-type limited WG responds well to therapy. We therefore selected PSL administration only against L-type limited WG. We have reported L-type limited WG with eosinophilia and the negative effects of c-ANCA at an early clinical stage.     

Necrotizing pneumonitis and empyema caused by Streptococcus cremoris from milk

A 24-year-old heterosexual male, HIV-infected intravenous drug addict, with necrotizing pneumonitis and empyema due to Streptococcus cremoris is presented. The patient had fever, severe dyspnea and chest pain. Chest roentgenogram demonstrated pleural effusion on the left side. A thoracocentesis revealed purulent exudate and S. cremoris was isolated. Fever and pleural effusion disappeared with penicillin and clindamycin therapy. The most likely source of the infection was ingestion of unpasteurized milk and cheese.     

Acute pneumonia and empyema caused by Mycobacterium intracellulare

Nontuberculous mycobacterial infection is rarely accompanied by pleural involvement. We report a very rare case of M. intracellulare pulmonary disease with pleural empyema. A 56-year-old man was admitted to our hospital because of fever, purulent sputum and pleuritic chest pain. A chest radiograph and CT revealed pneumonic consolidation in the left lower lobe and loculated hydropneumothorax. The sputum smear was positive for acid fast bacilli. The aspirated pleural fluid was grossly purulent and the smear of the pleural effusion was also positive for acid fast bacilli. M. intracellulare was identified by culture and PCR from sputum and pleural fluid specimens. The patient improved with percutaneous tube drainage of the purulent effusion and antibiotic treatment including clarithromycin, rifampicin, ethambutol and streptomycin.     

Pleural effusion: a rare manifestation of acute pulmonary blastomycosis

A 47-year-old woman presented with cough, pleuritic chest pain and fever of three weeks duration. Although the patient lived in an area where blastomycosis is endemic, this diagnosis was not initially considered owing to the presence of consolidation and a large pleural effusion on the initial chest roentgenogram. Cultures of sputa, bronchial washings and pleural fluid documented the presence of pleuropulmonary infection with Blastomyces dermatitidis. Therapy with amphotericin B was associated with rapid clinical, roentgenographic and bacteriologic resolution of both pleural and parenchymal lung disease.     

Pleural effusion due to Histoplasma capsulatum and idiopathic CD4 lymphocytopenia

Acute histoplasmosis is usually a benign, self-limited infection in endemic areas. Since protection against Histoplasma capsulatum infection requires specific, cell-mediated immunity, histoplasmosis is well documented in patients with acquired T cell deficiencies e.g. due to HIV infection. We report here for the first time a case of pleural effusion due to H. capsulatum infection in a patient with idiopathic CD4 lymphocytopenia (ICL). A 25-year-old woman presented with chest pain, dyspnea on exertion and a moderate weight loss. Chest X-ray showed a large left pleural effusion, and thoracentesis yielded an exudate. Histologic examination of pleural biopsies identified H. capsulatum. Laboratory tests revealed lymphocytopenia with low CD4+ T cell counts (<100/microl) and a decreased CD4/CD8 ratio. Serology, including HIV, was repeatedly negative. The diagnosis of pleural effusion due to H. capsulatum infection in a patient with idiophatic ICL was established. There was no evidence of any other opportunistic infection. Treatment with itraconazole was initiated and pleural effusion resolved within 2 weeks of treatment. Moreover, the patient was found to have idiopathic thrombocytopenic purpura, as confirmed by the detection of autoantibodies against thrombocytes. In a 1-year follow-up, the patient remained asymptomatic without relapse or any new infection. Treatment with itraconazole was given for 12 months. Because of persistent CD4+ T cell counts below 100/microl, prophylactic antibiotic treatment is continued.     

A case of hypereosinophilic syndrome associated with pulmonary infarction and hepatic vein obstruction (Budd-Chiari syndrome)

A 21-year-old man was admitted in March 1987 with low grade fever and chest pain. Eosinophilia had been pointed out and PIE syndrome was diagnosed in another hospital a month before admission. Steroid therapy had been started. On the first admission, the chest roentgenogram showed bilateral pleural effusion and a nodular shadow in the left lower lung field. Open lung biopsy was performed and a diagnosis of pulmonary infarction was made. Eosinophilia, low grade fever and chest pain were improved by steroid therapy. He was discharged in April 1987. He was readmitted in September 1987 because of fever, back pain and abdominal distension. On the second admission, eosinophilia (4,510/mm3) was pointed out. The case was diagnosed as hepatic vein obstruction by hepatic vein angiography, liver biopsy and ultrasonic examination. He had transient remission on corticosteroid and anti-coagulant therapy. This case was considered as a rare case of hypereosinophilic syndrome associated with pulmonary infarction and Budd-Chiari syndrome.     

Unexplained in-hospital fever following cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo.

In Part I of this study, the in-hospital course of 219 patients who had undergone a cardiac operation is analyzed. Fever (greater than or equal to 37.8 degrees C, rectal) was present after postoperative day 6 in 159 patients (73%) and was of unexplained cause in 118. Fever decay in the population of unexplained fever patients was exponential. All patients with unexplained postoperative fever were afebrile by postoperative day 19. In-hospital pericardial rub and pleuritic chest pain, widening of the mediastinum on chest film, and pleural effusion were not specifically associated with unexplained postoperative fever. In Part II, 67 patients with unexplained postoperative fever were given indomethacin (100 mg per day) or placebo for 7 days by a randomized, double-blind protocol. Indomethacin resulted in a shorter duration of fever (2.4 vs 3.5 days, P is less than 0.01) and in a shorter duration of chest pain, malaise, and myalgias compared to placebo. Sixty-seven percent of the patients in Part I and all of the patients in Part II were contacted 2-8 months following hospital discharge. Five percent had experienced an illness that we considered to be acute pericarditis, but its occurrence was unrelated to whether the patient had had in-hospital unexplained postoperative fever, in-hospital rub or chest pain, or in-hospital administration of indomethacin.