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    Home > Active Ingredient News > Immunology News > Repeated pleural effusion is not good, it may be caused by gout

    Repeated pleural effusion is not good, it may be caused by gout

    • Last Update: 2022-04-30
    • Source: Internet
    • Author: User
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    *For medical professionals only for reference significantly increased
    .

    The prevalence of hyperuricemia in different ethnic groups ranges from 2.
    6% to 36.
    0%, and the prevalence of gout ranges from 0.
    03% to 15.
    30%.
    In recent years, both of them have shown a marked increase and a younger trend [1]
    .

    Meta-analysis showed that the overall prevalence of hyperuricemia in China was 13.
    3%, and the overall prevalence of gout was 1.
    1%[2]
    .

    Gout is a disease that damages multiple organs in the whole body due to the disorder of purine metabolism and the increase of blood uric acid (SUA).
    The most common damaged organs are the joints, kidneys, heart and vascular system.
    Disease cases [3-5]
    .

    An 83-year-old man suffers from gout attacks and pleural effusion all the year round.
    So what is the relationship between these two diseases? Let's unravel the mystery of both! Case Introduction An 83-year-old man had red, swollen, and severe pain in both hallucinations, knee joints and back of foot 10 years ago, with more than 10 repeated and alternate attacks, 3 of which were due to acute arthritis attacks accompanied by shortness of breath, Cough, chest X-rays were taken in the local hospital, and left pleural effusion was found in all cases.
    All patients were discharged after thoracentesis with symptom relief, but no clear diagnosis was made
    .

     Recently, the patient was admitted to the hospital again due to shortness of breath and pain in the left big toe
    .

    After admission, chest CT showed a large amount of pleural effusion on the left side (Figure A).
    The X-ray films of both feet showed honeycomb-shaped defect areas of the first metatarsal phalanges on both sides, and the SUA was 902 μmol/L
    .

    Thoracentesis can draw out pale yellow liquid with a specific gravity of 1.
    018, Li Fanta test (±)
    .

    Since the diagnosis is still unclear, it is recommended that the patient undergo thoracoscopy and related pathological examinations to clarify the condition
    .

    Figure A What diseases need to be differentially diagnosed on chest CT? There are many reasons for the occurrence of pleural effusion, among which the common clinical ones are pneumonia-like pleural effusion, tuberculous pleurisy, malignant pleural effusion and congestive heart failure
    .

    Identifying the cause of pleural effusion by thoracoscopy and pleural effusion culture can help in clinical diagnosis! (1) Pneumonic pleural effusion: patients often have symptoms such as fever, cough and expectoration, chest pain, shortness of breath, etc.
    , blood routine, procalcitonin (PCT) and other infectious indicators are elevated, and chest X-ray first has lung parenchyma infiltration Shadow or lung abscess, bronchiectasis and other manifestations
    .

    Subsequently, pleural effusion occurs.
    The amount of effusion is generally small and it is exudate.
    The common pathogens are Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, etc.
    , and are often combined with anaerobic infection, pleural effusion smear, bacterial culture, etc.
    Helps to identify pathogenic bacteria
    .

     The relevant test results of the patient indicated: hemoglobin 110g/L, leukocyte 4×109/L, erythrocyte sedimentation rate 35mm/h, low leukocyte and inflammatory indexes, no cough, expectoration, fever and other symptoms, and a large amount of pleural effusion, pleural effusion Smears and bacterial cultures did not suggest pathogenic infection
    .

     (2) Tuberculous pleurisy: It is the most common cause of exudate in China, and it is more common in young adults.
    It usually has symptoms of chest pain, shortness of breath, and often accompanied by symptoms of tuberculosis poisoning
    .

    Pleural effusion is mainly lymphocytes, mesothelial cells are less than 5%, protein is more than 40g/L, ADA and gamma interferon are increased, pleural effusion can be positive for Mycobacterium tuberculosis, and PPD is strongly positive.
    Pleural biopsy can improve the diagnostic rate
    .

     The attending physician also thought about the possibility of tuberculous pleurisy, asked the patient about the condition, and learned that there was no history of tuberculosis and no symptoms of tuberculosis poisoning.
    Both were negative
    .

    Therefore, tuberculous pleurisy was excluded
    .

     (3) Malignant pleural effusion: mostly secondary to lung cancer, breast cancer, lymphoma, etc.
    , which directly invade or metastasize to the pleura, as well as malignant pleural mesothelioma, which is more common in middle-aged and elderly people, and patients often feel dull chest pain accompanied by hemoptysis , weight loss and other symptoms
    .

    Pleural effusion is mostly bloody, large in volume, and rapidly growing, carcinoembryonic antigen (CEA) > 20μg/L or pleural effusion/serum CEA > 1, lactate dehydrogenase (LDH) > 500U/L, exfoliative cytology, pleural biopsy, etc.
    aids in diagnosis
    .

     No abnormality was found in the patient's tumor markers, no weight loss, hemoptysis and other symptoms, pleural effusion was pale yellow liquid, CEA in pleural effusion was 5 μg/L, pleural effusion/serum CEA<1, LDH was 105U/L, exfoliative cytology, pleural effusion No cancer cells were found in the biopsy
    .

     (4) Congestive heart failure: It is a common cause of fluid leakage.
    Most of the patients have basic heart diseases such as hypertension, coronary heart disease, and rheumatic heart disease, which may be combined with signs such as enlarged cardiac boundary and heart murmur
    .

    Chest X-ray shows signs of heart enlargement and pulmonary congestion.
    Most of the pleural effusion is bilateral, but the right side is often more than the left side.
    Serum brain natriuretic peptide and echocardiography can assist in the diagnosis
    .

     The patient had a history of hypertension in the past, but echocardiography showed no significant expansion of cardiac chambers, no bilateral pulmonary congestion on chest X-ray, and pleural effusion occurred many times on the left side
    .

    The brain natriuretic peptide was 700pg/ml, and congestive heart failure was not considered for the time being
    .

     Finally, the patient underwent thoracoscopy (VATS) to confirm the condition
    .

    Intraoperative VATS findings: white deposits on the left pleura (Figure B)
    .

    Microscopic examination revealed a large number of needle-like uric acid crystals (Figure C)
    .

    Pathological results were diagnosed as gouty lung damage
    .

     Figure B, C VAST examination combined with the patient's symptoms, blood uric acid results, pathological results, the final diagnosis of gouty lung damage
    .

    Why does gout still affect the lungs? After the level of SUA increases, sodium urate (MsU) precipitates in the tissue, resulting in pathological changes in the tissue
    .

    The MsU crystals formed by precipitation are deposited in a large amount in tissues and organs such as joints, kidneys, hearts and blood vessels, and become the main factor of pathogenesis
    .

    Under certain incentives, such as injury, local temperature and pH reduction, or fatigue, alcoholism, etc.
    , crystallization is easy to precipitate
    .

    When MsU crystals are deposited in the alveoli and bronchi, they may form calculi, which are easily penetrated by X-rays, so chest X-ray films often do not show calculi shadows
    .

    The MsU crystals precipitated from lung tissue and pleura carry a negative charge, while the IgG in the globulin in the body fluid has a positive charge.
    The two have strong affinity and can quickly combine into MsU-IgG, becoming a special class of antigens
    .

    This antigen MsU-IgG can be phagocytosed by inflammatory cells, and the phagocytosed inflammatory cells can release inflammatory cell chemokines, which can promote unidirectional migration of inflammatory cells to the lung or pleura
    .

    Under the action of various factors, a large number of aggregated inflammatory cells are continuously disintegrated and broken, releasing chemical mediators and cytokines such as interleukins, prostaglandins, tumor necrosis factors, thrombosis-activating factors and polypeptides
    .

    These mediators and cytokines can dilate blood vessels and promote vascular leakage, tissue edema, inflammatory cell infiltration, proliferation of collagen fibers and smooth muscle fibers, etc.
    , which further lead to the formation of pulmonary fibrosis and pleural effusion [6]
    .

    How to diagnose gouty lung damage clinically? The clinical diagnosis of gout patients with pulmonary symptoms is difficult.
    Usually, patients who have been diagnosed with gout have various abnormal symptoms and signs of the respiratory system, and when chest imaging examination finds corresponding abnormal lung and pleural manifestations, the clinician should Pulmonary complications of gout should be considered, but other pulmonary complications should be strictly excluded
    .

    Some scholars believe that there are two main diagnostic criteria for gout lung damage: ① It is confirmed that gout exists; ② When there is lung damage and no other cause can be found, if it can be found in pleural effusion, sputum smear and lung stone test MsU crystallization, that is, the diagnosis can be established [7]
    .

    In the later stage of disease follow-up, the patient underwent thoracentesis in time, and at the same time received colchicine, allopurinol and other uric acid-lowering treatments, the symptoms were relieved and discharged
    .

    After discharge, the patient was instructed to have a low-purine diet and continued taking allopurinol.
    During the 2-year follow-up period, the blood uric acid was close to normal, and pleural effusion did not recur
    .

    The diagnosis of this case is a bit interesting.
    The patient has repeated pleural effusion, which may be the initial manifestation of gout! With the long-term misdiagnosis and mistreatment of gout leading to the delay of uric acid-lowering treatment, SUA continues to rise, which may lead to the occurrence and development of various complications
    .

    With the change of diet structure in our country, the intake of protein-rich foods and high-energy foods increases, and the factors that cause this disease exist, so that gout and its complications will continue to increase
    .

    Therefore, when the cause of the patient's lung disease cannot be found, it is necessary to consider whether there are causative factors of gout
    .

    When urate crystals can be found in the pleura or pleural effusion, clinicians can consider the diagnosis of gouty lung damage
    .

     References: [1]Dehlin M, Jacobsson L, Roddy E.
    Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors.
    Nat Rev Rheumatol, 2020,16(7):380-390.
    [2]Liu R , Han C, et al.
    Prevalence of Hyperuricemia and Gout in Mainland from 2000 to 2014: A Systematic Review and Meta-Analysis.
    Biomed Res Int, 2015,2015:762820.
    [3] Zhang Kaifu, Zhao Congxin, Zhang Liqun.
    Gout with thoracic cavity Two cases of effusion.
    Chinese Journal of Tuberculosis and Respiratory Medicine, 1995,(02):124.
    [4]Liu Dazheng, Xue Zhenying.
    One case of gout complicated with pleural effusion.
    Zhejiang Medicine, 1995,(03):16.
    [5]Yan Hongying , Mao Wenli.
    Clinical analysis of 12 cases of gout complicated with pulmonary damage.
    Journal of South China University (Medical Edition), 2001,(05):514-515.
    [6] Zhang Kaifu, Liu Lan, Han Youqin.
    Pulmonary complications of gout.
    Zhonghua Journal of Tuberculosis and Respiratory Medicine, 2000,(06):40-41+65.
    [7]Zou Ling.
    A case report of gout-induced lung disease in the elderly.
    Chinese Community Physician, 2005,(01):47.
    [8]Zhong Nanshan, Liu Youning Respiratory Medicine (2nd Edition) [M].
    2012: 798-800.
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