Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

We report a fatal case of toxic myopathy in a patient with a transplanted heart for severe ischemic coronary artery disease. He was on long-term cyclosporine, prednisone, and mycofenolate. Four months before the development of proximal muscle weakness, his simvastatin dose was doubled, and he was also started on colchicine for acute exacerbation of gout. He developed progressive muscle weakness leading to shortness of breath and hospitalization for respiratory failure. Colchicine and simvastatin were stopped on admission. He received high-dose methylprednisolone for continued muscle weakness while he was sedated with propofol. These changes led to a marked elevation of creatine kinase, peaking at 33,580 U/ml. The muscle biopsy revealed toxic vacuolization, mitochondrial damage, and no evidence of inflammation. Based on the timing of events, the combination of propofol, high-dose methylprednisolone, and cyclosporine have triggered rhabdomyolysis, which may have been facilitated by prior administration of colchicine and simvastatin.
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PMID:Fatal toxic myopathy attributed to propofol, methylprednisolone, and cyclosporine after prior exposure to colchicine and simvastatin. 1762 39

A 62-year-old white woman was admitted with shortness of breath, wheezing, and cough. While in the hospital a generalized pruritic skin rash developed on her trunk and upper and lower extremities. She did not have any fevers, chills, or night sweats. The patient was known to have chronic, difficult-to-control asthma despite being compliant with a treatment regimen consisting of inhaled albuterol, high-dose inhaled steroids, salmeterol, and montelukast. Her medical history was significant for hypertension and gout. She had no family history of asthma. The patient was a life-long nonsmoker and did not drink alcohol. During this hospitalization, she was started on prednisone 40 mg/d po in addition to her home medications.
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PMID:A 62-year-old women with persistent severe asthma, skin rash, and eosinophilia. 2509 63

Mufangji Decoction is a famous herbal formula from Synopsis of Golden Chamber. However,it is easy to be misunderstood due to so its unique compatability. The syndromes treated by Mufangji Decoction included the following aspects:(1) in terms of modern medicine,it could be used to treat acute and chronic heart failure,heart failure aggravated by lung infection,chronic obstructive pulmonary disease acute episode,pulmonary heart disease,bilateral pleural effusion,acute attack of gout,rheumatic fever,rheumatoid arthritis,and rheumatoid arthritis;(2) in terms of symptoms,it could be used to treat asthma,chest tightness,wheeze impacting prostration and dyspnea impacting sitting posture; gastric distention; dark face,cyanotic,and mitral valvular face; edema of head and extremities; dry mouth,thirsty,unwilling to wear thick clothes,intolerance of heat,and irritable; fatigue,shortness of breath,poor appetite,constipation,less urine,yellow color,poor response to diuretics,and diuretic resistance; fast heart rate,which is hard to be controlled by Western medicine and has no response to Zhenwu Decoction; dark red tongue,dry tongue with yellow fur,rapid pulse,or deep tight pulse. In emergency and severe cases,Yang deficiency and fluid retention are normal syndromes of heart failure,while Yang deficiency,fluid retention,and heat are metamorphic syndromes of heart failure,which possessed complex mechanisms of pathophysiology; the mechanisms of Shaoyin heat-conversion syndrome is similar to Yang deficiency,fluid retention,and heat syndrome; the reason of application of gypsum in Mufangji Decoction shall be further studied; the " empty" and " real" in modified Mufangji Decoction are physical signs,rather than pathogenesis.
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PMID:[Mufangji Decoction formula tracing and its effect on emergency and severe cases]. 3098 62