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)

The authors revealed heart failure in 7 of 216 patients with gout. Two of them showed isolated mitral valve insufficiency and two patients aortal insufficiency while combined aortal disease, combination of mitral and aortal insufficiency and combined mitral valve disease with aortal insufficiency occurred each in 1 patient. One could not find distinct dependence between the clinical variant of the course of gout and development of a definite heart failure. Clinical and electrocardiographic signs of the revealed kinds of cardiac abnormalities are described. The morphological changes of the valves are described on the basis of 2 autopsy cases. The possible mechanism of development of podagric heart failures is discussed.
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PMID:[Gouty heart defects]. 208 May 68

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

A 60-year-old African American man with end stage renal disease on hemodialysis (HD) for the past 2.5 years developed severe hyperparathyroidism. Other past medical history included atrial fibrillation, type II diabetes mellitus, hypertension, gout, pericardial effusion needing pericardial window, deep vein thrombosis, mitral insufficiency, and cardiomyopathy with implantable cardioversion device placement. His parathyroid hormone (PTH) level peaked at 4,191 pg/mL despite being on cinacalcet, sevelamer, and paricalcitol. He underwent a subtotal parathyroidectomy in January 2015, after which his PTH levels dropped to 184 pg/mL. Approximately 4 weeks later he developed extensive, painful necrotic skin lesions in both his lower extremities and buttocks, suggestive of calciphylaxis which was confirmed by tissue biopsy. The patient was treated with elaborate wound care, wound debridements, increased dialysis dose, and IV sodium thiosulfate (STS) during hemodialysis. Besides STS, he was treated with narcotics, gabapentin, topical lidocaine on intact skin, and oral steroids for pain control. Even though his lesions improved initially, he deteriorated due to recurrent sepsis, respiratory failure, and prolonged hospitalization which culminated in stopping dialysis before he passed away. Calciphylaxis, or calcific uremic arteriolopathy, is a life-threatening complication of end stage renal disease. Treatment of this condition is multidisciplinary which includes elaborate wound care, increasing dialysis dose, and discontinuing vitamin D supplements and calcium containing phosphate binders. Even though STS has been recommended off-label, several studies have shown promising results with resolution of lesions. Thus, sodium thiosulfate has become the mainstay of treatment. Parathyroidectomy is a recommended modality of treatment in those with high PTH levels. Our case was unique in that calciphylaxis developed after subtotal parathyroidectomy. We believe that this is due to a decreased PTH level and decreasing bone turnover which resulted in more circulating calcium facilitating vascular and soft tissue calcification. The exact mechanism of developing calciphylaxis after parathyroidectomy is unknown. Even though parathyroidectomy is an effective treatment for calciphylaxis, clinicians should be aware that it can rarely present after parathyroidectomy.
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PMID:Calciphylaxis after parathyroidectomy. 2906 76