Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 70-year-old man with uremia was referred because of hemoptysis. A chest X-ray showed diffuse infiltration in the right lung field. Laboratory data were remarkable for renal failure, anemia, and thrombocytopenia. Furthermore, laboratory evidence of microangiopathic hemolytic anemia was present. A kidney biopsy revealed diffuse crescentic glomerulonephritis with linear staining of IgA along the glomerular basement membrane (GBM). No thrombotic microangiopathy was noted on renal biopsy. Circulating IgG anti-GBM antibody was not detected, and IgA anti-GBM antibody was not tested. The patient was treated with plasmapheresis and pulse steroid therapy, which resulted in an immediate improvement in the pulmonary hemorrhage and hematological abnormalities. However, the patient did not regain renal function and remained on hemodialysis.
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PMID:IgA variant of anti-glomerular basement membrane glomerulonephritis associated with pulmonary hemorrhage and microangiopathic hemolytic anemia. 2240 99

Anti-glomerular basement membrane (GBM) disease is mediated by circulating autoantibodies, principally IgG, targeted at the type IV collagen of GBM. The IgA variant of anti-GBM disease has rarely been described. We report a 65-year-old man with uremia, undergoing hemodialysis, who was referred because of hemoptysis. A chest X-ray showed diffuse infiltration in the right lung field. Laboratory data were remarkable for renal failure, anemia, and thrombocytopenia. Furthermore, laboratory evidence of microangiopathic hemolytic anemia was present. A kidney biopsy revealed diffuse crescentic glomerulonephritis. Circulating IgA anti-GBM antibody was found, as well as the presence of significant IgA deposition in a linear pattern along the GBM, suggesting an anti-GBM antibody-mediated disease. The patient was treated with plasmapheresis and pulse steroid therapy, which resulted in an immediate improvement in the pulmonary hemorrhage and hematological abnormalities. However, the patient did not regain renal function and remained on hemodialysis.
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PMID:An unusual case of IgA-mediated anti-glomerular basement membrane disease. 2245 64

The various types of glomerulonephritis, including many forms of vasculitis, are responsible for about 15% of cases of end-stage renal disease (ESRD). Arterial hypertension represents a frequent finding in patients suffering from glomerulonephritis or vasculitis and hypertension also serves as an indicator for these severe types of diseases. In addition, there are symptoms and signs like hematuria, proteinuria and renal failure. Especially, rapidly progressive glomerulonephritis (RPGN) constitutes a medical emergency and must not be missed by treating physicians. This disease can either occur limited to the kidneys or in the context of a systemic inflammatory disorder, like a vasculitis. If left untreated, RPGN can lead to a necrotizing destruction of glomeruli causing irreversible kidney damage within several months or even weeks. With respect to the immunologically caused vasculitis, there are - depending upon the severity and type of organ involved - many clinical warning signs to be recognized, such as arterial hypertension, hemoptysis, arthalgias, muscle pain, palpable purpura, hematuria, proteinuria and renal failure. In addition, constitutional signs, such as fever and loss of body weight may occur concurrently. Investigations of glomerulonephritis or vasculitis must contain a careful and complete examination of family history and medications used by the respective patient. Thereafter, a thorough clinical examination must follow, including skin, joints and measurement of arterial blood pressure. In addition, a spectrum of laboratory analyses is required in blood, such as full blood screen, erythrocyte sedimentation rate, CRP, creatinine, urea and glucose, and in urine, including urinalysis looking for hematuria, red cell casts and proteinuria. Importantly, proteinuria needs to be quantified by the utilization of a random urine sample. Proteinuria > 3g/d is diagnostic for a glomerular damage. These basic tests are usually followed by more specialized analyses, such as a screening for infections, including search for HIV, hepatitis B or C and various bacteria, and for systemic inflammatory diseases, including tests for antibodies, such as ANA, anti-dsDNA, ANCA, anti-GBM and anti-CCP. In cases of membranous nephropathy, antibodies against phospholipase-A2-receptor need to be looked for. Depending upon the given clinical circumstances and the type of disease, a reasonable tumor screening must be performed, especially in cases of membranous and minimal-change nephropathy. Finally, radiological examinations will complete the initial work-up. In most cases, at least an ultrasound of the kidney is mandatory. Thereafter, in most cases a renal biopsy is required to establish a firm diagnosis to define all treatment options and their chance of success. The elimination of a specific cause for a given glomerulonephritis or vasculitis, such as an infection, a malignancy or a drug-related side-effect, remains the key principle in the management of these diseases. ACE-inhibitors, angiotensin receptor-blockers, aldosteron antagonists and renin-inhibitors remain the mainstay in the therapy of arterial hypertension with proteinuria. Only in cases of persistently high proteinuria, ACE-inhibitors and angiotensin receptor blockers can be prescribed in combination. Certain types of glomerulonephritis and essentially all forms of vasculitis require some form of more specific anti-inflammatory therapy. Respective immunosuppressive drug regimens contain traditionally medications, such as glucocorticoids (e. g. prednisone), cyclosporine A, mycophenolate mofetil, cyclophosphamide, and azathioprine. With respect to more severe forms of glomerulonephritis and vasculitis, the antibody rituximab represents a new and less toxic alternative to cyclophosphamide. Finally, in certain special cases, like Goodpasture's syndrome or severe ANCA-positive vasculitis, a plasma exchange will be useful and even required.
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PMID:[Glomerulonephritis and vasculitis as causes of arterial hypertension]. 2254 60

In leptospirosis, severe pulmonary hemorrhagic syndrome has replaced Weil's disease as the main cause of mortality, with rates of up to 75%. Four men, all farmers, were admitted to the intensive care unit between August 2009 and July 2010 with a diagnosis of acute respiratory distress syndrome. All patients presented with fever, hemoptysis, bilateral pulmonary infiltrates in chest radiographs, and thrombocytopenia and had compatible epidemiological history with leptospirosis; 3 patients had anemia, 3 had renal failure, 2 had increased creatine kinase, whereas bilirubin was slightly increased in only 1 patient. Leptospirosis was diagnosed serologically in all cases. Empirical therapy with ceftriaxone was administered immediately to all patients, while implementation of ARDSnet protective mechanical ventilation approach combined with an early goal-directed hemodynamic approach led to a relatively low mortality rate (25%). Acute Physiology and Chronic Health Evaluation II, Simplified Acute Physiology Score II and Sepsis-Related Organ Failure Assessment scoring systems were unable to predict the outcome of the patients with leptospirosis-associated severe pulmonary hemorrhagic syndrome.
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PMID:Anicteric leptospirosis-associated severe pulmonary hemorrhagic syndrome: a case series study. 2273 64

A 66-year-old man with uremia and on hemodialysis was referred to our hospital because of hemoptysis. A chest radiograph showed diffuse infiltration in the right lung field. Laboratory data were remarkable for renal failure accompanied by hematuria and proteinuria. A kidney biopsy revealed diffuse crescentic glomerulonephritis with linear staining of IgG along the glomerular basement membrane (GBM). Circulating IgG anti-GBM antibody was not detected. Because the findings of renal biopsy suggested anti-GBM disease, the patient was treated with plasmapheresis and pulse steroid therapy, which resulted in a rapid resolution of his pulmonary symptoms and chest radiograph abnormalities. However, sputum culture submitted on admission yielded Mycobacterium tuberculosis 3 weeks later. Therefore, immunosuppressive agents were discontinued and antituberculous agents were administrated. No relapse of pulmonary hemorrhage occurred during the next 1-year period of follow-up, but the patient did not regain renal function and remained on hemodialysis.
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PMID:Anti-glomerular basement membrane glomerulonephritis with subsequent pulmonary hemorrhage in the course of pulmonary tuberculosis. 2295 Aug 33

This case describes a 42-year-old female with longstanding history of rheumatoid arthritis (RA) and Felty syndrome (FS). She presented with acute renal kidney failure, skin rash and hemoptysis. A clinical suspicion of small vessel vasculitis (SVV) was thought, serology was also positive for various markers of SVV. However, these serology markers could be false-positive in a patient of rheumatoid arthritis. A renal biopsy was performed that led to the final diagnosis of cryoglobulinemic vasculitis. Patient was managed according to the standard guidelines for therapy (plasmafiltration and immunosuppression). It is challenging to manage a patient of RA, in the presence of Felty syndrome-related granulocytopenia and thrombocytopenia. Patient initially showed signs of improvement, but finally succumbed to complications of therapy. The case provides insight into the diagnosis and management of such cases.
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PMID:Female with rash, acute kidney failure and rheumatoid arthritis. 2302 60

The catastrophic antiphospholipid syndrome (CAPS) is a rare life-threatening form of the antiphospholipid syndrome characterized by disseminated vascular thrombosis resulting in multiorgan failure. On an exceedingly rare occasion, CAPS can be associated with severe hemorrhagic manifestations. We report a young woman with a history of several spontaneous miscarriages who presented with menorrhagia and hemoptysis. The patient developed respiratory failure due to diffuse alveolar hemorrhage. Laboratory tests demonstrated severe hemolytic anemia, profound thrombocytopenia, markedly elevated fibrin degradation products, and renal failure. Blood films revealed numerous schistocytes. Serologic tests disclosed hypocomplementemia and autoantibodies directed against several nuclear antigens. Coagulation studies revealed lupus anticoagulant. Echocardiography demonstrated reduced ejection fraction and moderate to severe mitral and tricuspid regurgitation. The patient was diagnosed with CAPS with hemorrhagic manifestations in the setting of new-onset SLE. The patient was treated with hemodialysis, high-dose glucocorticoids, plasma exchange, intravenous cyclophosphamide, and rituximab. Over the ensuing four weeks, the combination therapy led to hematological, cardiopulmonary, and renal recovery. This exceedingly rare case emphasizes that hemorrhagic manifestations, severe microangiopathic hemolytic anemia, and profound thrombocytopenia can dominate the clinical picture in CAPS.
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PMID:Catastrophic antiphospholipid syndrome with severe acute thrombotic microangiopathy and hemorrhagic complications. 2438 68

Diffuse alveolar hemorrhage (DAH) in patients with systemic lupus erythematosus is a rare but potentially fatal condition. Although the pathogenesis of this condition is unknown, high disease activity is the main characteristic; moreover, histopathology in some studies showed alveolar immune complex deposits and capillaritis. Clinical features of DAH include dyspnea, a drop in hemoglobin, and diffuse radiographic alveolar images, with or without hemoptysis. Factors associated with mortality include mechanical ventilation, renal failure, and infections. Bacterial infections have been reported frequently in patients with DAH, but also invasive fungal infections including aspergillosis. DAH treatment is based on high dose methylprednisolone; other accepted therapies include cyclophosphamide (controversial), plasmapheresis, immunoglobulin and rituximab.
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PMID:Diffuse alveolar hemorrhage in patients with systemic lupus erythematosus. Clinical manifestations, treatment, and prognosis. 2470 7

A 73-year-old previously healthy man presented with a 3-day history of rigours, abdominal pain, diarrhoea, haemoptysis and myalgia. He had not been abroad recently, but reported being a farmer and having had a recent rat infestation. Laboratory investigations revealed acute kidney failure, deranged liver function tests, raised C reactive protein and a chest CT revealed bilateral ground-glass opacities. This presentation was consistent with icteric leptospirosis which was confirmed by serological testing. Following haemofiltration and the administration of antibiotics the patient made an excellent recovery from his leptospirosis.
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PMID:The importance of "His" story. 2489 80

We describe a case of a patient who developed microscopic polyangiitis (MPA) in the setting of exposure to silicone after breast implantation. A 57-year-old Hispanic woman was admitted to our hospital with complaints of fever, cough, and hemoptysis. She had undergone silicone breast implantation two years prior to presentation. She was diagnosed as having microscopic polyangiitis (MPA) based on acute progressive renal failure, hematuria, pulmonary hemorrhage, and positivity for myeloperoxidase-anti-neutrophil cytoplasmic antibody (ANCA). A renal biopsy performed showed focal segmental necrotizing and crescentic glomerulonephritis. The patient received high dose steroids, cyclophosphamide, and plasmapheresis with remarkable clinical response. This case report raises the possibility of the development of MPA after silicone exposure from breast implantation.
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PMID:Microscopic Polyangiitis following Silicone Exposure from Breast Implantation. 2538 72


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