Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven patients with myasthenia gravis developed clinical signs of arthropathy. In two patients, the symptoms were due to a deforming rheumatoid arthritis and the myasthenic symptoms appeared as a transitory phase during the course of the disease. Muscle antibodies of IgG class were demonstrated with sera from both patients. Autoreactivity between muscle antibodies and rheumatoid factor was detected in one patient. Both patients died from sudden cardiac failure. Necropsy was performed in one and revealed a spotty myocardial necrosis. One patient had juvenile rheumatoid arthritis. Two patients had mild articular symptoms with indices of multivisceral disease and serological findings indicating a systemic lupus erythematous. One patient had classical ankylosing spondylitis, and one, unspecified arthropathy.
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PMID:Arthritis in myasthenia gravis. 110 89

An 82-year-old man with a history of myasthenia gravis and heart failure was admitted to the hospital with respiratory failure. Aminophylline and eventually theophylline therapy were initiated to improve respiratory status. During the hospital stay, the patient developed a resistant pseudomonal pneumonia. After failure with conventional antibiotics, ciprofloxacin was initiated because of favorable sensitivity and the planned avoidance of aminoglycoside therapy. Seventy-two hours after initiation of ciprofloxacin, the patient's theophylline level rose from a steady-state baseline of 9.8 micrograms/ml to 34.7 micrograms/ml. After the theophylline dose was reduced by approximately 67 percent, the patient's theophylline serum concentration returned to baseline (10 micrograms/ml). Until more data concerning the interaction of theophylline and ciprofloxacin are available, we recommend close monitoring of theophylline serum concentrations in patients receiving concomitant ciprofloxacin.
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PMID:Increased theophylline concentrations secondary to ciprofloxacin. 367 60

Giant cell myocarditis is a rare disease of unknown etiology, which develops as a myocardial isolated affection or associated to different diseases. Its characteristics are such as necrosis, inflammation and giant cell presence in the myocardium. We present the case of a woman who suffered of giant cell myocarditis, thymoma, myasthenia gravis, chronic lymphocytic thyroiditis, giant cell myositis, granulomatous infiltration in the lymph nodes of the hilus of the lung and hypogammaglobulinemia; multiple association that we have not found in any published medical paper and that suggest the autoimmune origin of this illness. The cardiovascular symptoms and the associated diseases are revised, and we discussed the diagnostic and therapeutic topics, pointing out the necessity to take it into account for any patient with thymoma or myasthenia gravis developing to heart failure or arrhythmias.
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PMID:[Giant-cell myocarditis: a systemic disease? Apropos a case]. 823 70

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10

Calcium signalling in cells is dependent on a communication between channels/ transporters in two membrane structures: the cell membrane and the membranes of endo- and sarcoplasmic reticula (ER/SR). In general, cytosolic Ca2+ can be raised by influx of calcium over the cell membrane through three types of channels: voltage-, receptor-, and store-operated channels (VOCs, ROCs and SOCs). This small Ca2+ influx is most often amplified by a Ca2+ release from the ER/SR through two types of channels: the IP3-receptor and the ryanodine receptor (RyR), which are huge proteins identified and cloned in recent years. We focus on the 'synaptic' connection between VOCs (L-type calcium channels) and RyRs of the SR in heart and skeletal muscle. Depolarization of the cell membrane (an action potential) opens the VOC and moves it in the membrane. One VOC triggers opening of a certain number of underlying RyRs that together release a quantum of calcium from the SR, a calcium spark. The communication between the VOC and RyRs is probably achieved primarily by a mechanical link in skeletal muscle (voltage-controlled calcium release), and by the small inward calcium flux through the VOC in the heart (calcium-induced calcium release, CICR). Conditions as different as heart failure, myasthenia gravis, malignant hyperthermia, and skeletal muscle fatigue, may be examples of deteriorated control or function of the RyR.
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PMID:Intracellular calcium signalling in striated muscle cells. 939 86

The management and clinical course of patients with myasthenia gravis admitted to a neurological intensive therapy unit (ITU) over a 66 month period were reviewed. Twenty-seven patients were admitted in myasthenic crisis, eight of whom had multiple admissions. One patient had a cholinergic crisis and a further patient an acute myocardial infarction. A specific aetiological factor precipitating myasthenic crisis was identified in 19 instances: infection (8), reduction in medication (5), menstruation (4), and steroid administration (2). Thirteen patients with crisis had had a previous thymectomy, six with thymoma. Twenty-three out of 35 (66%) patients admitted in crisis required intubation; nine subsequently needed a tracheostomy. Twenty-nine patients received plasma exchange and seven intravenous immunoglobulin. Four patients in myasthenic crisis died in ITU [adult respiratory distress syndrome (1), disseminated intravascular coagulation and cytomegalovirus (CMV) pneumonitis (1), cardiac failure (1) and multiple organ failure (1)]. Appropriate management of myasthenia gravis requires the easy availability of specialised neuro-intensive care facilities. Copyright Rapid Science Ltd
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PMID:The management and outcome of patients with myasthenia gravis treated acutely in a neurological intensive care unit. 1021 Aug 24

We report a 62-year-old man with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis (MG). He was diagnosed as having MG and invasive thymoma at the age of 45. After he had a myasthenic crisis at the age of 61, tacrolimus was indicated in order to improve his neurological symptoms, in addition to glucocorticoid. Three months later, he was readmitted to our hospital complaining of general fatigue and dyspnea. Serum level of creatine phosphokinase (9,835IU/L) and myocardium-derived troponin T (3.24 ng/mL) were elevated, and the ECG showed atrioventricular dissociation and accelerated idioventricular rhythm. In spite of glucocorticoid pulse therapies and high-dose immunoglobulin therapies, he died of cardiac failure within a few days. Autopsy was done, and histological examination of the myocardium and the skeletal muscle showed massive necrosis with infiltration of inflammatory cells including giant cells. These findings constituted giant cell myocarditis and myositis. Although it has been suggested that myocardial disorders can often occur in patients with thymoma and/or MG, the mechanism involved is still unknown. This report may provide new knowledge about the pathophysiology of giant cell myocarditis and myositis associated with thymoma and MG.
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PMID:[A patient with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis]. 1465 3

Today, dilated cardiomyopathy (DCM) represents the main cause of severe heart failure and disability in younger adults and thus is a challenge for public health. About 30% of DCM cases are genetic in origin; however, the large majority of cases are sporadic, and a viral or immune pathogenesis is suspected. Following the established postulates for pathogenesis of autoimmune diseases, here we provide direct evidence that an autoimmune attack directed against the cardiac beta(1)-adrenergic receptor may play a causal role in DCM. First, we immunized inbred rats against the second extracellular beta(1)-receptor loop (beta(1)-EC(II); 100% sequence identity between human and rat) every month. All these rats developed first, receptor-stimulating anti-beta(1)-EC(II) Ab's and then, after 9 months, progressive severe left ventricular dilatation and dysfunction. Second, we transferred sera from anti-beta(1)-EC(II)-positive and Ab-negative animals every month to healthy rats of the same strain. Strikingly, all anti-beta(1)-EC(II)-transferred rats also developed a similar cardiomyopathic phenotype within a similar time frame, underlining the pathogenic potential of these receptor Ab's. As a consequence, beta(1)-adrenergic receptor-targeted autoimmune DCM should now be categorized with other known receptor Ab-mediated autoimmune diseases, such as Graves disease or myasthenia gravis. Although carried out in an experimental animal model, our findings should further encourage the development of therapeutic strategies that combat harmful anti-beta(1)-EC(II) in receptor Ab-positive DCM patients.
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PMID:Direct evidence for a beta 1-adrenergic receptor-directed autoimmune attack as a cause of idiopathic dilated cardiomyopathy. 1514 32

We report an autopsy case of acute pancreatitis with a high serum IgG4 concentration complicated by systemic amyloid A amyloidosis and rheumatoid arthritis (RA). The patient was a 42-year-old Japanese female with a 22-year history of rheumatoid arthritis. She was diagnosed with myasthenia gravis when she was 31-year old. At the onset of pancreatitis, the patient was anti-nuclear antibody-positive, and had high serum gamma globulin and IgG4 levels. Dexamethasone and conventional therapy induced clinical remission and significantly decreased the serum IgG4 and gamma globulin. However, despite the decreased disease parameters, the patient developed a bleeding pseudocyst and died of cardiac failure. In the autopsy examination, it was determined that pancreatitis was probably caused by ischemia due to vascular obstruction caused by amyloid deposition in the pancreas. Even though acute pancreatitis is a rare complication in RA patients, we speculate that an autoimmune pancreatitis-related mechanism and ischemia due to vascular obstruction by amyloid deposition might be attributable to a single source that leads to acute pancreatitis in our particular case.
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PMID:An autopsy case of acute pancreatitis with a high serum IgG4 complicated by amyloidosis and rheumatoid arthritis. 1580 Oct 1

Giant cell myocarditis (GCM) is a serious condition that warrants immediate diagnosis and treatment. It often presents as rapidly progressive heart failure and/or malignant ventricular arrhythmias. Here, we describe a 34-year-old patient with myasthenia gravis who presented with GCM 2 weeks after resection of a thymoma. A cardiac biopsy confirming the diagnosis was done within 3 days after admission. After institution of an aggressive immunosuppressive drug regimen, implantation of an implantable cardioverter defibrillator, and intensive cardiac rehabilitation, the patient recovered dramatically. In control biopsies after 4 weeks and 6 months, no more giant cells were found. We conclude that, in the case of nonischemic acute heart failure in young patients, a biopsy should be performed as soon as possible to prevent an unfavourable outcome of this often fatal disease.
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PMID:Serial right ventricular endomyocardial biopsy in rapid-onset severe heart failure due to giant cell myocarditis. 1684 55


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