Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a patient who developed the Lambert-Eaton myasthenic syndrome (LEMS) in association with systemic lupus erythematosus (SLE). Severe proximal weakness with electrodiagnostic evidence of LEMS developed over 2 days during an exacerbation of cutaneous manifestations (bullous pemphigoid) associated with SLE. Following an increase in the daily dose of prednisone, there was complete clinical restitution of strength within 2 weeks and a slower resolution of electrodiagnostic abnormalities over 6 months. Marked serologic abnormalities were present at the onset and showed improvement over 6-8 months. LEMS had been infrequently described in association with SLE. The immunologic features of both SLE and LEMS suggest a linkage between the two diseases in this patient. We hypothesize that increased antibodies associated with exacerbation of SLE cross reacted with the neuromuscular junction membrane to produce LEMS.
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PMID:Transient Lambert-Eaton myasthenic syndrome associated with systemic lupus erythematosus. 274 33

Thirty patients with SLE were studied retrospectively and subjected to clinical neurological examination. The accumulated neurological manifestations from the beginning of the disease until the time of examination were thus collected. Twenty-five patients (83%) had experienced neuropsychiatric manifestations while 11 patients (37%) had neuromuscular manifestations. The most frequent single symptom was migraine which had occurred in 40% of the patients. This was followed by severe protracted headache in 20%, vertigo in 20%, and psychiatric problems in 17%. Carpal tunnel syndrome and muscular weakness both occurring in 23% of the patients were the most prevalent neuromuscular manifestations, followed by myositis in 10%.
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PMID:Clinical neuropsychiatric and neuromuscular manifestations in systemic lupus erythematosus. 283 97

We report a 34-year-old woman with mixed connective tissue disease (MCTD) who developed severe pulmonary and neuromuscular complications. At presentation, pulmonary function tests and pulmonary mechanics were suggestive of pulmonary vascular disease, and she subsequently developed clinical signs of pulmonary hypertension. These noninvasive tests may be useful in the timing of more invasive hemodynamic studies. She initially had myasthenia gravis and then developed polymyositis, profound peripheral neuropathy, and ventilatory muscle failure. She died despite aggressive immunosuppressive therapy and plasmapheresis. Autopsy showed spinal cord changes secondary to a peripheral neuropathy and signs of neurogenic atrophy confined to the ventilatory muscles. Peripheral neuropathy may be an important cause of ventilatory muscle weakness that can be found in MCTD and systemic lupus.
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PMID:Pulmonary and neuromuscular complications of mixed connective tissue disease: a report and review of the literature. 231 66

Internuclear ophthalmoplegia has been infrequently described in patients with systemic lupus erythematosus. We report a 23-year-old woman with lupus who presented with bilateral internuclear ophthalmoplegia and skew deviation. Additional neurologic findings included dysarthria, hemifacial weakness, hemiparesis, and dysmetria. Computed tomography of the patient's brainstem was unremarkable while magnetic resonance scanning demonstrated two areas of infarction. Magnetic resonance imaging is superior to computed tomography in both neuroradiographic study of the brainstem as well as evaluation of patients with neurologic complications of lupus.
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PMID:Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. 295 86

Diaphragmatic weakness has been identified as one of the pulmonary manifestations of systemic lupus erythematosus. Whether this weakness results from a neuropathic or myopathic process has not been established. Thirty patients with SLE were screened for the presence of inspiratory muscle (IM) weakness. Detailed studies were performed in nine with IM weakness. All nine were found to have diaphragmatic weakness (mean +/- SD, maximal transdiaphragmatic pressure 50 +/- 12 cmH2O). Phrenic nerve latencies, evaluated using transcutaneous stimulation, were normal in all individuals excluding a demyelinating neuropathy. Compound diaphragm action potential (CDAP) with phrenic nerve stimulation was normal in six of these nine patients. Reduced CDAP in three of nine patients was consistent either with axonal degeneration of the phrenic nerve or diaphragm myopathy. Nerve conduction and electromyographic studies on peripheral nerves and muscles respectively failed to demonstrate an associated generalized neuropathy or myopathy. We conclude that diaphragmatic weakness in patients with SLE is both common and is very unlikely to be caused by a phrenic neuropathy.
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PMID:Phrenic nerve function in patients with diaphragmatic weakness and systemic lupus erythematosus. 333 3

In 23 consecutive patients (mean age, 38.6 years) with systemic lupus erythematosus (SLE) and in 17 healthy subjects (mean age, 37.5 years) fatigue of respiratory (diaphragm, musculi intercostales externi) and leg muscles (musculus gastrocnemius) was determined comparatively by electromyography. Additionally, routine lung function parameters, including maximum inspiratory (PImax) and expiratory (PEmax) mouth pressures, were measured. The SLE patients showed lower values of vital capacity (VC), total lung capacity (TLC), thoracic gas volume (TGV), FEV1, PImax and PEmax than the healthy controls, while FEV1/VC, residual volume and specific airway conductance were not significantly different in either group. Lung compliance, corrected for TGV, was normal in the SLE group. Breathing through stenoses with increasing resistances resulted in fatigue of the diaphragm in 73% of the SLE group and in 41% of the control group. The corresponding values of the external intercostal muscles were 74% (SLE group) and 29% (control group). Electromyographic signs of respiratory and leg muscle fatigue occurred at lower loads in the SLE group than in the healthy subjects. The pattern of lung function data in patients with SLE was characteristic neither of lung restriction nor of airway obstruction. Respiratory muscle weakness can explain the decrease in TLC, VC, TGV, FEV1, PImax and PEmax.
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PMID:Lung function disturbances versus respiratory muscle fatigue in patients with systemic lupus erythematosus. 339 38

A previously healthy 62 years old man was admitted for weight loss, weakness and pigmentation of skin with increased tumor markers and altered hepatic tests. The final diagnosis was Systemic Lupus Erythematosus, despite clinical appearance. High doses of glucocorticoids were used and a sudden improving of the disease was obtained.
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PMID:[Systemic lupus erythematosus in an elderly man with hepatic involvement, skin hyperpigmentation and increase in tumor markers]. 340 61

We describe a case of histologically proven giant cell arteritis (GCA) in a 62-year-old woman who initially presented with upper limb girdle pain and weakness, and intermittent claudication. Clinical improvement was obtained with oral prednisolone. She subsequently developed a photosensitive rash and was diagnosed as having systemic lupus erythematosus. The features of the two conditions and the possibility of an association are discussed.
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PMID:Giant cell arteritis and systemic lupus erythematosus. 340 55

Polymyositis is an autoimmune, inflammatory disease affecting human skeletal muscle. In the presence of concomitant vasculitis in the skin, the term dermatomyositis is used. In contrast, systemic lupus erythematosus (SLE) is a multisystem disease in which involvement of the skin, kidneys, joints, brain, and other organs may be found. The clinical manifestations vary according to the organ/system involved. It is clinical and therapeutic importance to define which organ/system is involved during the course of the disease. We approached this problem by studying the specificity of autoantibodies that are generated in patients with SLE and polymyositis/dermatomyositis. Among such antibodies are those directed against nuclear components including a variety of ribonucleoprotein (RNP) complexes. We have utilized mammalian nuclear preparations enriched with RNP particles as the antigenic source for immunoblotting studies to identify specific antigenic polypeptides. In the study reported here, sera from five groups of patients were examined: 10 patients with dermatomyositis/polymyositis; six patients with SLE and myositis; 12 lupus patients with cerebral and/or renal disease; eight patients with SLE but no myositis, renal, or cerebral disease; and 5) 11 patients with muscle weakness or muscle disease not due to myositis. In the first two groups of patients with myositis, antibodies against a nuclear RNP protein of 56 KD was identified in 12 of 16 sera. In contrast, such antibodies were found in the serum of only two of 20 patients with SLE but without muscle involvement (groups 3 and 4), and were not found at all in patients with other muscle diseases. This study has identified a new marker, antibodies against a nuclear RNP protein of 56 KD for detecting muscle involvement among the autoimmune rheumatic diseases.
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PMID:Autoantibodies against a specific nuclear RNP protein in sera of patients with autoimmune rheumatic diseases associated with myositis. 349 67

The clinical features and biochemical profile of 10 patients with Renal Tubular Acidosis (RTA) were described. The commonest mode of presentation was muscular weakness due to severe hypokalaemia in 5 patients while the other 5 presented with renal colic, haematuria or passage of gravel. Nine patients had nephrocalcinosis on X-rays and one had rickets. All the patients had Type I RTA, 2 of whom presenting initially with Incomplete Type I RTA which progressed to Complete Type I RTA. Two other patients had associated features of proximal tubular involvement evidenced by hypophosphatemia, hypouricemia, hyperphosphaturia, aminoaciduria and glycosuria. Six of the 10 patients had secondary RTA: 2 associated with medullary sponge kidneys, 2 with gout, 1 with idiopathic hypercalciuria and hyperuricosuria and the remaining patient with systemic lupus erythematosus.
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PMID:Renal tubular acidosis. 370 33


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