Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinician with interest in neuromuscular disease must become familiar with the clinical manifestations of HIV infection. It is important to realize that not everyone who is infected with HIV will develop clinical AIDS. This includes patients with clinical manifestations related to HIV infection, for example, neuropathy. Thus, if treatment is successful, patients can continue a normal life. HIV infection should be considered in almost any neuromuscular syndrome, especially neuropathies with features of demyelination, which may be the first manifestation of HIV infection. Plasmapheresis may be the treatment of choice for these disorders. Steroids should be used with caution. AZT seems to be a promising new agent to combat AIDS.
 ...
PMID:Disorders of peripheral nerves associated with HIV infection. 215 12

In a few patients with Graves' disease, visual loss related to an optic neuropathy develops. Clinical and radiologic evidence suggests that the mechanism of visual loss is optic nerve compression in the orbital apex. Steroids may offer improvement, but often the condition recurs unless high doses are maintained. Orbital decompression provides dramatic visual and cosmetic improvement in most cases. A transorbital approach suitable to the experienced orbital surgeon for decompression of the orbital floor and medial wall has been presented in a companion article. Results of this approach in 12 eyes with visual loss unmanageable by steroid therapy indicate a gratifying improvement in vision. Strabismus is the most frequent complication. Results with follow-up ranging from six to 18 months are encouraging and comparable to the results obtained with other methods of surgical decompression.
 ...
PMID:Transorbital decompression. Indications and results. 689 28

Sporadic acute brachial plexus neuropathy occurs in approximately 1.64/100,000 population, but may present in epidemic form. Sporadic lumbosacral plexus neuropathy is far less common and has to be distinguished from more common disorders affecting the plexus and roots such as diabetes. Early this century, when serum therapy became popular to treat or prevent prevalent infectious diseases, it became apparent that a plexopathy could follow treatment. It has thus been assumed that many of the cases are due to an autoimmune or inflammatory lesion of the plexus. A wide variety of vaccines, infections and medications seem able to precipitate the disorder. Recent work has shown that cultured lymphocytes from affected patients, but not controls, are able to mount a blastogenic response to components of cadaver brachial plexus. This response seems to be selective not only to the brachial plexus, but also to discrete components of the plexus. The recovery rate in brachial plexus neuropathy is good, being almost 90% at 3 years. Recovery with lumbosacral disease is less satisfactory. Histological material and descriptions of acute brachial plexus neuropathy are rare. There is some evidence that an inflammatory process is present, but the role of demyelination and axonal atrophy in producing the observed clinical signs, is still uncertain. Virtually nothing is known about the histological changes in lumbosacral plexus neuropathy. Treatment is mainly supportive, but important in limiting disability. Steroids may help relieve pain in the acute stages, but do not seem to alter the prognosis.
 ...
PMID:Brachial and lumbar neuropathies. 792 88

The history of antiarrhythmic therapy reveals these agents to be associated with a high incidence of toxicity. Although several agents have ocular effects, amiodarone is the most widely recognized for producing adverse effects in the eyes. Corneal microdeposits are almost ubiquitous in patients being treated with amiodarone. However, they are, for the most part, benign and produce no changes in visual acuity. Lack of microdeposits should prompt the physician to investigate whether there is a problem with drug absorption or adherence to therapy. Other effects on the eye have been reported including optic neuropathy, but no causal link has been proved with amiodarone. The population of patients treated with amiodarone often have ischemic disease and/or diabetes, which affect retinal and optic nerve health. Many antiarrhythmic agents also affect lung function. The frequent association of procainamide with a lupus-like syndrome, where half the cases develop pleural-pericardial involvement, may require discontinuation of that drug. Although beta blockers and to a lesser degree, calcium antagonists, may cause bronchospasm in some patients, this is not usually a major clinical problem. Again, it is amiodarone that has the most widespread reputation for causing pulmonary toxicity. Although infrequent (< 1% incidence), it generates the most fear as it is sometimes fatal. Because of the lack of a diagnostic "gold standard," it is often overdiagnosed, placing patients at risk from overlooked congestive heart failure and infections and from recurrent arrhythmias after drug withdrawal. Patients with pre-existing pulmonary disease appear to be more at risk. Common features include indolent onset of cough, malaise and fever associated with patchy peripheral infiltrates, and severely decreased diffusion capacity. Several cases of pulmonary toxicity have had inordinately high serum desethylamiodarone to amiodarone ratios. Most cases recover with cessation of amiodarone therapy. Steroids are commonly used, but are of unproved efficacy. In terms of its toxicity, amiodarone remains the most feared of the antiarrhythmic agents. In the future, a better understanding of its pharmacokinetics, mechanisms of toxicity, and optimal dosing regimens should provide a possibility of better strategies for avoidance, early diagnosis, and more directed therapy of toxicities associated with amiodarone.
 ...
PMID:Clinical organ toxicity of antiarrhythmic compounds: ocular and pulmonary manifestations. 1056 58

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.
 ...
PMID:Neurological complications of sepsis: critical illness polyneuropathy and myopathy. 1175 54

We report a case of POEMS syndrome (Polyneuropathy, Organomegaly, Endocrinopathy, M protein and Skin changes) with unusual clinical features. A 62-year-old woman presented a severe polyneuropathy with dysphonia and vegetative symptoms, including bradycardia and sphincterial disorders. The clinical examination showed facial hyperpigmentation, cachexia, anasarca and splenomegaly. She also presented restrictive cardiomyopathy and endocrine disturbances. Nerve conduction studies revealed a severe demyelinating sensorimotor neuropathy. Cerebrospinal fluid analysis showed an elevated protein level. We detected a biclonal gammapathy (Ig G and Ig A with lambda light chain) and lytic pelvic bone lesions. Later, she developed a severe ventilatory failure due to a bilateral phrenic nerve paralysis leading to a mechanical ventilation. Steroids followed by localized radiotherapy partially improved the respiratory status and stabilized the neuropathy. Phrenic nerve paralysis, restrictive cardiomyopathy, vegetative symptoms and cranial nerve palsy are exceptional in POEMS syndrome. Moreover, this case emphasizes the importance of radiological investigations since the discover of plasmocytoma may improve the prognosis of POEMS syndrome.
 ...
PMID:[Bilateral phrenic nerve paralysis, dysautonomia and restrictive cardiomyopathy in a case of POEMS syndrome]. 1248 6

A case of giant cell arteritis with systemic and panocular involvement is reported here. This elderly Indian male presented with symptoms of unilateral temporal headache and intermittent jaw claudication for a month followed by diplopia and blurring of vision and later loss of vision in the right eye. The right eye showed some limitation of ocular movements, presence of relative afferent pupil defect, anterior segment ischaemic changes and anterior ischaemic optic neuropathy. Visual evoked potential showed an absent P1 wave while the left eye with normal 6/6 vision sowed a prolonged P1 wave. Fundus fluoresceine angiography showed delay in choroidal perfusion. His erythrocyte sedimentation rate (ESR) was 120 mm/hr and he was started on oral prednisolone. Superficial temporal artery biopsy obtained one week after starting steroids was positive for giant cell arteritis. Steroids led to the resolution of optic disc swelling, disappearance of anterior segment signs, full recovery of right ocular movements and no further deterioration of the fellow eye. On steroids, he developed insomnia and progressive myopathy which resolved and is now symptom free at lower doses of steroids.
 ...
PMID:Giant cell arteritis with panocular involvement in an Indian male. 1455 35

This series of articles on the management of glomerulonephritis (GN) has been prepared by a team of experts in the evidence-based format consistent with peer review of published data. Each author was asked to review the literature for his assigned histological type, with emphasis on therapy and limited to adult studies. The age limit was not considered for minimal change disease and focal segmental glomerulosclerosis, because of the high prevalence of these glomerulopathies in children. The particular treatment recommendations for each type of glomerular disease were graded by each author according to the amount of evidence provided in these reviewed studies. The first two articles concentrate on indications and techniques for kidney biopsy. Each subsequent article focuses on and describes the highest level of evidence supporting the recommendation for therapy in IgA nephropathy (Ig-GN), minimal change nephropathy (MCN) and focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN), lupus nephritis, ANCA-associated vasculitis, HCV-associated cryoglobulinaemia and renal involvement in paraproteinemic disorders. The article on IgA nephropathy emphasises the importance of carefully evaluating both clinical and histologic findings before settling on the treatment. The recent, renewed interest in steroids and many immunosuppressive agents is discussed in detail. Recommendations related to the patient's age are also provided. MCN and FSGS are treated together because these forms share similar evidence-based recommendations. For both of these diseases, in fact, the initial treatment approach in children should be prednisone or prednisolone for four to six weeks. The therapeutic response in adults is slower than in children, but adults experience fewer relapses and a more prolonged remission. There is also a discussion on treatment of relapse, frequent relapsing disease and true steroid-resistant disease as well as the role of new immunosuppressive agents. Membranous nephropathy is a frequent cause of nephrotic syndrome in adults and, in one third of these patients, leads to end-stage renal disease. However, the treatment of this form is as yet a matter of discussion. Based on extensive critical review of the literature, the following recommendations are put forward: (a) no treatment in the absence of nephrotic syndrome; (b) patients with heavy proteinuria should receive a 6-month treatment with i.v. methylprednisolone (MP) pulse therapy for three consecutive days followed by oral MP (0.4 mg/kg/day) (months 1, 3, 5) and chlorambucil or cyclophosphamide (months 2, 4, 6); (c) the dosage of chlorambucil or cyclophosphamide should be lowered in older patients; (d) cyclosporine is a second-choice treatment. The treatment of lupus nephritis depends on the histologic class. No specific treatment is usually necessary for class I and IIA. Oral steroids are indicated in patients with class IIb, proteinuria and active systemic disease. Steroids and azathioprine are the treatment of choice for patients with class III and IV, but cyclosporine can be an effective alternative therapy. Cyclophosphamide is more effective than azathioprine when severe acute renal involvement is present. The treatment of ANCA-associated vasculitis depends mainly on clinical presentation, oral prednisone + oral or i.v. cyclophosphamide are generally effective. In the most severe cases, the association of MP pulse therapy with cyclophosphamide is probably more effective. Plasma exchange is probably justified in unresponsive patients. Azathioprine should replace cyclophosphamide during the maintenance therapy. In HCV-associated mixed cryoglobulinemia the treatment also depends on the severity of renal involvement. The treatment for chronic HCV infection involves alpha interferon alone or preferably in combination with ribavirin. Aggressive therapy, including i.v. MP, plasmapheresis and cyclophosphamide is primarily reserved for patients with acute severe disease, as manifested by progressive renal failure, distal necroses requiring amputation, or advanced neuropathy. Uncontrolled studies suggest that this regimen can improve renal function. Renal involvement is a common problem in paraproteinemic disorders that include multiple myeloma, Waldentrom's macroglobulinaemia and monoclonal gammopathy. The most common renal diseases in this setting are cast nephropathy, primary amyloidosis cast nephropathy, primary amyloidosis, and light chain deposition disease that are related to the overproduction of monoclonal immunoglobulin light chains. The approach to therapy varies with the cause of the renal dysfunction. Patients with amyloidosis or light-chain deposition disease are generally treated with chemotherapy, but the most effective therapy for myeloma kidney is prevention by minimising the risk factors that promote light chain filtration and subsequent obstruction by cast formation within the tubules. Chemotherapy or stem cell or bone marrow transplantation to decrease filtered light chain load, prevent volume depletion and maintain high fluid intake to reduce light chain concentration within the tubular lumen are indicated in almost all the patients.
 ...
PMID:[Instructions and implementations for percutaneous renal biopsy. Guidelines for the therapy of glomerular nephropaties]. 1466 2

Ophthalmoplegic migraine is a rare condition, previously thought to represent a variant of migraine. Recent observations regarding its usual clinical presentation and common magnetic resonance imaging findings have given rise to speculation that this illness is more likely to represent an inflammatory cranial neuropathy. The recent revision of the International Headache Classification has reclassified ophthalmoplegic migraine from a subtype of migraine to the category of neuralgia. In this article, potential pathophysiological mechanisms are discussed. The typical clinical presentation of ophthalmoplegic migraine generally involves transient migraine-like headache accompanied by often long-lasting oculomotor, abducens or, rarely, trochlear neuropathy with diplopia and (if oculomotor nerve is involved) pupillary abnormalities and ptosis. Ophthalmoplegic migraine generally occurs in children, but a number of adult cases have been reported. Prognosis is good because symptoms almost always resolve, but, after several episodes, some deficits may persist. Differential diagnosis is rather large, although most other possible causes of ophthalmoplegia and headache have distinctive presentations or can be excluded with fairly straightforward diagnostic testing. Optimal prophylactic and acute treatment is still unclear, but migraine prophylactic medications such as b blockers and calcium channel blockers have been proposed. Steroids have been used with mixed results.
 ...
PMID:Ophthalmoplegic migraine. 1522 91

A patient with a history of pituitary tumour treated with yttrium 29 years before presented with an asymmetrical chiasmal neuropathy. Magnetic resonance imaging showed a partially thrombosed giant aneurysm of the right internal carotid artery, with enhancement of the chiasm and right optic tract adjacent to the aneurysm. It was thought that, in addition to the effects of compression, a peri-aneurysmal inflammatory reaction had developed, causing breakdown of the blood-brain barrier and consequent inflammatory changes in the optic chiasm. High dose steroid treatment led to significant improvement in vision within two weeks. Steroids may have a role in the acute preservation of vision in similar cases, as well as in cases of deterioration following coiling or embolisation of aneurysms where thrombosis within the aneurysm has been induced.
 ...
PMID:Optic chiasm enhancement associated with giant aneurysm and yttrium treated pituitary adenoma. 1531 30


1 2 3 Next >>