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)

Cryptococcosis is a known opportunistic infection in immunosuppressed hosts. We report our experience of all cases presenting to our Department between December 1975 and September 1988. Eight post-renal transplant patients and three systemic lupus erythematosus (SLE) patients were affected. All were receiving treatment with steroids, in association with either azathioprine or cyclosporin. The diagnosis of cryptococcal meningitis was initially based on a positive cerebrospinal fluid (CSF) cryptococcal antigen, by latex agglutination test, and subsequently confirmed by cultures. Common clinical presentations, in descending order of frequency, included headaches, fever, mental confusion, epilepsy and papilloedema. Meningism was not a prominent feature. CT brain scans were obtained in eight patients and one showed a focal lesion and one showed cerebral atrophy. Four patients also had an abnormal chest X-ray (CXR) and one had disseminated cryptococcosis. Amphotericin and 5-fluorocytosine were the mainstay of therapy, although ketoconazole alone was subsequently used in three selected patients with cure. Four early deaths occurred in patients with delayed diagnosis and treatment, usually in association with other severe concurrent infections. We conclude that awareness of cryptococcosis is essential in immunocompromised hosts presenting with headache with, or without, mental confusion or fever.
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PMID:Cryptococcosis in a renal unit. 228 81

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.
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PMID:Cerebral blood flow variations in CNS lupus. 229 89

Systemic lupus erythematosus (SLE) affects the nervous system in 75% of cases (1). A female with several neurological manifestations in the case history presented with severe headache, psychiatric disturbances, and increasing paraparesis. She was found to have bilateral subdural hematomas, and after evacuation her neuropsychiatric symptoms, including headache, disappeared. It is speculated that the reported low incidence of subdural hematomas in SLE may be more apparent than real. On the basis of our case, we recommend repeated neuroradiological investigations to uncover this important, treatable and otherwise potentially fatal cause of headache.
Cephalalgia 1990 Feb
PMID:Subdural hematoma presenting as headache in systemic lupus erythematosus. 231 50

This study was conducted to analyze the prevalence and features of chronic or recurrent headache in Systemic Lupus Erythematosus (SLE), and also the relationship of such headache with other manifestations of the disease. A total of 76 patients (69 women and 7 men) with a mean age of 40 years (r: 24-74 years) were included. An overall severity index for SLE was applied. Fifty-two patients (68%) presented headache, 27 (52%) being vascular and 25 (48%) muscle contraction type. Headache in general was more frequent after the onset of SLE (p less than .001). Prevalence of muscle contraction headache in particular was greater following manifestations of SLE. Family history of migraine was recorded in 54% of the patients with vascular headache. This antecedent was more common in patients in whom migraine started before the onset of SLE (p = .05). A greater number of neuropsychiatric symptoms was observed in the patients with vascular headache and family history (p less than .02). Patients with thrombocytopenia presented headache less frequently (p less than .05). Our results showed headache, of both vascular and muscle contraction types, to be frequent in SLE. We note that there is an increased frequency of muscle contraction headache after the onset of SLE, and that there is a migraine-like headache directly related to SLE. Migrainous patients with familial history have a greater probability to suffer neuropsychiatric manifestations. Finally, it is suggested that severity of SLE is not related to presence of headache.
Headache 1990 Mar
PMID:A prospective study of chronic or recurrent headache in systemic lupus erythematosus. 233 79

We describe six cases of cerebral venous thrombosis in patients with systemic lupus erythematosus. In one patient, cerebral venous thrombosis was the initial manifestation of lupus; in the five others, it occurred 1-33 years after the diagnosis of lupus. The main clinical features of cerebral venous thrombosis were persistent headache in all six patients, focal symptoms in four, and seizures in three; papilledema was present in only one patient. Cerebral venous thrombosis was diagnosed based on angiography or magnetic resonance imaging. Both the transverse (in five patients) and the superior sagittal (in three) sinuses were involved. Extracranial arterial and/or venous thrombosis were present in three patients, abortion in two, thrombocytopenia in four, and lupus anticoagulant in three. The neurologic symptoms resolved rapidly in five patients treated with steroids and heparin. Cerebral venous thrombosis should be suspected in patients with lupus who complain of persistent headache, especially in the presence of neurologic symptoms.
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PMID:Cerebral venous thrombosis in systemic lupus erythematosus. 200 96

At the age of 29, a woman developed central nervous system manifestations of incontinence, psychosis and a grand mal seizure in February 1982. She was diagnosed as having systemic lupus erythematosus (SLE) based on photosensitivity, oral ulcers and elevated antinuclear and anti-DNA antibodies titers. Three years and one month later the patient had episodes of severe headache and vomiting during the course of maintenance treatment. CT examination of the head revealed blood within subarachnoid cisterns, and a small berry aneurysm was found at the distal portion of the basilar artery by cerebral angiography. The possible role of SLE-associated cerebral vascular changes in the development of this aneurysm is discussed.
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PMID:A case of central nervous system lupus associated with ruptured cerebral berry aneurysm. 250 73

The Authors submitted 53 randomly selected patients affected by systemic lupus erythematosus (SLE) to neurologic evaluation to investigate the prevalence of neurologic manifestations, establish relationships to clinical and epidemiological findings and antinuclear antibodies and/or lupus anticoagulant (LAC), as well as to assess the usefulness of electroencephalogram (EEG), saccadic eye movements (SEM) analysis, brain computerized tomography (CT). Twenty-two patients (41.5%) had nervous system involvement on anamnestic and/or clinical examination: there were seizures in 5 patients, headache in 3, involuntary movements in 3, psychosis in 2 and cerebrovascular disorders in 9. The patients were subdivided into 2 groups, with neuro-SLE and without neuro-SLE, according to clinical and/or anamnestic evidence of nervous system involvement. There were no differences between the two groups of patients regarding disease duration, disease activity, presence of antinuclear antibodies and/or LAC. EEG and/or SEM and/or brain CT abnormalities were found in 38 cases, 18 of which had no clinical evidence of neuro-SLE. Instrumental evaluation can thus document subtle nervous dysfunction and offers the possibility of classification into: a) non-neuro-SLE; b) subclinical neuro-SLE; c) overt neuro-SLE.
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PMID:[Neurological manifestations of systemic lupus erythematosus. Study of 53 cases]. 251 98

Magnetic resonance (MR) imaging and computed tomography (CT) are useful for the evaluation of central nervous system (CNS) lupus. This report describes the use of cranial MR and CT in 21 patients with systemic lupus erythematosus (SLE) with acute neuropsychiatric symptoms manifested by headache, seizures, focal neurological deficits, psychosis, or organic brain syndrome. Computed tomography was found to be insensitive and detected only diffuse atrophy (two cases), cerebral infarct (one case), and intracerebral haemorrhage (one case) in the 21 patients. Cranial MR images obtained with a General Electric 1.5 tesla Signa unit detected labile and fixed areas of increased proton intensity interpreted as focal oedema (eight cases), infarct (10 cases), haemorrhage (one), atrophy (seven), and acute sinusitis (two). Focal oedema was characterised by labile, high intensity lesions in the gray or white matter of the cerebellum, cerebrum, or brain stem, which completely resolved after aggressive corticosteroid treatment. Most high intensity reversible or fixed lesions evident on MR were not apparent on cranial CT images. In several patients sequential MR images were valuable in monitoring the efforts of treatment. Although histological confirmation of the high intensity brain lesions apparent on MR is desirable, prior necropsy studies suggest that pathological confirmation may be difficult owing to the paucity of recognisable brain lesions in patients with CNS lupus. It is concluded that for the evaluation of acute neuropsychiatric SLE MR is useful and provides more information than cranial CT.
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PMID:Magnetic resonance and computed tomographic imaging in the evaluation of acute neuropsychiatric disease in systemic lupus erythematosus. 261 53

A case of anti-phospholipids auto-antibodies syndrome is reported; it was an unusual expression of Systemic Lupus Erythematosus (SLE). The patient is a 38 years old woman, with a history of recurrent peripheral thrombosis, pulmonary and cerebral embolism, thrombocytopenia, abortions; moreover she suffered from arterial hypertension, and headache. Features of onset, with several episodes of relevant clinical severity and the long period without clinical and laboratory hallmarks of SLE suggest a serious caution in the diagnosis of "pure" anti-phospholipids auto-antibodies syndrome.
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PMID:[Antiphospholipid antibody syndrome: description of a case]. 264 52

The three best-described genetic polymorphisms of drug metabolism--the debrisoquin/sparteine type of oxidative polymorphism (hereafter referred to as the debrisoquin polymorphism), the polymorphism of N-acetylation, and the mephenytoin type of oxidative polymorphism--are reviewed. For all three polymorphisms, the poor-metabolizer phenotype is inherited as an autosomal recessive trait. The debrisoquin and mephenytoin oxidative polymorphisms involve defects in two separate cytochrome P450 enzymes. The prevalence of the poor-metabolizer phenotype for debrisoquin ranges between 2% and 10% for groups of various ethnic origins. The poor-metabolizer phenotype for mephenytoin comprises about 5% of the Caucasian population and about 20% of the Japanese population. N-acetyltransferase is a cytosolic enzyme whose clinical polymorphism was discovered using isoniazid as the substrate probe. The prevalence of the slow-acetylator phenotype among American and European Caucasian and American black groups is about 50%; among the Japanese it is about 10%. More than 20 agents are substrates for debrisoquin hydroxylase, about 15 for N-acetyltransferase, and 3-5 for mephenytoin. In poor metabolizers, debrisoquin can cause hypotension, and sparteine can cause blurred vision, headache, and dizziness. Clinical consequences of the slow-acetylator phenotype include increased susceptibility to systemic lupus erythematosus induced by procainamide and hydralazine, peripheral neuropathy induced by isoniazid, hydralazine, and dapsone, and sulfasalazine-induced dose-related leukopenia, nausea, vomiting, headache, and vertigo. After administration of mephenytoin, poor metabolizers have increased somnolence and intellectual impairment. Awareness of genetic polymorphisms of drug metabolism should improve understanding of interindividual variability in drug disposition and response.
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PMID:Polymorphic drug metabolism. 268 60


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