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)

A 17-year old girl received prednisone and azathioprine for the treatment of systemic lupus erythematosus. She developed a fever and hallucinations 18 months later; cryptococcal meningitis was diagnosed. An internal ophthalmoplegia with loss of accommodation and dilation of the pupils developed together with bilateral lateral rectus palsy. Treatment with intravenous amphotericin resulted in disappearance of papilledema, muscle palsy, and internal ophthalmoplegia. We believe that the internal ophthalmoplegia was secondary to involvement of the accommodative and pupillary fibers of both third nerves at the base of the brain.
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PMID:Cryptococcal meningitis and internal ophthalmoplegia. 44 40

Eleven patients with systemic lupus erythematosus (SLE) also had headaches and/or visual hallucinations typical of those found in migraine. These migrainous symptoms were commonly associated with exacerbations of SLE and abated as disease activity subsided. In some cases corticosteroids were more effective than conventional antimigraine therapy in controlling headaches and scotomas. The data suggest that migraine-like phenomena may arise as a result of vascular dysfunction in SLE.
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PMID:Migrainous phenomena in systemic lupus erythematosus. 62 96

Sensory neuroophthalmic abnormalities due to cerebral lupus erythematosus, with involvement of visual pathways posterior to the optic chiasm, occurred in 12 patients with systemic lupus erhthematosus. Five underwent detailed evaluation because of an hallucination, 4 for visual loss, and 3 for both. Hallucinations were either unformed (for example, bright lights, straight lines) or highly formed (for example, faces), in which case they were invariably recognized by the patient as inappropriate. In no instance did they occur in association with delirium, confusion, or use of hallucinogenic drugs. Patients with loss of vision had scotomas, homonymous field defects, and cortical blindness. These features indicate disease in the posterior cerebral artery circulation, a localization often supported by ancillary neurologic findings, for example, vocal cord paralysis, diminished gag reflex. Thus, various visual dysfunctions may occur in systemic lupus erythematosus due to cerebral vasculitis. At times they may be the most prominent and disabling feature of the disorder.
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PMID:Cerebral disorders of vision in systemic lupus erythematosus. 114 49

Central nervous system (CNS) dysfunction in patients with systemic lupus erythematosus (SLE) is highly variable, although it is often described under a single heading of "neuropsychiatric" or "CNS" SLE. To clarify these CNS abnormalities, we studied 91 lupus patients, 63 of whom had CNS symptoms or signs, over 599 patient years. By placing patients in relatively homogeneous clinical groups (stroke, seizure, suicide attempt, hallucination, confusion, decreased alertness) we detected significant (but variable among groups) correlations with other manifestations of SLE, suggesting separate mechanisms for each CNS disorder. These correlations were lost if all "CNS-SLE" was considered as a single group. Patients with decreased alertness often had undetected systemic infections and had a high death rate from infection, rather than from CNS-SLE. The understanding of the pathogenesis and potential treatment of CNS disorders in lupus will depend on classifying the patients into homogeneous groups.
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PMID:Central nervous system disease in patients with systemic lupus erythematosus. 151 50

A review of the literature regarding central nervous system side effects of the nonsteroidal anti-inflammatory drugs (NSAIDs) revealed three general categories: aseptic meningitis, psychosis, and cognitive dysfunction. Aseptic meningitis is found most commonly in patients with lupus treated with ibuprofen, but it should be considered in any patient with meningitis if the patient has used NSAIDs. Psychosis, although infrequently reported with NSAIDs, should be suspected in an elderly patient started on a regimen of indomethacin who acutely develops disorientation, paranoia, or hallucinations. Finally, there appears to be some potential for memory dysfunction and attention deficits in elderly patients treated with NSAIDs. Until further studies are available on the incidence and severity of these cognitive changes, physicians should use low doses of NSAIDs in the elderly and remain alert to the possibility of such adverse side effects.
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PMID:Central nervous system side effects of nonsteroidal anti-inflammatory drugs. Aseptic meningitis, psychosis, and cognitive dysfunction. 206 81

In summary, procainamide is a useful agent for suppressing premature depolarization frequency. Its short half-life of elimination requires a dosing frequency of every 3 hours with regular dosage forms or every 6-8 hours with a sustained action dosage. Because of the extreme unpredictability of plasma concentration, the dosage must be titrated in each patient with electrocardiographic monitoring serving as the most useful method of evaluating efficacy. Maximum and minimum plasma concentrations are helpful in monitoring the achievement of therapeutic plasma levels and adjusting the frequency of dosing, especially in the presence of impaired renal function or low cardiac output. Adverse effects of procainamide include anorexia, nausea, vomiting, fatigue, insomnia, visual hallucinations, and disorientation; these are minor and cease with discontinuation of the drug. Agranulocytosis has rarely been reported. Long-term treatment has resulted in the occurrence of a lupus-like syndrome that is reversible when the drug is stopped. Procainamide is excreted in breast milk and infants of mothers receiving procainamide should not be nursed.
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PMID:Pharmacokinetics of a sustained release procainamide preparation. 703 27

We report a 10-year-old girl with reflex seizures characterized by visual and acoustic hallucinations, induced by visual and acoustic stimulations. The EEG showed atypical spike-wave discharges on the left temporo-occipital area, markedly activated by visual and acoustic stimuli (intermittent light, pattern-reversal stimulation and monoaural right pure tone). The patient was treated with carbamazepine and seizure stopped within 7 months. After 10 months from the start of the therapy she developed signs of systemic lupus erythematosus.
Lupus 1993 Aug
PMID:Reflex seizures as initial manifestations of systemic lupus erythematosus in childhood. 826 79

A rare SLE patient with central nervous system involvement (CNS-SLE) who relapsed presenting new symptoms associated with the development of serum anti-Sm antibody and was then successfully treated with cyclophosphamide (CY) pulse therapy is presented here. A 47-years old housewife was admitted to Kushiro City General Hospital because of fever, limb erythema and drowsy consciousness in September 1995. On the basis of convulsion, proteinuria, leukopenia, thrombopenia, serum positive tests for both anti-nuclear antibody and anti-SSA antibody and low complement levels, as well as elevations of IgG index and IL-6 in the cerebrospinal fluid (CSF), she was diagnosed as having CNS-SLE. Serum tests for anti CL-beta 2 GPI antibody and lupus anticoaglant was negative. Serum test for HBs antigen was positive. She was treated successfully with methylprednisolone (mPSL) pulse therapy and plasma exchange (PE). Prednisolone was gradually tapered to the dosage of 17.5 mg per day and she was discharged in April 1996. She was re-admitted because of fever, an exacerbation of skin eruption and arthralgia in October 1996. Serum anti-Sm antibody was found to be positive. mPSL pulse therapy was not effective. On the basis of hallucination and elevations of IgG index and IL-6 in the CSF, a diagnosis of relapsed CNS-SLE was made. However the level of IFN-alpha in the CSF was normal. Although PE was not effective, CY pulse therapy was markedly effective.
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PMID:[A recovered case of SLE with central nervous system involvement who relapsed presenting new symptoms associated with development of serum anti-Sm antibody]. 956 77

A 20-year-old woman with arthralgia, serositis, thrombocytopenia, proteinuria, muscle weakness, elevated creatinine kinase, and positive anti-Sm antibody was diagnosed as having polymyositis and systemic lupus erythematosus (SLE). She had persistent high temperature, sinus tachycardia, hyperhidrosis, mydriasis, visual disturbance, hallucination, and loss of consciousness. Levels of plasma adrenaline, noradrenaline, and dopamine and cerebrospinal fluid interleukin (IL)-6 and IL-8 were all high. A diagnosis of sympathetic hyperfunction accompanied by central nervous system (CNS) involvement in SLE was made parenteral. Pulse administration of high dose corticosteroid therapy was effective. This is the first reported case of a connective tissue disease with CNS involvement manifesting as sympathetic hyperfunction with high plasma catecholamine levels.
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PMID:Acute sympathetic hyperfunction in overlapping syndromes of systemic lupus erythematosus and polymyositis. 971 13

Thirty patients (24 inpatients and 6 outpatients) with a clinical diagnosis of SLE were examined between September 1, 1998 and August 1, 1999 in the rheumatology clinic of Jichi Medical School Hospital. All of these patients fulfilled the 1982 revised criteria of the American Rheumatism Association for the classification of SLE and had some psychiatric manifestations (psychiatric SLE; P-SLE group). Mean patient age was 38.6 +/- 13.0, and there were 5 males and 25 females. When classified into 5 subgroups according to the most prominent symptoms, the distribution was as follows: consciousness disturbance group: 6 (20%), schizophrenia-like group: 5 (16.7%), mood disorder group: 7 (23.3%), neurosis-like group: 10 (33.3%), and convulsive disorder group: 2 (6.7%). Among all 37 psychiatric episodes, symptoms appeared in 37.8% of cases during the acute phase of SLE (during onset or recurrence) and in 62.9% during the chronic phase (during remission). The profile of the P-SLE group showed that the psychiatric symptoms of the SLE patients were milder and more chronic than those described in previous reports. To begin to comprehend the psychopathology of SLE, we put forward the concept of "Psychiatric basal state" and "psychiatric conjugated state". The former is considered a direct reflection of the acute-phase SLE process on mental condition. It is defined clinically as psychiatric symptoms that parallel the activity of SLE and respond well to steroid therapy. The latter include all other psychiatric problems in which one cannot rule out the effects of pharmacological, somatic, personality, and environmental effects on psychiatric symptoms. Only 3 patients in the P-SLE group fulfilled the criteria for the "psychiatric basal state". All three patients belonged to the consciousness disturbance group, whose clinical features were defined as slight clouding of consciousness, so-called "Amentia" in the sense of the German terminology. The clinical profile of this state is: 1. the patients are young (about 16 years old), 2. the onset of psychiatric symptoms is within 5 years after the onset of SLE, 3. confusion and disorientation are the most characteristic features, and 4. the clinical course of this state is almost 2 months. The experience structure of the "psychiatric basal state" consists of: 1. difficulty in selecting and holding a topic in cognition, 2. confusion and emotional instability as the basal mood, and 3. primitive and floating forms of delusions and hallucinations. Using this concept of the "psychiatric basal state" as a clue, we can hypothesize the continuity of diverse psychiatric symptoms in SLE. The "proper process of SLE (Harada)" has a disintegrating effect on the "ego" and it allows various psychopathological phenomena to emerge in the experience field. Against this background, additional factors, such as secondary organ damage, personality structure, and social environment, induce organization of the "psychiatric conjugated state".
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PMID:[A clinical study of psychopathology in systemic lupus erythematosus]. 1102 78


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