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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 panel of nine monoclonal antibodies raised against human hemopoietic cells was used for immunohistological labeling of frozen sections of human nervous tissues and tumors. Three antibodies showed a remarkably consistent labeling pattern when tested on 18 samples of normal or reactive tissue, on 31 neurogenic and 17 non-neurogenic tumors in an indirect immunofluorescence technique. VIM C6, an antibody recognizing cells of the granulocyte series, showed surface labeling of normal and reactive glial cells and of all types of glioma regardless of the grade of malignancy. VIT 13, an antibody recognizing activated T-cells, labeled the processes of normal, reactive, and neoplastic glia in a manner very similar to but not identical with glial fibrillary acidic protein (GFAP). VIB C5, an antibody recognizing B cells and granulocytes, showed surface labeling restricted to malignant cells (malignant gliomas and primitive neuroectodermal tumors) and fetal brain, thus recognizing, within the nervous system, an oncofetal antigen. Due to this operational specificity within the nervous system, some of the antibodies described here might have a role as diagnostic markers for CNS tumors. This study confirms and expands previous data that sharing of antigenic determinants by hemopoietic cells and nervous tissue or neurogenic tumors is common. However, the significance of such cross-recognition is still obscure. It is tempting to speculate that cross-reacting auto-antibodies might contribute to tissue damage in some immune-mediated neurologic diseases (myasthenia gravis, multiple sclerosis, CNS involvement in
systemic lupus erythematosus
) or to impairment of immunoregulation in multiple sclerosis or glioma patients. Furthermore, sharing of surface determinants might be responsible for the dual tissue tropism of some viruses, including the lymphotrophic virus (HTLV) in the
encephalopathy
of the acquired immune deficiency syndrome (AIDS).
...
PMID:Shared antigenic determinants between human hemopoietic cells and nervous tissues and tumors. 241 Oct 97
Magnetic resonance imaging was sued to examine the brains of 13 patients with
systemic lupus erythematosus
(
SLE
) who had experienced symptoms and signs of
encephalopathy
. All the patients had normal computerized tomographic scans. Four patients with abnormal magnetic resonance imaging studies had active central nervous system disease. None of the 9 patients with normal scans had active nervous system involvement at the time of study. Parenchymal lesions were usually located in the region of the corticomedullary junction or in the deep periventricular white matter. In coronal sections, some of the corticomedullary lesions extended centripetally as thin irregular lines into the white matter approximating the course of penetrating arterioles of the brain. The parenchymal lesions resolved in 4 months in 1 patient, but persisted unchanged in the others despite clinical improvement or a stable clinical course. It is likely that the parenchymal lesions of these patients represent intrinsic vasculopathy of small cerebral vessels and perivascular microinfarctions associated with
SLE
.
...
PMID:Central nervous system lupus erythematosus: the value of magnetic resonance imaging. 339 69
Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated
lupus
, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension,
encephalopathy
, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
...
PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33
Phenobarbital and phenytoin have good antiepileptic effect, but clinically significant untoward effects occur during their long-term use. Phenobarbital may cause hyperactivity, behavioral problems, sedation, and even dementia; these effects are dose related to some extent. Side effects of phenytoin include sedation, a cerebellar syndrome, phenytoin
encephalopathy
, psychosis, locomotor dysfunction, hyperkinesia, megaloblastic anemia, decreased serum folate level, decreased bone mineral content, liver disease, IgA deficiency, gingival hyperplasia, and a
lupus
-like hypersensitivity syndrome. Especially susceptible to the neurotoxic effects of phenytoin are epileptic children with severe brain damage who are on multiple drugs. In those children, balance disturbance may develop and be followed by gradual loss of locomotion. Among 131 mentally retarded epileptic patients, phenytoin intoxication occurred in 73 (56%), of whom 18 experienced persistent loss of locomotion. There is experimental evidence that the toxic action of phenytoin lies at the cellular level, predominantly in the cerebellum. Many experts avoid the long-term use of phenytoin because of its insidious and potentially dangerous side effects.
...
PMID:Side effects of phenobarbital and phenytoin during long-term treatment of epilepsy. 642 97
An analysis of two new cases and four previously reported cases produced evidence for a syndrome of arterial-occlusive retinopathy and
encephalopathy
. All six patients were women; they ranged in age from 21 to 40 years. The clinical features of this condition include multiple branch retinal arterial occlusions and
encephalopathy
in which behavioral and memory disturbances predominate early. Hearing loss is frequent. Except for cerebrospinal fluid pleocytosis and an increased cerebrospinal fluid protein level, there are few laboratory or radiographic abnormalities. The disease may be responsive to corticosteroid therapy. There are some similarities between this syndrome and
systemic lupus erythematosus
but it appears to be a distinct disease entity. A comparison of the retinal findings with those described in experimental allergic encephalitis suggests that this may be a virally induced immune-mediated disease. Although only four clearly documented examples of this syndrome have been reported, we suspect that cases may have been overlooked because of failure to recognize arterial branch occlusions in the peripheral retina.
...
PMID:A syndrome of arterial-occlusive retinopathy and encephalopathy. 647 46
Paired serum and cerebrospinal fluid specimens from 19 patients with
SLE
and central nervous system dysfunction were studied with respect to cerebrospinal fluid IgG index (a measure of intrathecal IgG synthesis), isoelectric focusing using immunoperoxidase staining techniques to detect oligoclonal IgG, and determination of the cerebrospinal fluid/serum albumin quotient (Q albumin) as a measure of blood-brain barrier integrity. Twenty-five patients without neurologic disease and 70 patients with a variety of non-
SLE
neurologic disorders were also studied for comparison. Of most interest was the observation that 42 percent of the patients with
SLE
had cerebrospinal fluid oligoclonal IgG, usually in association with elevation of the cerebrospinal fluid IgG index. In addition, two of the cerebrospinal fluid specimens that exhibited oligoclonal IgG also had increased titers of alpha-interferon. Q albumin was normal (under 9.0) in 12 of 13 patients with
SLE
, who had seizure, psychosis, or cranial neuropathy as principal central nervous system manifestations (mean +/- SD = 5.3 +/- 2.4), but was significantly elevated (mean +/- SD = 27.4 +/- 18.8, p less than 0.001) in five of six patients with diffuse, major central nervous system injury, for example,
encephalopathy
with coma, transverse myelopathy, paraparesis. Blood-brain barrier impairment was not correlated either with presence of circulating immune complexes or with other clinical or serologic evidence for extra-central nervous system disease activity. Taken together, the data suggest that, within the limitations of the techniques used, impairment of the blood-brain barrier in
SLE
may be secondary to the central nervous system lesion, rather than a result of systemic immune complex injury. In addition, substantial evidence is provided for an ongoing humoral immune response within the central nervous system in this disorder, which, in certain patients, may be associated with the production of intrathecal alpha-interferon.
...
PMID:Intrathecal IgG synthesis and blood-brain barrier impairment in patients with systemic lupus erythematosus and central nervous system dysfunction. 683 7
Neurologic complications of
systemic lupus erythematosus
(neuro-SLE) are common. The most frequent manifestations of neuro-
SLE
are seizures,
encephalopathy
, and behavioral changes, but a wide variety of other neurologic abnormalities affecting the central and peripheral nervous system and muscle also occur. Although the prevalence of neuro-
SLE
is high, the diversity of clinical presentations, the multiple potential etiologies, and the absence of sensitive and specific diagnostic tests render diagnosis difficult. Recent advances in understanding mechanisms of neuronal dysfunction combined with advances in imaging techniques, including functional imaging, should help in diagnosis and management. The mechanisms of neurologic injury can be divided into three broad categories. First, neuronal dysfunction may result from direct effects of the immune system on brain cells such as autoantibody binding to cell surface, immune complex deposition with secondary inflammation, and effects of cytokines. Second, immune- mediated injury to supportive structures such as the vasculature may also affect the nervous system by producing ischemia. Finally, the neuraxis may be affected by any one of several immune and non- immune effects of infection, toxins, and metabolic disturbances.
...
PMID:Systemic lupus erythematosus: immunopathogenesis of neurologic dysfunction. 748 26
The authors report the case of a sixty-five year old woman initially suffering from a thrombocytopenia. The patient was diagnosed as having an autoimmune disease with a
lupus
anticoagulant, positive antinuclear antibodies and negative anti-DNA antibodies. She then developed an
encephalopathy
which was fatal despite corticosteroids. Brain pathology revealed a vasculitis with some giant cells, evoking a granulomatous angiitis of the central nervous system. These clinical and biological features suggest a
systemic lupus erythematosus
with vasculitis or a primary granulomatous angiitis of the central nervous system. Taking into account the clinical manifestations and the presence of a
lupus
anticoagulant, we finally preferred to identify it as a primary antiphospholipid antibodies syndrome, despite absence of anticardiolipin antibodies. Contrary to thrombosis, vasculitis is rarely associated with an anticardiolipin antibody or a
lupus
anticoagulant. However, vasculitis in the course of primary antiphospholipid antibodies syndrome has been reported previously as in this case report.
...
PMID:Association of cerebral vasculitis with a lupus anticoagulant. A case with brain pathology. 769 67
From 1977 till 1991, the diagnosis of
systemic lupus erythematosus
was made on 137 children aged 18 years or under in Chang Gung Memorial Hospital. The medical records were reviewed and the clinical data were analysed with emphasis on the morbidity and mortality of this disease. The clinical and laboratory characteristics were similar to the findings from most other reports. Renal failure accounted for 8% of the initial presentation. The non-infectious complications were, in the order of frequencies, hypertension, avascular necrosis of femoral head, cataract,
encephalopathy
, and venous thrombosis. Sepsis, cutaneous infection and urinary tract infection were the frequently encountered infectious complications. The major causes of death in childhood onset
systemic lupus erythematosus
were sepsis (42%) and renal failure (30.7%). Forty patients were lost to follow-up. The 5-year survival rate, calculated by life-table, was 76.3%.
...
PMID:The morbidity and mortality associated with childhood onset systemic lupus erythematosus. 806 33
We report a case of acute postinfectious
encephalopathy
in a child following Campylobacter jejuni enteritis. Serial MR scans showed lesions involving predominantly gray matter and the adjacent subcortical white matter--findings different from those in other immune-mediated disorders, such as
systemic lupus erythematosus
, in which either white or gray matter may be involved, and acute disseminated encephalomyelitis, in which white matter abnormalities predominate with involvement of the subcortical white matter.
...
PMID:Postinfectious encephalopathy in a child following Campylobacter jejuni enteritis. 845 26
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