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)

The aim of the study was to evaluate the prevalence of headache in patients with systemic lupus erythematosus (SLE), its classification and estimation if they are the symptoms of central nervous system (CNS) involvement in patients with SLE causing any pathologies in EEG and neuroimaging methods like SPECT and MRI. We examined 83 patients with systemic lupus erythematosus (81 females and 2 males) aged between 19 and 71 years. All patients had neurological examination and EEG complemented with SPECt and MRI in some cases. 65 patients reported headache, 45 of them complained of idiopathic headache and 20--symptomatic one. The group with symptomatic headache had more frequently paroxymal changes in EEG while changes in background activity were more often notified in patients with idiopathic headache. Both SPECT and MRI showed more cerebral pathologies in patients with idiopathic headache. In SPECT the most common were multiple perfusion deficits and in MRI small hyperintensive lesions in white matter of cerebral hemispheres. Headache is the most common neurological complaint in SLE. Headache associated with pathological results of EEG or neuroimaging methods indicate the presence of central nervous involvement in patient with SLE.
Pol Arch Med Wewn 2003 May
PMID:[Headache in patients with systemic lupus erythematosus: analysis of clinical EEG and neuroimaging studies]. 1476 79

The author presented the present classification, clinical course, diagnostic and prognostic problems and own remarks in juvenile systemic lupus erythematosus and juvenile dermatomyositis.
Pol Merkur Lekarski 2004 Mar
PMID:[Connective tissue diseases in childhood]. 1519 Jun 7

We report the case of a 22-year-old male survivor of myocardial infarction as the first symptom of systemic lupus erythematosus and antiphospholipid syndrome. The diagnosis of myocardial infarction was based on typical ECG and enzymatic chanches and subsequently confirmed by technetium 99 scintigraphy. However, coronary arteries appeared to be normal at angiography. The authors conclude that myocardial infarction in SLE could be caused by a combination of cardiac microvascular thrombosis and inflammation accompanying the antiphospholipid syndrome.
Pol Arch Med Wewn 2004 Feb
PMID:[Myocardial infraction as the first manifestation of systemic lupus erythematosus in a 22-year-old man]. 1523 Feb 34

The concentration measurement of the acute phase proteins in blood serum has been applied in differential diagnosis of inflammatory arthritis since a long time. However, it appeared that the qualitative changes such as the presence of different glycoforms of the acute phase protein that was a glycoprotein, enabled to differentiate acute inflammatory conditions including the chronic ones, and to determine the dynamics of inflammatory process. This phenomenon is defined as a main heterogeneity, whereas the determination of the proportions of particular glycoforms is known as glycosylation profile. The changes of this profile are well known in the course of acute inflammatory conditions such as: bacterial sepsis, skin burns complicated with bacterial infections or acute pancreatitis. Considerably less observations concern the chronic conditions as: rheumatoid arthritis, systemic lupus erythematosus and degenerative joint disease. The examination encompassed 25 patients with rheumatoid arthritis, 21 with systemic lupus erythematosus, 19 with reactive arthritis and 21 patients with degenerative joint disease whose diagnosis was established on the basis of international diagnostic criteria. In all these patient the changes of C-reactive protein (CRP), acid glycoprotein (AGP) as well as glycosylation profile of the AGP were evaluated. For this purpose the electrophoresis method of two affinity directions with concanavalin A was applied, whereas the concentration of particular acute phase protein was determined by Laurell's immunoelectrophoresis method. The variants of glycoprotein resulted from electrophoresis were calculated with aid of planimetric method, and the results were presented as a coefficient of glycosylation. The characteristic patterns of glycosylation profile in the course of systemic lupus erythematosus, rheumatoid arthritis and reactive arthritis may be useful in differential diagnosis of the above mentioned diseases.
Pol Merkur Lekarski 2004 Oct
PMID:[Analysis of the acid glycoprotein heterogeneity in patients with arthritis]. 1569 Jun 99

We present a 15-year-old boy with massive venous thrombosis who was admitted to hospital with non-specific complaints. Transesophageal echocardiography and spiral computer tomography showed pulmonary embolism. A coagulation screen was performed to identify hypercoagulability. Lupus anticoagulant was detected and the diagnosis of antiphospholipid syndrome was established. Therapeutic options in such condition are discussed and review of the relevant literature is presented.
Pol Arch Med Wewn 2004 Oct
PMID:[Venous thromboembolism in a 15-years old boy with antiphospholipid syndrome]. 1577 36

We present case of 55 years old female with systemic lupus erythematosus (SLE) and necrotic ulcerations in lower limbs. Etiology of this lesions was complex. In the presented case, vasculitis (microvasculitis) accompanying systemic inflammatory connective tissue disease coincides with deficiency of protein S and venous insufficiency lower limbs. It could determine necrotic type of ulcerations and location of lesions. In this case vasculitis was crucial importance and ulcerations were healed after immunosuppressive therapy. In similar cases it is often difficult to find factors responsible for development of ulcerations and it need different investigations. But detailed determine of etiopathogenesis gives guarantee therapeutic success.
Pol Arch Med Wewn 2005 Jan
PMID:[A case of cutaneous vasculitis in a patient with systemic lupus erythematosus]. 1613 Jun 3

Since the association between human foamy virus (HFV) with rheumatic autoimmune diseases remains controversial, this study was designed to determine the relationship between HFV and systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), or progressive systemic sclerosis (PSS). The bel1 and Pol sequences of HFV were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) in plasma and by PCR in peripheral blood mononuclear cells (PBMC) from patients with SLE, RA, and PSS. Antibodies against Bel1 and Pol were assessed by enzyme-linked immunosorbent assay. Active HFV infections were detected by a Bel1-responsive indicator cell line. The bel1 sequence was detected in the plasma (SLE 59, RA 32, and PSS 63%) and PBMC (SLE 54, RA 71, and PSS 57%). However, active HFV infection existed only in patients with the bel1 sequence in both plasma and PBMC. In SLE patients, antibodies against Bel1 (7.1%) and Pol (4.5%) were also detected. The results suggest a possible association between HFV infection and these autoimmune rheumatic diseases.
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PMID:Human foamy virus bel1 sequence in patients with autoimmune rheumatic diseases. 1636 88

Epileptic seizures may be an early symptom of systemic lupus erythematosus, while at the same time some of the epileptic drugs, namely carbamazepine (CBZ), phenytoin (PHT), valproic acid (VPA), ethosuximide (ETM), primidone (PRM), lamotrigine (LTG), zonisamide (ZNS) can cause lupus. A separate clinical problem is the fact that few cases of systemic lupus have as yet been identified by giving antiepileptic drug. We present the case of a 30-year-old woman with frequent simple partial seizures and few secondarily generalized seizures since the age of 18. She was treated with VPA for three years. Then, because of side effects the drug had to be withdrawn and was replaced by CBZ. After eight months duration of the treatment with CBZ, the dose was increased because a secondarily generalized seizure occurred again. After another two months, painful swelling of all joints and leucopenia were observed. During additional studies, LE cells and high titer of ANA antibodies were found. Systemic lupus erythematosus was diagnosed and prednisone therapy was introduced. In spite of the withdrawal of CBZ, the increased titer of ANA antibodies persisted for several years and skin and muscle biopsy performed five years from the onset of clinical symptoms disclosed inflammatory infiltration and presence of IgG and IgM deposits in skin and vessel walls. Control serological examinations, skin and muscle biopsy carried out after eight years of observation and lack of clinical manifestations permitted to exclude a connective tissue disease in our patient.
Neurol Neurochir Pol
PMID:[Carbamazepine-induced systemic lupus erythematosus--a case report]. 1662 12

In our article we describe the case of 24 years old woman with overlap syndrome under form of systemic sclerosis and systemic lupus erythematosus complicated by secondary antiphospholipid syndrome (APS). The first manifestation of antiphospholipid syndrome was intrauterine fetal death. Afterwards pulmonary embolism occurred. After several weeks in result of catastrophic course of antiphospholipid syndrome coronary artery thrombosis and myocardial infarction occurred with following prominent left ventricle systolic failure and multi organ failure. The patient died about one month after discharge from the hospital.
Pol Merkur Lekarski 2006 Mar
PMID:[Secondary lethal catastrophic antiphospholipid syndrome in 24-years old female patient with overlap syndrome (systemic sclerosis and systemic lupus erythematosus)]. 1678 Feb 70

In recent years new potential therapies of systemic lupus erythematosus, called biological therapies, have been developed. These agents influence some immunological reactions, essential for genesis of systemic lupus erythematosus, ie. T cells and B cells activation, antibodies production, cytokines and complement components activation. Pathogenic basis of using these therapies, their safety and efficacy assessment have been presented.
Pol Merkur Lekarski 2006 Mar
PMID:[Biological therapies of systemic lupus erythematosus]. 1678 Feb 79


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