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 pancerebellar syndrome of subacute progression associated with cerebellar atrophy is highly suggestive of a paraneoplastic cerebellar degeneration (PCD). We describe a 27-year-old woman with systemic lupus erythematosus (SLE) that presented with a subacute pancerebellar syndrome. Serum and CSF anti-Yo, anti-Hu and anti-Ri antibodies were not found neither in blood, nor in CSF. Brain MRI showed a cerebellar atrophy. The cerebellar ataxia improved markedly following corticosteroids administration. This case probably demonstrates that an antineuronal antibody negative subacute cerebellar disease may not only be a manifestation of paraneoplastic disease, but that it can also be associated with SLE.
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PMID:Subacute pancerebellar syndrome associated with systemic lupus erythematosus. 883 90

Cerebral venous thrombosis is a rare cause of focal neurological damage in patients with SLE. We describe a patient with SLE who presented with a focal neurological deficit and subsequently developed increased intracranial pressure. A superior sagittal sinus thrombosis was diagnosed by MRI. The association between SLE and superior sagittal sinus thrombosis is discussed. Early diagnosis is essential because treatment leads to a positive clinical outcome.
Lupus 1996 Aug
PMID:Superior sagittal sinus thrombosis in a patient with systemic lupus erythematosus. 886 8

A 55-year-old woman with a several-decade history of thyroid goiter is presented here as a case of myasthenia gravis complicated with hyperthyroidism and thymoma with serological evidence of systemic lupus erythematous (SLE). She had had right eyelid ptosis since July 1992, with a positive tensilon test. The acetylcholine receptor antibody titer was 4.01 nmol/L. A thyroid function test revealed T3: 162 ngidl, T4: 14.98 micrograms/dl, TSH:0.09 microIU/ml and positive anti-microsomal antibody (1:400). An MRI of the chest showed a thymoma in the left thymus. Other autoantibody screenings include ANA (1:320, speckled pattern) and anti-ds DNA (+) suggesting a serological association with SLE. After three courses of plasmapheresis, she received an extended maximal thymomectomy and a subtotal thyroidectomy. She was then treated with prednisolone, Mestinon, Eltroxin and discharged without complications. The coexistence of myasthenia gravis, hyperthyroidism, thymoma and a serological evidence of SLE have not previously been documented in the literature.
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PMID:Myasthenia gravis complicated with hyperthyroidism, thymoma and serological evidence of systemic lupus erythematosus: a case report. 887 Mar 31

We report a patient with medial medullary infarction who showed deep sensory impairment as his prominent neurological manifestation. A 54-year-old man with a history of hypertension was admitted to our hospital with numbness of the bilateral upper and lower extremities, followed by dysarthria and right hemiparesis. Physical examination revealed no abnormalities except for high blood pressure. He hiccuped continuously. On neurological examination, he exhibited dysarthria, mild dysphagia and right hemiparesis without facial or lingual paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and thromboxane synthetase inhibitor. His hiccups stopped within two weeks, and his right hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive lupus anticoagulant. MRI showed bilateral infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities. Neurological manifestations of our patient are not typical of medial medullary infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable hiccups to the bilateral medial medullary lesions, and emphasize the importance of lupus anticoagulant as one of the risk factors in brainstem infarction.
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PMID:[A case of medial medullary infarction with prominent deep sensory impairment]. 892 33

The 11-year-old girl had hypertension and generalized tonic-clonic convulsions during the steroid pulse therapy. Her cranial T2-weighed MRI showed small areas of high signal intensity in the right occipital lobe. Her neurological findings were normal. After 2 months of steroid pulse therapy, multiple high signal intensities were demonstrated on T2-weighed MRI. After 5 months of the therapy, however, only a small T2-weighed MRI spot of high signal intensity in the white matter was observed, and the multiple lesions disappeared. On follow up, she did not show any neurological defects. It is postulated that not only steroid pulse therapy-induced hypertension but also SLE-induced angiopathy caused such flexible lesions. According to the literature, these lesions can be considered to be edema around small vessels. Such MRI findings have been reported in adult patients with SLE, but to our knowledge there have not been reports on children with SLE.
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PMID:[Reversible changes of cranial MRI in a girl with SLE]. 898 98

A 26-year-old woman was admitted to our hospital because of fever of unknown origin. She had been treated with prednisolone, elcatonin and alfacalcidol under the diagnosis of systemic lupus erythematosus (SLE) and aseptic necrosis of femoral bone head. Six months ago she began to have a fever and subsequently left low back pain, for which extensive examinations were performed in other hospital but their causes remained unclear. She was referred to our hospital for further evaluation and therapy in October 1995. Bacteriological, immunological or serological examinations did not reveal the origin of fever. CT and ultrasonic examination did not show any abnormality. However, MRI, which was taken for the evaluation of aseptic necrosis of femoral bone head, showed the abscess shadow in sacroiliac joint. Open biopsy was performed and Mycobacterium tuberculosis bacilli were detected from the abscess. To our best knowledge, this is the first report of SEE with tuberculosis sacroiliac arthritis.
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PMID:[A case with systemic lupus erythematosus complicated with tuberculosis sacroiliac arthritis]. 912 22

A 34-year-old woman was admitted to our hospital because of ptosis, dysarthria, muscle weakness of upper limbs and skin lesions. At the age of 22 years, she was diagnosed as having systemic lupus erythematosus (SLE) due to the presence of arthritis and high titer of antinuclear antibody. On admission, the high antiacetylcholine receptor antibody titer, along with the positive tensilon test and electromyography established a diagnosis of myasthenia gravis (MG). The demonstration of anti-intercellular antibodies both in cutaneous tissue and blood confirmed the diagnosis of pemphigus. MRI showed hypertrophic thymus. After thymectomy, the myasthenic symptoms aggravated and SLE and pemphigus erythematosus relapsed despite anti-cholinesterase treatment with plasmapheresis. She was then placed on corticosteroid therapy with an improvement of her all symptoms. This very rare case of MG associated with SLE and pemphigus erythematosus suggests that these diseases share common immunological abnormalities.
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PMID:[A case of myasthenia gravis associated with systemic lupus erythematosus and pemphigus erythematosus]. 916 41

Transient musculoskeletal pain may occur in renal transplant patients on cyclosporin (CyA). Of 28 consecutive patients transplanted in this unit between 20 January 1995 and 2 May 1996, eight (two published elsewhere) developed this problem. Before transplantation, three of the patients had received prednisone intermittently or continuously for 15, 5 and 2 years, for asthma, crescentic GN and SLE, respectively. All patients had normal hand radiographs prior to transplantation. Five developed acute rejection following transplantation requiring treatment with methylprednisolone; one also required OKT3 (7 days). Weight-bearing joints of the lower limbs became affected at 3-40 weeks (mean 14) following transplantation. MRI changes (T1-, T2-weighted and STIR images) were consistent with acute bone-marrow oedema. Bone scintigrams showed enhanced tracer uptake in affected joints. A spontaneous complete remission occurred in five patients within 4-16 weeks, and this was supported by serial imaging. The other patient underwent core decompression of the femoral heads with relief of symptoms, but MRI showed bilateral avascular necrosis (AVN) of the femoral heads. MRI proved useful in detecting acute bone-marrow oedema and its possible progression to AVN. The former may be either a distinct entity or a forerunner of AVN.
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PMID:Acute bone-marrow oedema in cyclosporin-treated renal transplant recipients. 920 72

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
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PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

A 56-year-old woman with systemic lupus erythematosus developed septic arthritis and bursitis of the left shoulder due to an atypical mycobacterium, M. xenopi. Plain radiography, ultrasound (US), and MRI were performed. Articular disease by tuberculous and nontuberculous mycobacteria have similar presentations, clinically as well as radiologically, and have to be differentiated from other chronic bacterial or fungal infections, pigmented villonodular synovitis, rheumatoid arthritis, gout, hemophilia, and synovial chondromatosis. Although atypical mycobacterial involvement of the skeleton and soft tissues is relatively uncommon, its incidence is increasing, as is the incidence of extrapulmonary tuberculosis in western countries. The triad of Phemister is reemphasized, and the US and MRI findings are demonstrated. The definitive diagnosis has to be made by culturing biopsied synovium or synovial fluid.
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PMID:Nontuberculous mycobacterial bursitis and arthritis of the shoulder. 950 8


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