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At least 19 recordsLinked to original sources
PubMed1994

Chilblain lupus erythematosus (lupus pernio): clinical review of the Mayo Clinic experience and proposal of diagnostic criteria.

Five cases of chilblain lupus erythematosus were retrospectively reviewed regarding their clinical, histopathologic, serologic, and immunofluorescence findings. Ages at onset of chilblain lupus erythematosus varied from 26 to 73 years, with a female-to-male ratio of 3:2. Since other entities can be confused with this disorder, we propose the following diagnostic criteria. The two major criteria are skin lesions in acral locations induced by exposure to cold or a drop in temperature, and evidence of lupus erythematosus in the skin lesions by results of histopathologic examination or direct immunofluorescence study. The three minor criteria are coexistence of systemic lupus erythematosus or other skin lesions of discoid lupus erythematosus, response to anti-lupus erythematosus therapy, and negative results of cryoglobulin and cold agglutinin studies. We conclude that chilblain lupus erythematosus can be diagnosed and treated. Discoid lupus erythematosus lesions respond more quickly to treatment than chilblain lupus erythematosus lesions. Treatment with antimalarial agents, prednisone, pentoxifylline, or dapsone was of benefit to our patients.

Adult↗
PubMed2000

An unusual case of systemic lupus erythematosus, lupus nephritis, and transient monoclonal gammopathy.

A 23-year-old female patient suffering from active systemic lupus erythematosus (SLE) was treated with azathioprine (2 mg/kg per day) and prednisone. Lupus nephritis class III with increasing proteinuria developed 28 months after disease onset. Treatment was switched to monthly pulse cyclophosphamide administered intravenously for 6 months (total dose 6.3 g), followed by oral azathioprine and low-dose prednisone to maintain partial remission. Eight months later, the patient developed an acute exacerbation of SLE with fever, proteinuria of 9.1 g/day, pancytopenia, and cerebral involvement with cephalgias and a grand mal seizure. She responded well to high-dose corticosteroids (500 mg prednisolone pulses over 3 days, i.v.) and was azathioprine switched from to methotrexate (12.5-15 mg per week). Under this treatment, lupus activity gradually decreased and the patient felt well again. Five years after the initial diagnosis of SLE, a rapidly increasing immunoglobulin G-kappa type (IgG-kappa) monoclonal gammopathy developed, reaching a maximal serum paraprotein concentration of 73.5 g/l. Bone marrow biopsy revealed 15% of moderately abnormal, highly differentiated plasma cells arranged in small clusters and expressing IgG-kappa. No bony lesions were detectable on skeletal radiographs. Pulses of dexamethasone (40 mg) were administered and led to a transient decrease of paraproteinemia to a minimum of 31.9 g/l, followed by an increase to 62 g/l. At that point, high-dose chemotherapy supported by autologous stem cell transplantation was considered. Due to an intermittent pneumococcal septicemia, methotrexate was discontinued and dexamethasone was replaced by 5-10 mg cloprednol. At this point, totally unexpectedly, the paraprotein decreased spontaneously without any further cytostatic treatment and was no longer detectable 1 year later. Concomitantly, plasma cell counts in bone marrow biopsies fell to below 5%. As SLE remained inactive, the patient became pregnant and gave birth to a healthy child. During late pregnancy, SLE activity flared up with rising proteinuria and blood pressure. Therefore, after delivery, cyclophosphamide (100 mg/day, orally) was readministered for 4 months, resulting in an improvement of kidney function with stable proteinuria of 1-2 g/l to date. Paraproteins are no longer detectable. In conclusion, this case report documents the rare event of transient paraproteinemia in a patient with SLE. A self-limiting regulatory defect in the control of a terminally differentiated B-cell clone may be the origin of this phenomenon.

Adult↗
PubMed1981

Noninflammatory renal microangiopathy of systemic lupus erythematosus ('lupus vasculitis').

5 (group 1) of 9 patients with systemic lupus erythematosus (SLE) who underwent a kidney biopsy during a 1-year period had a noninflammatory renal microangiopathy which significantly narrowed or occluded the lumens of arterioles and terminal segments of interlobular arteries. Though these lesions resemble those of malignant hypertension and the thrombotic microangiopathies, their distinctive features, revealed by light, immunofluorescence and electron microscopy, differentiate them from the others. 4 of these 5 (group 1) patients developed hypertension; in 3 the microangiopathy predated the hypertension. None of the remaining 4 (group 2) patients without these lesions has become hypertensive. One group-1 patient with extensive lesions involving 40% of intrarenal arterioles at biopsy developed renal failure shortly thereafter with increasing arteriolar involvement but unchanged glomerular histology.

Adult↗
PubMed1999

[Idiopathic thrombocytopenic purpura as first manifestation of systemic lupus erythematosus lupus].

OBJECTIVES: We studied SLE whose initial symptoms were related to idiopathic thrombocytopenic purpura (ITP) in order to determine if they share clinical and immunologic manifestations. METHODS: We reviewed the clinical backgrounds of 150 SLE (according to the ACR criteria) periodically followed from 1980 until 1998. We found 12 patients with both these conditions. RESULTS: All patients were female with a mean age of 32 at the time of ITP diagnosis and 36 at the time of SLE diagnosis. The most usual clinical manifestations were: arthritis (92%), cutaneous (58%) and hematologic involvement with lymphopenia (58%) and thrombocytopenia again (33%) after the initial ITP episode, always together with autoimmune hemolytic anemia (Evans syndrome). None of these patients presented with neurologic involvement and only one presented with renal involvement. 50% were positive for anti-DNA antibodies, 50% were Ro(+) and 16% were RNP (+). 66% were positive for antiphospholipid antibodies and 33% for lupus anticoagulant. Thrombocytopenia was controlled just with steroids in only 16% of the patients. Splenectomy controlled thrombocytopenia with complete remission achieved in 80% (4 from 5) of the patients and 20% (1 from 5) were refractory to this therapy after a medium follow-up time of 6.5 years. CONCLUSIONS: 1) SLE whose initial symptoms are related to ITP were characterized by joints, cutaneous and hematologic involvement without renal and neurologic manifestations. 2) Splenectomy was able to control refractory thrombocytopenia in the majority of these patients.

Adult↗
PubMed1989

A patient with probable systemic lupus erythematosus, lupus anticoagulant and myocardial infarction.

The case history of a 31-year-old woman is described. She had a history of thrombosis; in the past there had been an arterial embolus of the left superficial femoral artery and venous thrombosis of the right leg. The patient was admitted to hospital because of fever of unknown origin. During the hospital stay the diagnosis of probable SLE was made. She died of myocardial infarction. At autopsy, thrombosis of the small arterioles of the heart was found without sclerosis of the coronary arteries. A lupus anticoagulant could be demonstrated in her blood and seems to have been the cause of this rare complication. Treatment with anticoagulants is advised for patients with LAC and a history of thrombosis.

Adult↗
PubMed1994

[Kaposi-Irgang lupus erythematosus profundus. Lupus erythematosus panniculitis].

Lupus panniculitis is a rare variant of cutaneous lupus erythematosus. Two typical cases demonstrate the association of lupus panniculitis with signs of discoid lupus erythematosus and systemic lupus erythematosus. Clinically it is characterised by subcutaneous nodules or plaques, which may ulcerate leaving depressed atrophic scars. Histologically the lesions show lobular panniculitis. A positive immunofluorescent band test with deposition of IgG, IgM and C3 at the dermal-epidermal junction and blood vessel walls helps to confirm the diagnosis. The knowledge of the clinical features and histopathology of the disease is important because lupus panniculitis may precede systemic lupus erythematosus by some years.

Adipose Tissue↗
PubMed1997

Animal models of cutaneous lupus erythematosus and lupus erythematosus photosensitivity.

Over the past decade, the most exciting and important finding in SLE-prone mice is the discovery of Fas/Fas ligand systems in the pathogenesis of autoimmune phenomena. A human model for murine lpr/gld disease has also been reported recently. Furthermore, as shown in Table 2, studies on Ig variable region genes, TCR genes and MHC class II genes have given us much information concerning human and murine SLE. With respect to cytokines, IL-2 deficiency and the key role of IL-6 have been found in SLE-prone mouse strains, and Th2 cytokine production has been demonstrated to play a more pathogenic role than Th1 cytokine production in human and murine SLE except for MRL/pr mice. TGF is also very intriguing because TGF-beta knockout mice show SLE-like autoantibodies and Sjögren syndrome-like lymphoproliferation. Apart from these basic scientific investigations, there are also many promising and practical therapeutic approaches. In particular, treatments with anti-CD4 antibody and murine CTLA4Ig which bound B7 and blocked binding of CD28 to B7 are outstanding. However, it remains obscure whether such new approaches are effective for the skin lesions of SLE-prone mice, although some immunosuppressive agents such as FK506, cyclosporin and Chinese herbal medicines have been evaluated to determine their selective effects on the skin lesions of MRL/lpr mice. Needless to say, mouse models are not identical, but similar, to human diseases. However, they are important in the search for the underlying pathogenesis of autoimmune diseases on the basis of careful evaluation of the similarities and differences between human diseases and these models. If such studies are steadily performed, then inbred or experimental models will become more promising tools for the investigation of cutaneous lupus erythematosus.

Animals↗