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PubMed1986

Progressive multifocal leukoencephalopathy complicating systemic lupus erythematosus.

Two patients with systemic lupus erythematosus who developed progressive multifocal leukoencephalopathy (PML) are described. Although the time of PML onset could not be determined with certainty, it probably developed after steroid-induced immunosuppression. However, high-dose corticosteroids appeared to produce transient amelioration in the neurologic disorder. We suggest that PML is an important addition to the list of conditions to be considered in the differential diagnosis when a patient with systemic lupus erythematosus develops neurologic abnormalities.

Adult↗
PubMed2006

[Terbinafine-induced Stevens-Johnson syndrome and aggravation of systemic lupus erythematosus].

BACKGROUND: There have been published reports of induction and aggravation of subacute systemic lupus erythematosus of lupus by terbinafine. We report the case of female patient with systemic lupus erythematosus who, after treatment with terbinafine, presented a Stevens Johnson syndrome eruption, together with renal exacerbation of her connective tissue disease. OBSERVATION: A 25 - year-old woman was followed for 4 years for systemic lupus erythematosus was no renal involvement. The patient was stable under corticosteroids (20 mg/d) and chloroquine (200 mg/d). She was treated with terbinafine onychomycosis caused by Trichophyton rubrum. Seven days after trunk and limbs, with cheilitis affecting the mucous membrane and bilateral conjunctivitis. This rash was followed by epidermolysis involving 10% of the cutaneous area. Stevens-Johnson syndrome was diagnosed. Laboratory tests indicated massive hematuria and proteinuria, and the renal needle biopsy sample showed signs of class III lupus glomerulonephritis. The anti-histone antibodies were highly positive. The patient was treated with systemic corticosteroids (1 mg/kg/d), chloroquine was recommenced and cyclophosphamides were given in a bolus. The outcome of the patient's eruption and lupus was favorable. DISCUSSION: Although induction and worsening of lupus by terbinafine have already been reported, the present case differs through the concomitant occurrence of eruption on treatment with terbinafine and severe relapse of lupus, thus suggesting the involvement of a shared immunological mechanism.

Adult↗
PubMed2001

An update on the genetics of systemic lupus erythematosus.

The development of systemic lupus erythematosus has a strong genetic basis. The techniques to study the genetics of SLE have improved, and family-based studies have been gaining importance due to advances in the human genome project. Recently, complete genome scans with microsatellite markers and linkage analysis have been performed in human systemic lupus erythematosus in various populations. These studies represent the first step of a process towards the identification of susceptibility genes in SLE. We review here the results of the human genome scans performed until now and provide an update of the latest advances on the genetics of SLE in linkage studies and association analyses of candidate genes.

Female↗
PubMed1990

Response of discoid and subacute cutaneous lupus erythematosus to recombinant interferon alpha 2a.

Ten patients suffering from discoid lupus erythematosus (DLE) or subacute cutaneous lupus erythematosus (SCLE) were treated with interferon alpha 2a. A marked improvement or clearing of cutaneous lupus erythematosus lesions was observed in eight of them. However, the response to interferon was of short duration and within a few weeks after interferon withdrawal all patients who were improved or cleared relapsed. This study suggests that interferon alpha 2a represents a new interesting approach in the treatment of DLE and SCLE. Ongoing trials will define the optimal treatment schedule for the maintenance of interferon-induced improvement of cutaneous lupus erythematosus.

Dose-Response Relationship, Drug↗
PubMed1985

Splenectomy does not cure the thrombocytopenia of systemic lupus erythematosus.

Fourteen patients with systemic lupus erythematosus had splenectomies done between 1960 and 1982 for treatment of severe thrombocytopenia. Thrombocytopenia persisted or recurred within 1 month postoperatively in five patients and within 6 months in three others. Three patients had late recurrence (18, 30, and 54 months after splenectomy); in two it was probably related to withdrawal of immunosuppressive agents or corticosteroids. Median lowest platelet count before splenectomy and median platelet count at relapse or failure of splenectomy were both 8000/microL. Only two patients maintained normal platelet counts without need for corticosteroids or other treatment. These results differ from those in patients with idiopathic thrombocytopenic purpura. Other treatments should be tried before splenectomy is done for thrombocytopenia in patients with systemic lupus erythematosus.

Adult↗
PubMed1986

Lupus band test: anatomic regional variations in discoid lupus erythematosus.

Seventy-one patients with discoid lupus erythematosus were studied for anatomic regional variations in the lupus band test. The test was positive in 82% of biopsies from the scalp, face, neck, and upper extremity. Only three out of fourteen biopsies (21%) from the trunk were positive. Discoid lupus erythematosus could be confirmed or strongly suspected in the light microscopic sections from all cases. Truncal lesions should not be selected for the lupus band test in discoid lupus erythematosus if there are other choices.

Abdomen↗
PubMed1999

Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus.

Neuropsychiatric forms of systemic lupus erythematosus (SLE) vary, most commonly consisting of seizures, psychiatric disturbances, or focal central nervous deficits. This is a new case of neuromyelitis optica or Devic's syndrome during the course of SLE. Few reports of this association exist in the literature. Our objective is to report this unique case of Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus. A 28-year-old woman had been diagnosed as having SLE with cutaneous and articular involvement in 1987 when she was 17 years old. She was treated with a synthetic antimalarial agent associated with corticosteroids. In 1994, during the fourth month of pregnancy, she had signs of transverse myelitis with a sensory level at T6 associated with an optic neuropathy suggesting a Devic's syndrome. The patient was managed by plasmapheresis sessions and intravenous corticosteroids. Transverse myelitis recurred postpartum and three years later at the same thoracic level. Management by bolus administration of a steroid and cyclophosphamide resulted in remission again. There have only been around a dozen reports in the literature of patients who had both Devic's neuromyelitis optica and SLE. Magnetic resonance imaging is contributive to diagnosis and therapeutic follow-up, showing spinal cord lesions with increased intensity on T2-weighted sequences. Although the clinical course of the present patient has been favourable so far, the prognosis of this neurologic disease is generally considered to be poor with elevated mortality.

Adrenal Cortex Hormones↗
PubMed1990

Recombinant interferon alpha 2a is effective in the treatment of discoid and subacute cutaneous lupus erythematosus.

Ten patients suffering from either discoid lupus erythematosus (DLE) or subacute cutaneous lupus erythematosus (SCLE) were treated with interferon alpha 2a. Eight received low or intermediate doses (18-45 x 10(6) U/week) for a short period of time (4-8 weeks), with marked improvement of skin lesions in six, an exacerbation in one patient and no change in the other. Two patients with SCLE received high doses (100-120 x 10(6) U/week) over 12 weeks, with complete clearing of the lesions in one and a marked improvement in the other. The responses were of short duration and within a few weeks of stopping treatment all who had improved or cleared relapsed. The side-effects in all the patients were fever and a flu-like syndrome which necessitated a reduction of the dose in one case. In two patients there were increases in the liver enzyme levels, but no haematological toxicity was noted.

Adult↗
PubMed2002

Peripheral neuropathy in pediatric systemic lupus erythematosus.

Peripheral neuropathy is an uncommon manifestation of systemic lupus erythematosus and has not yet been characterized in pediatric patients. We report the clinical and electrophysiologic features of peripheral neuropathy in one child and three adolescents with lupus erythematosus. There were three females and one male. The peripheral neuropathy followed the onset of lupus erythematosus by a mean of 3 years. The onset of the neuropathy correlated with lupus erythematosus activity and presented with either severe pain or dropfoot. Nerve conduction studies revealed sensory and motor polyneuropathy in all patients and mononeuritis multiplex in two patients. Only one patient had associated central nervous system involvement at that time. All patients were positive for IgM and IgG anticardiolipin antibodies. Patients were treated with steroids, gabapentin, carbamazepine, azathioprine, and cyclophosphamide. Response to treatment was variable: two patients recovered and two had a partial response. Although an unusual manifestation, peripheral neuropathy should be kept in mind as part of the neurologic spectrum in lupus erythematosus. It is not necessarily associated with central nervous system disease. A role for antiphospholipid antibodies in the pathogenesis is suggested.

Adolescent↗
PubMed2000

Chlorpromazine induces apoptosis in activated human lymphoblasts: a mechanism supporting the induction of drug-induced lupus erythematosus?

OBJECTIVE: Drug-induced lupus erythematosus is a serious side effect of certain medications, such as procainamide, quinidine, hydralazine, chlorpromazine, and isoniazid, the underlying pathogenesis of which is unresolved. In this study, we examined the influence of these drugs on the regulation of apoptosis, or programmed cell death, in quiescent and activated human lymphocytes. We also discuss the dysregulation of apoptosis as a pathogenetic factor in systemic lupus erythematosus. METHODS: Peripheral blood mononuclear cells or activated lymphoblasts from normal donors were incubated with different concentrations of each of the above-mentioned drugs. RESULTS: We did not find induction of apoptosis in quiescent cells over a broad concentration range. In contrast, lymphoblasts readily underwent apoptosis when cultured with chlorpromazine, but not any of the other drugs, after stimulation with interleukin-2 (IL-2) in a dose-, time- and cell cycle-dependent manner. By several lines of evidence, toxicity was ruled out. Characteristic features of apoptosis-like incorporation of propidium iodide (PI), such as increased annexin V binding, changes in mitochondrial membrane potential, and induction of DNA breaks (as evidenced by TUNEL techniques), could be induced in lymphoblasts after chlorpromazine treatment. Chlorpromazine did not cause apoptosis by inhibition of cytokine binding or blockade of early intracellular signaling. The protease inhibitor Z-VAD and the ceramide inhibitor sphingosine 1-phosphate effectively blocked chlorpromazine-induced apoptosis (by PI staining and by externalization of phosphatidylserine), in contrast to the caspase 3/CPP32 inhibitor DEVD, which had only minor effects. Western blot analysis revealed IL-2-mediated phosphorylation of extracellular signal-regulated kinase, which was sensitive to chlorpromazine. Using lymphoblasts from a patient with Canale-Smith syndrome, we found that chlorpromazine-mediated apoptosis is Fas/ APO-1 independent. CONCLUSION: These data suggest that chlorpromazine mediates apoptosis in human lymphoblasts through specific activation of intracellular proapoptotic signaling cascades. This mechanism might lead to an unsynchronized inflow of apoptotic break-down products and thereby to the induction of (auto)immunity against nuclear components.

Apoptosis↗
PubMed1985

Embolic stroke complicating systemic lupus erythematosus.

Embolic stroke complicating systemic lupus erythematosus has been infrequently reported. We examined a 25-year-old woman who suddenly became hemiplegic. Two-dimensional echocardiography identified a source of emboli. At cardiac surgery, friable thrombotic vegetations were found adhering to the mitral valve leaflets, left ventricular septal wall, and chordae tendineae. At autopsy several weeks later, careful pathologic examination of the heart failed to reveal evidence of thrombus formation or endocarditis. An embolus identical in appearance to the thrombotic vegetations described at cardiac surgery was found lodged in the left middle cerebral artery underlying the recent brain infarction. To our knowledge, this is the first report of embolic stroke in systemic lupus erythematosus caused by extensive cardiac thrombus formation in the absence of underlying endocarditis.

Adult↗
PubMed1989

Complement system protein C4 and susceptibility to hydralazine-induced systemic lupus erythematosus.

21 patients with systemic lupus erythematosus induced by long-term treatment with hydralazine were investigated to see whether susceptibility to this syndrome was associated with deficiency of the classical pathway complement protein, C4. 16 of 21 (76%) patients had one or more C4 null (ie, non-productive) alleles compared with 35 of 82 normal subjects (43%). This difference was significant. The HLA-DR4 antigen, known to be in linkage disequilibrium with the C4B null allele, was also significantly more frequent in the patients (14 of 21 patients compared with 31 of 81 normal subjects). Susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythematosus, may depend partly upon genetically determined C4 levels.

Alleles↗
PubMed1981

[Development of "mixed connective tissue disease" (MCTD) from discoid lupus erythematosus].

A patient with discoid lupus erythematosus is reported which turned into a mixed connective tissue disease (MCTD) within five months. THe patient developed a severe polysymptomatic clinical picture with frailty, myositis, generalized erythema and livedo racemosa features, but without renal involvement. Combined therapy with prednisolone and azathioprine led to rapid regression of all symptoms. After releasing from the hospital a mitigated relapse could be controlled by increasing the dose of cortico-steroids. No other relapse occurred during the following year. Since the onset of disease the indirect immunofluorescence showed antinuclear antibodies of the speckled pattern. Also we could mark antibodies against ENA. We regard this finding as an indication, that in patients with discoid lupus erythematosus and antinuclear antibodies of the speckled pattern the risk of progressing into MCTD had to be considered. Repeated controls for symptoms of other collagenoses, therefore, should follow for a period of two years.

Antibodies, Antinuclear↗
PubMed2005

Discoid lupus erythematosus in an infant.

Discoid lupus erythematosus (DLE) is rare in childhood. We report the case of a 15-month-old female infant who presented with erythematous telangectatic lesions and photosensitivity involving the sun-exposed areas. Histological examination confirmed the diagnosis of DLE. Direct immunofluorescence (DIF) on lesional skin showed granular IgM deposits along basement membrane zone. Laboratory tests were normal. External photo-protection and topical corticosteroids lead to complete healing. Summer recurrences that responded to topical corticosteroids were noted but there was no progression to systemic lupus erythematosus. Several authors note the absence of female predominance in children with DLE; prevalence of photosensitivity is controversial. Histological confirmation of DLE is easy and important for diagnosis. DIF is not specific but can be helpful in establishing the diagnosis of DLE. Laboratory tests rarely show low titers of antinuclear antibodies. Treatment is based on sun avoidance and photoprotection. Topical corticosteroids are indicated for active lesions. For resistant cases antimalarials are the treatment of choice. Progression to SLE is probably more frequent in children than in adults.

Female↗
PubMed2006

Lymphopenia at presentation is associated with increased risk of infections in patients with systemic lupus erythematosus.

BACKGROUND: Patients with systemic lupus erythematosus (SLE) frequently suffer from infections, but the predisposing risk factors, as well as the exact frequency and nature of such infections, are not fully understood. AIM: To describe the frequency, types and risk factors for infections in a group of Chinese patients in the early stage of SLE in Hong Kong. DESIGN: Retrospective record study. METHODS: We reviewed the case records of 91 Chinese SLE patients, presenting <12 months after SLE diagnosis. Details of major infections (requiring intravenous antimicrobial therapy, or any confirmed mycobacterial infection) and minor infections were reviewed. Clinical and laboratory features, the systemic lupus erythematosus disease activity index (SLEDAI) at presentation and drug treatment were recorded and analysed. RESULTS: There were 48 major infections and 62 minor infections during 260 patient-years of follow-up. A lymphocyte count < or =1.0 x 10(9)/l at presentation was independently associated with an increased risk for major infection: hazard ratio 4.7 (95%CI 1.6-13.7), p = 0.005. SLEDAI, use of corticosteroids and immunosuppressive therapy were all not associated with increased risk of infection. DISCUSSION: Lymphopenia was an important risk factor for major infections in this group of Chinese patients in the early stages of SLE. SLE patients with lymphopenia at presentation should be closely monitored for the development of infective complications.

Adolescent↗
PubMed1979

[New studies on the pathogenesis of lupus erythematosus].

The pathogenesis of the lupus erythematosus results from co-operation of three principles: (1) genetical disposition, (2) increased reactivity of the immune system, (3) different exogenic influences. The genetical disposition is confirmed by family investigations, metabolic disorders and immune anomalies as well as by parallels to animal models. The reaction manner of the immune system is genetically determined. Exogenic factors influence the immune system (behaviour) either as starter or by modifying the genetical material. The most striking humoral immune phenomenon is an immense number of (auto-)antibodies. Investigations of xeroderma pigmentosum as well as with DNA of different antigenity have shown that an increase of the antigenicity is unlikely for this phenomenon. In the serum of patients there were established and partially characterized factors (mitogens, granulocytic adherence-factor) for increasing the immune reactivity. The increase of such factors may be the sequence of a T-suppressor cell-defect. Like-wise no interdigitating cells in systemic lupus erythematosus have been found, cells which may be responsible for the terminal differentiation of T-lymphocytes. The mode of action of exogenic factors is represented and discussed with the example of the UV provocation.

Antibodies↗
PubMed1995

Bullous systemic lupus erythematosus: revised criteria for diagnosis.

Blistering in systemic lupus erythematosus has been divided into three groups. A specific subgroup of 'bullous systemic lupus erythematosus' has been defined by Gammon et al. on the basis of a number of criteria. From our experience of seven patients with bullous systemic lupus erythematosus, and after reviewing the literature, we suggest that the current classification is too narrow. Our patients displayed clinical and immunohistological (based on direct and indirect immunofluorescence and Western immunoblotting) heterogeneity. Sera from two patients bound to epidermal epitopes in sodium chloride-split skin, but immunoblotting was negative. In neither of these patients could the target antigen be type VII collagen, the only antigen identified as pathogenic in this disease. Patients with epidermal binding should not be excluded from a diagnosis of bullous systemic lupus erythematosus. SLE is a disease in which there is a genetic predisposition to form antibodies to type VII collagen, along with other autoantibodies, many of which may be implicated in blistering. We suggest that the criteria for the diagnosis of BSLE should be revised. We define this disease as an acquired subepidermal blistering disease in a patient with SLE, in which immune reactants are present at the basement membrane zone on either direct or indirect immunofluorescence.

Adult↗