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At least 1,063 records · Page 59Linked to original sources
PubMed2004

[Hyperprolactinemia in systemic lupus erythematosus. A prospective study of 38 cases].

OBJECTIVE: To study prospectively the serum prolactin concentrations among patients with systemic lupus erythematosus and their possible relationship to disease activity and manifestations. METHODS: Serum prolactin levels were measured by radioimmunoassay in 38 patients with systemic lupus erythematosus and 22 age matched controls. Patients with known secondary causes for hyperprolactinaemia, such as pregnancy, lactation, prolactinoma and taking medications known to induce prolactin secretion, were excluded from the study. Demographic, clinical and laboratory features of the patients were obtained. Patients were divided into two subgroups according to their disease activity. Mean prolactin levels from both groups were compared using student test, and prolactin from patients with systemic lupus erythematosus was correlated with variables of disease activity, including the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). RESULTS: Mean prolactin levels were higher in patients with systemic lupus erythematosus (15.4) than healthy controls (9.83); however, the difference did not reach statistical significance (p=). Hyperprolactinemia was found in 24 patients with systemic lupus erythematosus and 5 controls. The frequency of hyperprolactinaemia in systemic lupus erythematosus group was higher than healthy controls. No significant difference in mean prolactin levels was found between patients with active versus inactive disease (18.9 vs 18.5). CONCLUSION: Hyperprolactinaemia occurred significantly in patients with systemic lupus erythematosus, but did not correlate with disease activity.

Case-Control Studies↗
PubMedDate not supplied

Isoniazid-induced lupus erythematosus presenting with cardiac tamponade.

An estimated incidence of drug-induced lupus erythematosus caused by all drugs is 15,000 to 20,000 cases a year, and represents approximately 5 to 10% of the total number of patients with systemic lupus erythematosus. Approximately 22% of the patients treated with isoniazid for a mean of 6 months develop antinuclear antibodies. Isoniazid-induced lupus erythematosus affects either sex equally and the most common presenting feature is arthralgia or arthritis with anemia. Fever and pleuritis occur in approximately half of the cases, and pericarditis in approximately 30% of cases. IgG antibody to the (H2A-H2B)-DNA complex appears specific for the isoniazid-induced lupus erythematosus. The drug-induced lupus presenting with cardiac tamponade is a recognized feature of many drugs such as hydralazine, procainamide, and sulfasalazine. Reported here is a case of isoniazid-induced lupus erythematosus presenting with cardiac tamponade. A 73-year-old man was treated with isoniazid for 8 months at a dose of 300 mg a day. The patient responded to the withdrawal of the isoniazid therapy and placement of a pericardial window. The existing literature on the subject is reviewed.

Aged↗
PubMed1979

[Diagnosis of lupus erythematosus].

For the exact classification of lupus erythematosus, morphological criteria alone (clinical picture, histopathology, immunopathology from involved skin, immunoelectron microscopy) are not sufficient. It is the aim of this paper to discuss briefly the known criteria for the diagnosis of systemic lupus erythematosus with particular reference to the interpretation of more recent deagnostic methods (determination of certain antinuclear antibodies; lupus band test; C1q-binding assay.

Antibodies, Antinuclear↗
PubMed1997

[Treatment of discoid lupus erythematosus with sulfasalazine: 11 cases].

INTRODUCTION: Antimalaria agents and thalidomide are two reference drugs for discoid lupus erythematosus. In non-responders or after secondary resistance or contraindications, there are a number of alternative therapeutics which are less effective and more toxic. We therefore conducted an open study in patients with discoid lupus erythematosus treated with sulfasalazine. PATIENTS AND METHODS: Seven men and four women (mean age 40 years) with severe discoid lupus erythematosus (mean duration of disease 14 years) were treated with sulfasalazine (2 g/d). This treatment was initiated after a previous failure or contraindication of antimalarial drugs or thalidomide. The acetylation phenotype was predicted in all patients with N-acetyltransferase 2 genotyping. Genome DNA was tested for mutations causing an N-acetyltransferase deficiency. Homozygous individuals or those with heterozygous composites for the tested mutations were predicted slow acetylators and those with a homozygous or heterozygous genotype for an allele carrying a normal sequence at the mutation sites were predicted rapid acetylators. RESULTS: We had 7 complete responses, 1 partial response and 3 failures. Mean delay to efficacy was 7 weeks, longer for lesions involving the scalp (4 to 5 months). Six of the 8 responders were given sulfasalazine exclusively. The effect was suspensive and dose-dependent; the minimal effective dose was 1.5 g/d. Excepting light sensitization requiring discontinuation, there were no clinically significant side effects. Neutropenia occurred in one patient and moderate and transient live enzyme movements did not require treatment withdrawal. The only immunoallergic side effect (light sensitization) observed occurred in a slow acetylator. All responders except one were rapid acetylators. DISCUSSION: Salazosulfapyridine, or sulfasalazine, is composed of a derivative of 5-aminosalicylic acid and a sulfamide fraction, sulfapyridine. It is only marginally used in dermatology except for psoriasis. Its efficacy in chronic lupus erythematosus has been reported in one case. We confirmed the role of this compound in the treatment of chronic lupus erythematosus. The rare observations of induced lupus and development of antinuclear antibodies are not a contraindication, but require close regular clinical and biological surveillance. The potential risk is that possible hypersensitivity could lead to reserving sulfasalazine for severe resistant chronic lupus erythematosus after failure with antimalarials and thalidomide. Nevertheless, our study demonstrates that the slow acetylator phenotype predicts immunoallergic events, as observed by other authors, and would be a factor predicting nonresponse. If these results are confirmed by other studies, it would be possible to propose sulfasalazine as a treatment for discoid lupus erythematosus in rapid acetylators.

Acetylation↗
PubMedDate not supplied

Systemic and discoid lupus erythematosus: analysis of pulmonary function.

To determine the prevalence of pulmonary dysfunction in lupus erythematosus, 24 patients with systemic lupus erythematosus (SLE) and 5 patients with discoid lupus erythematosus (DLE) were studied. Diffusing capacity for carbon monoxide was abnormal in 17 (71 percent) SLE patients. A restrictive ventilatory defect was present in 6 (25 percent) and arterial hypoxemia in 4 of 23 (17 percent). The mean ratio of forced expiratory volume in one second to forced vital capacity (FVC) was 83 percent. To test for the presence of small airways disease, maximum expiratory flow rate at 50 percent of FVC was measured on air and on an 80 percent helium-20 percent oxygen mixture. Ten patients (5 smokers and 5 nonsmokers) with SLE were nonresponders to helium suggesting small airways disease. Pulmonary dysfunction was present in 90 percent (9/10) of SLE patients with a previous history of pleuritis and/or pneumonitis, and in 71 percent (10/14) without respiratory symptoms or history of lung disease and with a normal chest radiograph. Pulmonary function tests were normal in DLE patients except for an abnormal response to helium and/or mild arterial hypoxemia in two patients, all of whom were smokers. These data indicate that there is a high prevalence of pulmonary function abnormalities in SLE including patients without clinically evident pleuropulmonary disease.

Female↗
PubMed2005

New insights into the pathogenesis of systemic lupus erythematosus.

Although the etiology of systemic lupus erythematosus is unknown, recent studies have shed light on the pathogenetic pathways that lead to tissue damage. The immune system in systemic lupus erythematosus is characterized by a complex interplay between overactive B cells, abnormally activated T cells, and antigen-presenting cells. This leads to the production of an array of inflammatory cytokines, diverse autoantibodies, and immune complexes that in turn activate effector cells and the complement system leading to the clinical manifestations of the disease.

Autoimmunity↗
PubMed2004

Intestinal pseudo-obstruction as a presenting manifestation of systemic lupus erythematosus: case report and review of the literature.

A case of intestinal pseudo-obstruction as a presenting manifestation of systemic lupus erythematosus is presented. Systemic lupus erythematosus is an autoimmune disease with a wide spectrum of unpredictable multisystemic presentations. A case of systemic lupus erythematosus that was diagnosed in a patient whose initial presentation for the disease was acute renal failure, hydronephrosis, intestinal pseudo-obstruction, and false-positive syphilis serologies is presented. There have been 18 other cases of intestinal pseudo-obstruction associated with systemic lupus erythematosus to date in the English literature. A variety of gastrointestinal syndromes have been increasingly recognized as possible manifestations of systemic lupus erythematosus, and this case illustrates in particular that intestinal pseudo-obstruction may be a presenting manifestation of this disorder.

Adult↗
PubMed1995

[Systemic lupus erythematosus and Salmonella enteritidis osteomyelitis].

Infections in systemic lupus erythematosus are frequent. However, osteoarticular Salmonella infections are rarely reported. We report a case of systemic lupus erythematosus diagnosed in a 15 year-old girl. Seven months later, she presented with fever and a localized collection of the upper extremity of the left tibia related to a Salmonella enteritidis acute osteomyelitis (sub periosteal abscess). The out-come was chronic and led to death. The authors emphasize the severity of non typhoidal salmonellosis in systemic lupus erythematosus.

Adolescent↗
PubMedDate not supplied

Facial telangiectasia-an unusual complication of neonatal lupus erythematosus: report of one case.

Neonatal lupus erythematosus (NLE) is an uncommon passive autoimmune disease caused by transplacental passage of anti-Ro/SSA and/or anti-La/SSB or anti-U1RNP maternal autoantibodies. Common clinical manifestations include cutaneous lupus lesions, cardiac disease, notably congenital heart block, hematologic abnormalities, and hepatobiliary disease. The cutaneous lesions of NLE are usually transient, disappearing about six months after birth when maternal antibodies disappear from the infant's circulation. Persistent telangiectasia is a rare complication of NLE. We report a 3-year-old female who had cutaneous lupus with persistent facial telangiectasias over the frontal area. She was diagnosed with NLE at 2 months of age. Her findings then included cutaneous lupus, hemolytic anemia, a high titer of antinuclear antibodies (1: 640) with a speckled pattern, positive anti-Ro/SSA and anti-La/SSB antibodies, and absence of anti-dsDNA antibodies. Her mother had systemic lupus erythematosus with the presence of high titer of antinuclear antibodies (1: 1260) with a speckled pattern and positive anti-Ro/SSA and anti-La/SSB antibodies. The child's cutaneous lupus and hemolytic anemia disappeared at 6 months of age, but the telangiectasia persisted.

Antibodies, Antinuclear↗
PubMed1982

Cutaneous localization of the membrane attack complex in discoid and systemic lupus erythematosus.

Biopsy specimens of skin lesions from three patients with discoid lupus erythematosus and six patients with systemic lupus erythematosus contained the membrane attack complex, which comprises C5b through C9, as well as immune complexes at the dermal-epidermal junction. The basilar epithelium in these areas was vacuolated and edematous, and the dermis contained an inflammatory infiltrate. In contrast, 19 of 29 specimens of normal-appearing skin from patients with discoid or systemic lupus erythematosus showed only immune complexes at the dermal-epidermal junction, without the membrane attack complex. The other 10 specimens, all from patients without cutaneous involvement, showed neither immune complexes nor membrane attack complexes. These data suggest that immune complexes within skin lesions selectively generate the assembly of the membrane attack complex, which mediates membrane injury. A synergistic interaction of immune complexes and cofactors may be required to activate complement in areas of skin that are predisposed to tissue injury.

Adult↗
PubMed1992

Genetic and immunological mechanisms in the pathogenesis of systemic lupus erythematosus.

Recent research in systemic lupus erythematosus and animal models of lupus has provided new insight into the pathogenesis of this complex autoimmune disease. Progress has been made towards understanding the genetic contributions to disease susceptibility and induction, as well as towards elucidation of the lymphocyte abnormalities involved in pathogenic autoantibody production.

Animals↗
PubMed1995

Population and family studies of three disease-related polymorphic genes in systemic lupus erythematosus.

The contribution to systemic lupus erythematosus (SLE) of three lupus-associated polymorphisms (involving the C4A2 complement component, Humhv3005 and the T cell antigen receptor alpha chain gene) are investigated in 81 individuals from 14 multiplex SLE families, 41 unrelated lupus patients, and 88 unrelated healthy controls. The results show a strong association between C4A deletion and SLE in these families. While the current study confirms the previously reported association between hv3005 deletion and sporadic SLE, the study fails to support this association in familial SLE patients. Moreover, no correlation is detected between the occurrence of hv3005 deletion and C4A null alleles in lupus patients, suggesting that the effects of these genetic polymorphisms on predisposition to lupus are independent. The previously reported lupus-associated T cell receptor (TCR) alpha chain polymorphism is not detected in any of the individuals studied here. The combined data suggest that C4A null alleles predispose strongly to development of lupus, whereas the influence of hv3005 deletion is relatively weak. The results also suggest that contributions of weak susceptibility genes such as hv3005 to disease predisposition may be obscured by the effects of stronger genetic factors and thus need to be examined in patients lacking these factors.

Base Sequence↗
PubMed1994

Lupus erythematosus panniculitis: an immunohistochemical study.

An immunohistochemical study on a case of lupus erythematosus panniculitis (LEP), without discoid lupus erythematosus (DLE) or systemic lupus erythematosus (SLE) signs, showed that the cells in skin infiltrates were immunologically committed lymphocytes (OKT4, OKT8, OKT11 and HLA-DR positive cells) and elements of the monocyte-macrophage lineage (Leu M3 and Leu M5 positive). No immunophenotypically identifiable B-lymphocytes were seen. Immunofluorescent IgG, IgM, C3 and C4 deposits were found in blood vessel walls of the deep dermis. These findings, similar to that described in the skin changes of SLE and DLE, suggest that immunological mechanisms are operative in localized LEP, where the dermal lesions are the only expression of the disease.

Disease Progression↗
PubMedDate not supplied

Histopathology of cutaneous lupus erythematosus.

The basic histopathologic feature of all cutaneous lesions of lupus erythematosus involves a perivascular mononuclear cell infiltrate with subsequent involvement of the epidermis and appendages. The various histologic alterations affecting the epidermis, dermis, and adnexal structures reflect the particular type of lesion biopsied and the duration of the lesion at the time of biopsy. The different clinical and serologic forms of lupus erythematosus cannot reliably be distinguished histologically, which supports the premise that lupus erythematosus is a disease with a wide spectrum of clinical manifestations but with a common underlying pathogenesis.

Humans↗
PubMed1991

Occlusive vasculopathy in systemic lupus erythematosus. Association with anticardiolipin antibody.

Patients with systemic lupus erythematosus and with antiphospholipid antibody are subject to sudden occlusion of multiple blood vessels. We describe two patients with systemic lupus erythematosus with acute, catastrophic, widespread non-inflammatory visceral vascular occlusions associated with high-titer antiphospholipid antibody. The histopathologic features clearly distinguished these patients from classic systemic lupus erythematosus vasculitis. We further suggest that, based on a probable pathogenesis related to the presence of antiphospholipid antibody, and based on the non-inflammatory vascular occlusion, steroids and other immunosuppressive medications are of limited value. Plasmapheresis along with anticoagulant therapy should be considered.

Adult↗
PubMed2005

Infantile systemic lupus erythematosus presenting with pulmonary hemorrhage.

Systemic lupus erythematosus in infants born to healthy mothers is a rare entity. We describe a male infant who presented at 1 month of age with pulmonary hemorrhage and glomerulonephritis due to systemic lupus erythematosus, confirmed serologically and histologically. He was managed with a combination of prednisone and intermittent cyclophosphamide, but also received mycophenolate mofetil, with a complete serological and clinical remission at 30-month follow-up. This case underscores the importance of a broad approach to the evaluation of pulmonary hemorrhage and glomerulonephritis in the very young and the need for aggressive immunosuppressive therapy to achieve sustained serological and clinical remission.

Cyclophosphamide↗
PubMed1991

Neonatal lupus erythematosus syndrome.

Three cases of neonatal lupus erythematosus (NLE) syndrome are described. The key diagnostic sign is the erythematous and annular clinical appearance of lesions. The histopathologic findings may be subtle in NLE syndrome compared with discoid or subacute cutaneous lupus erythematosus. Direct immunofluorescence testing may be useful in supplementing the histopathologic evaluation. Detection of immunoglobulins, complement, or both at the basement membrane zone in lesional skin by immunofluorescence occurs in approximately half of cases; a negative study does not preclude the diagnosis of NLE syndrome. Clinical and serologic evaluation of both the infant and the mother are important in establishing a diagnosis of NLE syndrome, particularly when histopathologic findings are subtle.

Fluorescent Antibody Technique↗