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Lupus erythematosus, or LE, is a connective tissue disease that affects a number of organ systems. Patients with this condition can experience several other serious conditions--bleeding, infection, endocarditis, adrenal insufficiency and mucocutaneous disease--that can affect the provision of dental care. The authors describe considerations for managing dental treatment of patients with LE.
Diagnosis of systemic lupus erythematosus (SLE) requires documentation of multisystem involvement and the presence of antinuclear antibodies. In almost all cases of SLE, these autoantibodies are detected at significant titer with a sensitive screening test such as the fluorescent antinuclear antibody test. After other diagnostic possibilities, such as rheumatoid arthritis, have been excluded, several laboratory tests (hematocrit determination, complement tests, anti-native DNA assays) are available to monitor the response to therapy.
Cutaneous manifestations of lupus erythematosus (LE) are, usually, characteristic enough to permit an easy diagnosis. However, some patients may present less typical lesions, associated or not to the classic ones. Therefore, irrespectively of the variety of LE (acute, subacute and chronic), in absence of the typical butterfly rash, erythematosquamous papules or plaques, or any of the characteristic cutaneous alterations, it is important (even though not always easy) to recognize the uncommon and/or atypical changes of the skin.
Patients with systemic lupus erythematosus (SLE) are prone to develop opportunistic infections. Nevertheless, arthritis due to Pseudomonas aeruginosa in SLE is very rare and seems to be related to corticosteroid therapy and previous penetrating injury. A 17-year-old girl with SLE and Pseudomonas arthritis and discitis which followed laparotomy is described. Arthritis is a common manifestation of SLE, but arthritis due to infection with Pseudomonas is very serious and the diagnosis should not be missed.
Systemic lupus erythematosus (SLE) is a connective tissue disease most commonly affecting women of a fertile age. It is recommended that pregnancy is planned during periods with remission or low activity of he disease because it seems that SLE is more likely to be exacerbated by pregnancy when the disease is active at the time of conception. Presence of circulating anti-phospholipid antibodies is associated with a poor prognostic outcome for the foetus and increases the risk of complications related to pregnancy.
Patients with systemic lupus erythematosus (SLE) appear to be at increased risk for development of neoplastic disease. We describe the case of a male teenager with SLE and Burkitt's lymphoma. His presentation was similar to that of an exacerbation of his underlying SLE. We believe this to be the first case of Burkitt's lymphoma in a patient with SLE. The association of SLE and malignancy, with emphasis on lymphoproliferative states, is discussed.
Patients with systemic lupus erythematosus (SLE) often develop leg ulceration, particularly those with antiphospholipid antibodies or with vasculitis. Pyoderma gangrenosum (PG) is an idiopathic ulcerative neutrophilic dermatosis that is commonly associated with inflammatory bowel disease or seronegative polyarthritis. Although PG-like lesions have been commonly described in patients with the antiphospholipid antibody syndrome, the occurrence of PG as a preceding manifestation of SLE has only rarely been reported. We present a patient who developed PG roughly 8 years prior to developing SLE.
Patients with systemic lupus erythematosus (SLE) are at increased risk for infections. Insufficiency of the reticuloendothelial system caused either by immunosuppressive therapy or inadequate opsonisation are mechanisms by which Salmonella infections in particular appear in these patients. Salmonella infections can provoke a polyarticular reactive arthritis while Salmonella bacterial arthritis usually is monarticular. We report on the seriousness of a Salmonella infection (enteritis complicated by polyarticular bacterial arthritis) in a patient with SLE.
Autoantibodies in systemic lupus erythematosus which cross-react with double stranded DNA and intermediate filament proteins are frequently reported. However, little is known about the origin and the target of these antibodies. In this paper, a polyspecific monoclonal antibody, XY12, produced by the immunization of genetically non-autoimmune mice with a DNA-protein complex is detailed. Its antigen binding patterns are very similar to the autoantibodies. The data suggest that these autoantibodies may be triggered by a circulating nucleoprotein.
Systemic lupus erythematosus (SLE) is an uncommon childhood illness that is characterized by the formation of autoantibodies and immune complexes, which mediate inflammatory responses in multiple organ systems. Children who develop SLE are frequently very ill at the time of presentation and need careful evaluation to determine which organ systems are involved and how severely, meticulous control of medications to suppress active disease, and close monitoring to avoid complications from both the disease and its treatment.
Systemic lupus erythematosus (SLE) was diagnosed in 31 black Zimbabweans over a six year period. Renal involvement (71%) was more common and photosensitivity (16%) and serositis (23%) less common than in the United States. Lymphopenia (48%) was the commonest haematological abnormality. Unusual complications included subarachnoid haemorrhage, cardiac rhythm disturbance, portal and superior mesenteric vein thrombosis, and a non-Hodgkin lymphoma. Tuberculosis was a common differential diagnosis that was difficult to exclude. Nine patients (29%) died within one year of diagnosis. SLE is being recognised more commonly in Zimbabwe.
Photosensitivity associated with lupus erythematosus (LE) is well established. The photobiologic basis for this abnormal response to ultraviolet radiation, however, has not been determined. This paper summarizes the criteria for elucidating possible photobiologic mechanisms and reviews the literature relevant to the mechanism of photosensitivity in LE. In patients with LE, photosensitivity to wavelengths shorter than 320 nm has been demonstrated; wavelengths longer than 320 nm have not been adequately evaluated. DNA is a possible chromophore for photosensitivity below 320 nm. UV irradiation of skin produces thymine photodimers in DNA. UV-irradiated DNA is more antigenic than native DNA and the antigenicity of UV-irradiated DNA has been proposed, but not proven, to be involved in the development of clinical lesions. UV irradiation of mice previously injected with anti-UV-DNA antibodies produces Ig deposition and complement fixation that appears to be similar to the changes seen in lupus lesions. Antibodies to UV-irradiated DNA occur in the serum of LE patients although a correlation between antibody titers and photosensitivity was not observed. Defective repair of UV-induced DNA damage does not appear to be a mechanism for the photosensitivity in LE. Other mechanisms must also be considered. The chromophore for photosensitivity induced by wavelengths longer than 320 nm has not been investigated in vivo. In vitro studies indicate that 360-400 nm radiation activates a photosensitizing compound in the lymphocytes and serum of LE patients and causes chromosomal aberrations and cell death. The mechanism appears to involve superoxide anion. Further research is required to establish the action spectrum for long wavelength photosensitivity in vivo and to elucidate the mechanisms for the photosensitivity at all wavelengths.
Systemic lupus erythematosus, a disease of unknown cause and protean manifestations, continues to excite substantial investigational interest. These papers bring together recent advances in concepts of its immunopathogenesis, evidence for a major genetic role in the causation of the process, developing systems for the morphologic assessment of its often fatal nephritis, and data from ongoing trials of cytotoxic drugs in its management.
Fever in systemic lupus erythematosus (SLE) may be caused by exacerbation of the disease itself or by infection. We report on a patient with a long standing history of SLE that was complicated by fever and pancytopenia with no splenomegaly. SLE disease activity was suspected because of an elevated DNA-antibody titer. The early positive response to corticoid therapy may have masked the underlying infection. Visceral leishmaniasis was diagnosed by a repeated bone marrow biopsy and serological testing.
Patients with systemic lupus erythematosus (SLE) may be complicated with serious cerebrovascular accidents and pulmonary alveolar haemorrhage. The authors report an autopsy-proven angioinvasive zygomycosis in a patient with SLE. The clinical features of systemic zygomycosis in this patient masqueraded as SLE-related stroke and pulmonary haemorrhage. The case demonstrates that the simultaneous occurrence of complications that clinically suggest pulmonary haemorrhage and multiple brain infarcts in SLE patients should include the rare disseminated zygomycosis in the differential diagnosis.
BACKGROUND: Cutaneous neonatal lupus erythematosus (NLE) is an uncommon disease described mainly through isolated case reports. OBJECTIVE: Our purpose was to examine the cutaneous spectrum, clinical associations, and course of disease in babies with anti-Ro-positive NLE. METHODS: This is a retrospective case series evaluation of newborns with anti-Ro-positive NLE seen at a single ambulatory care university center over a 20-year period. Cases were drawn from a population of 3.2 million. Follow-up was at least 3 years. RESULTS: Four boys and 14 girls were included in our evaluation. Distribution of skin lesions in 18 babies was as follows: face, 17; periorbital "owl-eye" or "eye mask" facial rash, 14; scalp, 15; arms and legs, 13; trunk and groin, 6. Crusted lesions were predominant in 3. Photosensitivity was seen in 12, and features of cutis marmorata telangiectasia congenita were observed in 4. In 17 neonatal lupus was not suspected until the dermatology consultation. Noncutaneous manifestations included thrombocytopenia in 4, cholestatic hepatitis in 3, and congenital heart block in 3. Four patients had residual telangiectasia that persisted for 3 or more years but eventually cleared in 2 patients. Three babies had dyspigmentation that spontaneously cleared within 22 months. None had atrophy or scarring. CONCLUSION: Periorbital, scalp, and extremity lesions are common in cutaneous NLE. Crusted lesions predominated in male infants. In children selected by cutaneous involvement, thrombocytopenia and hepatic disease were present as frequently as cardiac disease and occurred more frequently in male babies with crusted skin lesions. Children with cutaneous NLE should be evaluated for hematologic and hepatic as well as cardiac involvement.
Hemoptysis in systemic lupus erythematosus (SLE) may occur in up to 17% of cases. The vast majority of the cases are secondary to bacterial, tuberculosis or opportunistic infections. Also uremia, pulmonary embolism and lung hemorrhage must be considered. The majority of the above referred entities are usually alarming events in any patient with SLE. In contrast, we describe a patient with inactive SLE, who developed hemoptysis secondary to Paragonimus sp., which was treated "easily" with praziquantel. Fluke infection must be considered in the differential diagnosis of hemoptysis in SLE.
Parkinsonism complicating systemic lupus erythematosus (SLE) is extremely rare. We report two girls with SLE who developed extrapyramidal parkinsonian features after an initial stormy course. One patient presented with generalized tonic clonic seizure and was then noted to have akinetic mutism and masked face. MRI brain revealed abnormal signals in bilateral basal ganglia and single photon emission computed tomography (SPECT) showed hypoperfusion in the same area. EEG background was slow and disorganized. Symptoms persisted despite high dose intravenous methylprednisolone and cyclophosphamide. Intravenous immunoglobulin (IVIG) was prescribed empirically and was followed by complete recovery. Both EEG and MRI brain were normal on follow-up. The second patient was found unconscious and then developed bradykinesia, mutism and shuffling gait. MRI and SPECT both detected abnormalities in basal ganglia. EEG was slow. Intravenous immunoglobulin was given after methylprednisolone and cyclophosphamide. This was followed by clinical improvement. The pathogenesis of basal ganglia injury in SLE, along with the management of cerebral lupus and the mechanisms of action of IVIG, are discussed.