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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Strongyloides stercoralis is an intestinal nematode which infects a large portion of the world's population. Individuals with infection confined to the intestinal tract are often asymptomatic but may have abdominal pain, weight loss, diarrhea, and other nonspecific complaints. Enhanced proliferation of the parasite in compromised hosts causes an augmentation of the normal life-cycle. Resultant massive invasion of the gastrointestinal tract and lungs is termed the hyperinfection syndrome. If the worm burden is excessive, parasitic invasion of other tissues occurs and is termed disseminated strongyloidiasis. A variety of underlying conditions appear to predispose to severe infections. These are primarily diseases characterized by immunodeficiency due to defective T-lymphocyte function (Table 1). Individuals with less severe disorders become compromised hosts because of therapeutic regimens consisting of corticosteroids or other immunosuppressive medication. The debilitation of chronic illness or malnutrition also predisposes to systemic stronglyloidiasis. The diagnosis of strongyloidiasis can be readily made by microscopic examination of concentrates of upper small bowel fluid, stool, or sputum. Important clues suggesting this infection include unexplained gram-negative bacillary bacteremia in a compromised host who may have vague abdominal complaints, an ileus pattern on X-ray, and pulmonary infiltrates. Eosinophilia is helpful, if present, but should not be relied upon to exclude the diagnosis. The treatment of systemic infection due to Strongyloides stercoralis with either thiabensazole 25 mg/kg orally twice daily is satisfactory if the diagnosis is made early. Because of several unusual features of this illness in compromised hosts, the standard recommendation for 2 days of therapy should be abandoned in such patients. Immunodeficiency, corticosteroids, and bowel ileus reduce drug efficacy. Thus a longer treatment period of at leuch as blind loops or diverticula necessitate longer treatment. Stool specimens and upper small bowel aspirates should be monitored regularly and treatment continued several days beyond the last evidence of the parasite. In particularly difficult situations where either worm eradication is impossible or reinfection is probable, short monthly courses of antihelminthic therapy seem to be effective in averting recurrent systemic illness. Finally, prevention of hyperinfection or dissemination due to Strongyloides stercoralis can be accomplished by screening immunocompromised hosts with stool and upper small bowel aspirate examinations. These would be especially important prior to initiating chemotherapy, or before giving immunosuppressive medications or corticosteroids to patients with nonneoplastic conditions such as systemic lupus erythematosus, nephrotic syndrome, or renal allografts.
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PMID:Overwhelming strongyloidiasis: an unappreciated opportunistic infection. 36 22

Four cases of fatal strongyloidiasis were reported from Thailand; two were malnourished young inmates from the same Government-Institution while two were adults receiving corticosteroid therapy for pemphigus vulgaris and systemic lupus erythematosus. The clinical and pathological findings of all cases were briefly described. Special emphasis is made in treatment of malnourished young children especially those living in the institution with possibility of such parasitic hyperinfection superimposed by other organisms. A single course of thiabendazole in strongyloidiasis is inadequate, especially in those immunosuppressive hosts.
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PMID:Fatal strongyloidiasis in Siriraj Hospital, Bangkok, Thailand. 665

The reactive hemophagocytic syndrome is a condition characterized by systemic proliferation of benign hemophagocytic histiocytes, fever, cytopenia, abnormal liver function, and frequently coagulopathy and hepatosplenomegaly. Its occurrence has been documented in association with viral, bacterial, fungal and parasitic infections; a wide spectrum of malignant neoplasms; some miscellaneous disorders; and phenytoin. Disseminated strongyloidiasis is reported in a patients with systemic lupus erythematosus treated with corticosteroids in whom a reactive hemophagocytic syndrome developed and who finally died. This reactive hemophagocytic syndrome is reported for the first time in strongyloidiasis and may not have been recognized in former patients.
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PMID:Case report: reactive hemophagocytic syndrome associated with disseminated strongyloidiasis. 868 29

We describe a case of disseminated strongyloidiasis involving a female patient with active systemic erythematosus (SLE). The cause of death was massive pulmonary hemorrhage induced by a filariform larvae infection. This was initially diagnosed during examination of the bronchoalveolar lavage fluid just 2 days before her death. The case indicated that immunosuppressed individuals would be paid attention to possible parasitic infection prior to starting therapy even in non-endemic areas as well as other microorganisms.
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PMID:SLE with death from acute massive pulmonary hemorrhage caused by disseminated strongyloidiasis. 938 54

We present an interesting case of recurrent paralytic ileus due to strongyloidiasis in a woman who was being treated with corticosteroids and immunosuppressants for systemic lupus erythematosus (SLE). She was also a carrier of human T-cell leukemia virus type I. She had a history of strongyloidiasis 8 years earlier. Recurrent episodes of paralytic ileus due to strongyloidiasis occurred during treatment of her SLE with corticosteroids. Ivermectin was given and improved the symptoms. This case shows that symptomatic strongyloidiasis can be induced in immunocompromised hosts by immunosuppressive therapy. It is important to rule out strongyloidiasis prior to starting immunosuppressive therapy in patients from endemic areas.
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PMID:Recurrent paralytic ileus associated with strongyloidiasis in a patient with systemic lupus erythematosus. 1662 24

Pleuropulmonary manifestations of systemic lupus erythematosus (SLE) have been reported to be of variable prevalence, depending on the diagnostic methods used. The objective of this study was to determine the anatomopathological prevalence and the nature of lung involvement associated with SLE and to define if there were differences in the grade and type of pulmonary involvement in patients who had died at different time periods, before or after 1996. Complete autopsy studies of 90 patients with SLE diagnosis carried out between 1958 and 2006 and their clinical records were studied. All patients fulfilled the American College of Rheumathology (ACR) diagnostic criteria for SLE. Two groups of patients were analyzed: patients who had died before 1996 and those deceased in 1996-2006. Some pleuropulmonary involvement was detected in 97.8% of the autopsies. The most frequent findings were pleuritis (77.8%), bacterial infections (57.8%), primary and secondary alveolar haemorrhages (25.6%), followed by distal airway alterations (21.1%), opportunistic infections (14.4%) and pulmonary thromboembolism (7.8%), both acute and chronic. No cases of acute or chronic lupus pneumonitis were found. Opportunistic lung infections were invasive aspergillosis, disseminated strongyloidiasis, mucormicosis and Pneumocystis carinii. Only three of 23 patients with alveolar haemorrhage showed capillaritis. The four patients with primary pulmonary hypertension (PHT) had plexiform lesions. Deceased patients' age at death (46.09 +/- 11.01 vs 30.3 +/- 11.5 years, P < 0.0001) as well as survival time from diagnosis date (11.8 +/- 11.2 vs 4.4 +/- 4.9 years, P < 0.0001) in the second time period evaluated were significantly higher. However, there were no statistically significant differences in the prevalence of any of the pulmonary manifestations. Sepsis was considered the major cause of death without significant differences in both groups. Our results show that pulmonary manifestations directly caused by systemic lupus erythematosus are very uncommon and that their prevalence has not changed in the past 10 years. Pulmonary infection is still the most frequent affection, and it is an important cause of death in patients with lupus.
Lupus 2009 Oct
PMID:Pulmonary involvement of systemic lupus erythematosus: analysis of 90 necropsies. 1976 78

We describe a case of systemic lupus erythematosus complicated by strongyloidiasis. The parasitic infection appeared with diarrhoea, weight loss and peripheral eosinophilia in association with recurrence of polyarthritis, probably due to a flare of systemic lupus erythematosus. The literature about the coexistence of systemic lupus erythematosus and strongyloidiasis has been reviewed.
Lupus 2010 Jun
PMID:Systemic lupus erythematosus and strongyloidiasis: a multifaceted connection. 2002 23

Strongyloidiasis is a parasitic disease caused by Strongyloides stercoralis, a nematode predominately endemic to tropical and subtropical regions, such as Southeast Asia. Autoinfection enables the organism to infect the host for extended periods. Symptoms, when present, are non-specific and may initially lead to misdiagnosis, particularly if the patient has additional co-morbid conditions. Immunosuppressive states place patients at risk for the Strongyloides hyperinfection syndrome (SHS), whereby the organism rapidly proliferates and disseminates within the host. Left untreated, SHS is commonly fatal. Unfortunately, the non-specific presentation of strongyloidiasis and the hyperinfection syndrome may lead to delays in diagnosis and treatment. We describe an unusual case of SHS in a 30-year-old man with a long-standing history of systemic lupus erythematosus who underwent a partial colectomy. The diagnosis was rendered on identification of numerous organisms during histologic examination of the colectomy specimen.
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PMID:Strongyloidiasis hyperinfection in a patient with a history of systemic lupus erythematosus. 2509 15

Introduction. Pulmonary hemorrhage secondary to disseminated strongyloidiasis is an unusual, well-recognized entity in immunocompromised patients with autoimmune disease, which is associated with the hyperinfection syndrome, sepsis, and a high mortality rate. Case Presentation. We present a case of a 44-year-old Mexican woman with systemic lupus erythematosus and acute bacterial meningitis who developed pulmonary hemorrhage with acute respiratory failure requiring mechanical ventilation, treated with broad spectrum systemic antibiotics and high dose methylprednisolone, who subsequently developed a characteristic purpuric skin eruption and septic shock and died two days later of refractory hypoxemia caused by massive pulmonary bleeding. The postmortem examination reports filariform larvae of S. stercolaris in lung, skin, and other organs. Conclusion. This case highlights the importance of considering disseminated strongyloidiasis in the differential diagnosis of diffuse alveolar hemorrhage in systemic lupus erythematosus, and screening for S. stercolaris infection before initiation of immunosuppressive therapy should be considered, especially in endemic areas. Disseminated strongyloidiasis has a high mortality rate, explained in part by absence of clinical suspicion.
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PMID:Pulmonary Hemorrhage Secondary to Disseminated Strongyloidiasis in a Patient with Systemic Lupus Erythematosus. 2610 72

We review the most characteristic clinical and histopathologic findings of the cutaneous manifestations of the occlusive nonvasculitic vasculopathic disorders. Clinically, most of these conditions are characterized by retiform purpura. Histopathologic findings consist of occlusion of the vessel lumina with no vasculitis. Different disorders may produce nonvasculitic occlusive vasculopathy in cutaneous blood and lymphatic vessels, including embolization due to cholesterol and oxalate emboli, cutaneous intravascular metastasis from visceral malignancies, atrial myxomas, intravascular angiosarcoma, intralymphatic histiocytosis, intravascular lymphomas, endocarditis, crystal globulin vasculopathy, hypereosinophilic syndrome, and foreign material. Other times, the occlusive disorder is due to platelet pugging, including heparin necrosis, thrombocytosis secondary to myeloproliferative disorders, paroxysmal nocturnal hemoglobinuria, and thrombotic thrombocytopenic purpura. Occlusive vasculopathy may also appear in cold-related gelling agglutination, like that occurring in cryofibrinogenemia, cryoglobulinemia, cold agglutinin syndrome, and crystalglobulinemia. Microorganisms may also occlude the vessels lumina and this is especially frequent in ecthyma gangrenosum, opportunistic fungi as aspergillosis or fusariosis, Lucio phenomenon of lepromatous leprosy and disseminated strongyloidiasis. Systemic coagulopathies due to defects of C and S proteins, coumarin/warfarin-induced skin necrosis, disseminated intravascular coagulation, and antiphospholipid antibody/lupus anticoagulant syndrome may also result in occlusive nonvasculitic vasculopathy. Finally, vascular coagulopathies such as Sneddon syndrome, livedoid vasculopathy, and atrophic papulosis may also cause occlusion of the vessels of the dermis and/or subcutis. Histopathologic study of occlusive vasculopathic lesions is the first step to achieve an accurate diagnosis, and they should be correlated with clinical history, physical examination, and laboratory findings to reach a final diagnosis.
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PMID:Occlusive Nonvasculitic Vasculopathy. 2775 98


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