Practical approach to monitoring and prevention of infectious complications associated with systemic corticosteroids, antimetabolites, cyclosporine, and cyclophosphamide in nonmalignant hematologic diseases.

Corticosteroids constitute a first-line therapy for adults and children suffering from nonmalignant immune-mediated hematologic diseases. However, high disease relapse rates during the tapering period or upon drug discontinuation result in long-term corticosteroid use that increases the risk of infection. This same concept applies to other immunosuppressive agents, such as antimetabolites, calcineurin inhibitors, and cyclophosphamide. Corticosteroids are associated with a length-of-treatment and dose-dependent risk for infection. Screening and antimicrobial prophylaxis against tuberculosis, hepatitis B, Strongyloides stercoralis, and Pneumocystis jirovecii pneumonia (PJP) might be indicated in patients who are scheduled to be on high-dose corticosteroids for >4 weeks (>30 mg of prednisone-equivalent dose [PEQ]) or in patients chronically treated (≥8 weeks of continuous or intermittent corticosteroid use) with moderate doses (≥15 to <30 mg PEQ). Antimetabolites (azathioprine, mycophenolate) increase the risk of progressive multifocal leukoencephalopathy (PML); however, other opportunistic infections and viral reactivation have also been reported. In case of new onset of neurological symptoms, PML needs to be considered, and an urgent neurology consultation should be obtained. Cyclophosphamide-induced myelosuppression can lead to serious infections related to neutropenia. PJP prophylaxis should be considered with combination therapy of cyclophosphamide and corticosteroids until a PEQ dose ≤ 5 mg/d is reached. Data on infectious risk when cyclosporine is used in patients with nonmalignant hematologic diseases are lacking. Discontinuation of any immunosuppressive agent during an episode of infection is recommended. In all patients, adherence to an age-based immunization schedule is appropriate.

Recurrent paralytic ileus associated with strongyloidiasis in a patient with systemic lupus erythematosus.

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.

Strongyloidiasis pre and post autologous peripheral blood stem cell transplantation.

Hyperinfection with strongyloides stercolis occurs in the setting of chronic strongyloides infection in conjunction with immune suppression. Although malnutrition remains the major secondary cause worldwide in the developed world, iatrogenic immune suppression is an important precipitant. Autologous stem cell transplantation recipients are significantly immunocompromised albeit temporarily. Despite the increasing use of haemopoetic stem cell transplantation, hyperinfection with strongyloides has rarely been reported. We describe two cases of patients transplanted with chronic strongyloidiasis. In one case eradication therapy was given prior to the transplant which was uncomplicated. In the second case strongyloidiasis was diagnosed post transplant which was complicated by infection and respiratory compromise. Fatal hyperinfection subsequently developed after corticosteroid therapy was started for a disease progression in the CNS.

Fatal strongyloidosis following corticosteroid therapy in a patient with chronic idiopathic thrombocytopenia.

A patient with chronic idiopathic thrombocytopenia and fatal strongyloides hyperinfection syndrome following prolonged corticosteroid therapy is briefly described. Diagnosis was difficult to perform due to absence of eosinophilia and diarrhea at presentation, as well as to the negativity of multiple stool specimens examined by direct microscopy of saline smear, formol-ether concentration techniques, and Baermann's test. The striking hypoalbuminemia in the setting of the normal results of liver function tests and prothrombin time was assumed to be due to enteropathy. Therefore, an upper endoscopy was undertaken, revealing Strongyloides stercoralis (SS) larvae in the biopsy specimens of the gastric and duodenal mucosa. The SS larvae were also demonstrated in the multiple specimens of the concentrated sputum. Despite thiabendazol treatment, death ensued. On autopsy, SS larvae were recovered in the gastrointestinal tract and lungs. The importance of early diagnosis and of ruling out strongyloidosis prior to administration of corticosteroids are discussed, as well as the pathogenetic aspects of strongyloidosis in the patient under corticosteroids.