Biomedical subjects
Publications and source records attributed to N T Ilowite.
We present a 12-year-old girl with skin lesions, arthritis and clinical response to tetracycline consistent with Mucha-Habermann's disease. She also showed serological evidence of reactivated Epstein-Barr virus (EBV) infection. We believe this represents the first such association of Mucha-Habermann's disease with EBV infection.
Explore the source record for details and available documents.
We report a 10-month-old infant who had arthritis as the initial clinical manifestation of ulcerative colitis. Arthritis is considered to be the most common extraintestinal manifestation of IBD in adults and children. This case emphasizes that arthritis may be the earliest manifestation of IBD even in the very young infant.
Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoproteinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
The case of an adolescent female with cutaneous polyarteritis nodosa and thromboses of the superior and inferior venae cavae is presented. Although thromboses of major vessels have been well described in systemic lupus erythematosus and Behçet's disease, this is only the second case of thromboses of major vessels in association with cutaneous polyarteritis nodosa. Possible pathophysiologic mechanisms are discussed.
A patient with polyarthritis and subcutaneous nodules was studied for expression of rheumatoid factors (RF) by numerous techniques for 5 months after presentation. Assays for RF binding human or rabbit IgG in whole sera, assays for hidden RF binding human or rabbit IgG, and assays for expression of the major RF cross-reactive idiotype (RCRI) in whole sera or by pokeweed mitogen induced plasma cells were performed (PWM-PC). In this patient, increased expression of RCRI in sera and among PWM-PC preceded detectable RF binding human IgG, and paralleled hidden RF and RF binding rabbit IgG expression.
Explore the source record for details and available documents.
Immunologic abnormalities described in juvenile rheumatoid arthritis (JRA) have been largely confined to mitogen or antigen driven proliferation assays. We studied antigen specific antibody production using the neoantigen bacteriophage phi X 174 in vivo and in vitro; defective responses were found in all 8 patients with JRA studied. These could not be attributed to circulating anti-T cell antibodies, but may relate to lymphocyte subset abnormalities found by 2 color analyses. These immunologic aberrations may play a direct role in the pathogenesis of JRA or, alternatively, may be a secondary event.
We describe a 12-year-old boy with Wiskott-Aldrich syndrome who developed a pulmonary vasculitis associated with lymphoreticular proliferation, consistent with the histological and clinical diagnosis of lymphomatoid granulomatosis. The lesions were responsive to cyclophosphamide and steroids. The patient has had severely depressed immune function and was shown to have abnormal Epstein-Barr virus (EBV)-specific cellular and humoral immune responses. Lymph nodes obtained at autopsy were positive for EBV genome. In this patient, reactivated EBV infection resulting from impaired immune surveillance of the virus may have been responsible for the development of this paraneoplastic disorder.
We report a 14-year-old boy with systemic lupus erythematosus and anticardiolipin antibodies. He developed asymptomatic superior vena cava thrombosis and silent pulmonary embolism. Computed tomographic scan of his chest and abdomen showed features of long standing obstruction secondary to superior vena cava thrombosis. Asymptomatic thrombosis of the major vessels and silent pulmonary emboli are part of the disease spectrum of pediatric antiphospholipid syndrome.