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The administration of 100 mg of methylprednisolone intravenously (IV) 1/2 h prior to rituximab decreases the incidence of acute infusion reactions (AIRs). However, this pretreatment adds considerable time and conveys potential risk. We performed an open-label prospective assessment of oral prednisone as a pretreatment to rituximab. This was a 26-week open-label trial of 40 mg of oral prednisone given 1/2 h prior to rituximab as a prophylaxis against AIRs in patients with rheumatoid arthritis (RA). The primary endpoint was AIRs in the first 24 h after their initial infusion. Secondary endpoints include AIRs during the 24 h following their second infusion and any adverse events experienced during the 26-week study; efficacy measures were also followed as secondary endpoints. Sixty-four subjects were screened, and 50 subjects qualified. Fourteen out of the 50 (28 %) subjects had AIRs within 24 h of their first infusion. There were four AIRs (8.3 %) within 24 h of their second infusion. One of day 0 AIRs required drug discontinuation (wheezing/bronchospasm). Forty out of 50 (80 %) subjects experienced an adverse event during the 26 weeks. There were three SAEs deemed not to be study-drug related. The DAS28 and HAQ-DI all improved significantly at weeks 8, 16, and 26 compared to baseline. Historical controls demonstrate that 27 % of RA subjects experience AIRs with their first rituximab infusion. Our data suggest a smaller dose of oral prednisone is an effective alternative to IV methylprednisolone as a pretreatment for rituximab in patients with RA.
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Totally 192 healthy Sprague-Dawley (SD) rats were selected and divided into three groups including PD7, PD15 and PD60 corresponding to three age-groups in human, i.e., the full-term newborn, one-year-old infant and adult, respectively. According to the therapeutic regime for infantile spasms, the dose of prednisone and ACTH was designed as 6 mg/(kg.d) and 150 U/(m(2).d) respectively. SD rats of different age-groups were treated with prednisone or ACTH and normal saline as the control for 4 days. The specimens were collected on Day 4 or 3 weeks after treatment. Body and brain weights were measured when the rats were sacrificed. Histological studies on the tissues of frontal lobe and hippocampus were performed by Nissl staining. Ultrastructural changes of brain were observed by the transmission electron microscopy. Expression of apoptosis-related proteins Bcl-2 and Bax in neurons was detected by immunohistochemistry. Neuronal apoptosis was detected by TUNEL. Mitochondria membrane potential of neurons in frontal lobe and hippocampus were detected by flow cytometry, and the Caspase-3 activity was detected by spectrophotometric assay.
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We present a case of a young woman presenting with irritative lower urinary tract symptoms and microscopic hematuria who was diagnosed with systemic lupus erythematosus (SLE). Abdominal ultrasound revealed bilateral hydronephrosis and a thickened bladder wall. Cystoscopic evaluation revealed severe diffuse inflammation, erythema and hemorrhage at the trigone with punctate extensions to the bladder base. She was treated with prednisone and mycophenolate mofetil with improvements in her symptoms and ultrasound findings. Lupus cystitis is a rare manifestation of SLE.
Vogt-Koyanagi-Harada disease is an uncommon cause of uveitis in children. The clinical characteristics of pediatric Vogt-Koyanagi-Harada disease in South India resembled those described in cohorts from other regions. Although children in our cohort tended to do well with prompt diagnosis and treatment, long-term vision loss can occur.
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Fibrillary glomerulonephritis (FGN) is a morphologically defined entity characterized by glomerular accumulations of non-branching, randomly arranged fibrils; these differ from amyloid fibrils by their larger size and lack of reactivity with Congo red and other amyloid-specific dyes. FGN is a rare disease and may mimic membranous nephropathy under routine light microscopy and immunohistochemistry. However, electron microscopy shows the fibrillary nature of these glomerular deposits. We report a rare case of membranous nephropathy complicated by fibrillary deposits in a 60-year-old man with a history of bone tuberculosis.
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A 44-year-old woman with a medical history of chronic pain syndrome presented with a 3-day history of a painful "rash" that started on her face and spread to her legs. Further history revealed that she recently started a new medication, varenicline, 7 weeks prior to admission and had a long-standing history of intranasal cocaine use. Review of systems was significant for rhinitis, nasal congestion, joint pain, and a febrile episode 2 days prior to admission. Physical examination revealed centrally violaceous, tender, stellate, and retiform purpuric patches and plaques on her extremities, nasal dorsum, and cheeks. Approximately 1.0-centimeter tender purpuric nodules were noted on her bilateral second proximal interphalangeal joints. She was afebrile. Initial laboratory data revealed a mild leukopenia, normal serum urea nitrogen and creatinine without hematuria, and an elevated erythrocyte sedimentation rate. Further analysis showed a normal complement level, negative antinuclear antibody, human immunodeficiency virus, rapid plasma reagin, and hepatitis panel. Trace cryoglobenemia and a positive anti-streptolysin O were noted, along with a positive antineutrophil cytoplasmic antibody (c-ANCA) (> 8.0 U) and perinuclear antineutrophil cytoplasmic antibodies, or p-ANCA (1.5 U). The hypercoagulable workup was negative. A skin biopsy taken from the left thigh was consistent with leukocytoclastic vasculitis. After several weeks of high-dose oral prednisone taper, the patient's symptoms improved, but flared upon discontinuation. On follow-up, she admitted to frequent relapses of cocaine abuse and had developed tender purpuric plaques on her nose, ears, and extremities, some with ulcerations (Figure 1 and Figure 2). She also had significant edema and joint pain that limited her ambulation. Further evaluation revealed normal chest x-ray results; however, computed tomography of her sinuses demonstrated thickened maxillary sinuses consistent with subacute/ chronic sinusitis. She also developed hematuria. Mass spectrometry analysis ofhair and urine samples tested positive for cocaine and levamisole. A presumptive diagnosis of levamisole-induced Wegener's vasculitis was made. She was restarted on high-dose prednisone and methotrexate with improvement and advised to discontinue cocaine use, so as to avoid exposure to both substances.
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GR-beta and TGF-beta1 might be involved in NP pathogenesis, but their role in modulating GC sensitivity is still unclear.
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We reported a case of peritoneal disseminated recurrence after total gastrectomy for perforated gastric malignant lymphoma. A 73-year-old man underwent total gastrectomy for perforated gastric diffuse large B cell lymphoma on day 5 of RCHOP (rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisolone) chemotherapy. He has rejected chemotherapy and received no additional treatment after gastrectomy. Computer tomography 13 months after surgery revealed peritoneal dissemination and abdominal lymph node metastasis. R-CHOP chemotherapy was performed, and after 4 courses of chemotherapy, peritoneal dissemination and metastatic abdominal lymph nodes disappeared. Chemotherapy was discontinued for a time, however, the tumors relapsed 2 months after stopping chemotherapy. He underwent chemotherapy with etoposide, but died of tumor progression 21 months after gastrectomy.
Hodgkin lymphoma (HL) has become a curable malignancy for most patients during the last decades. However, many controversies still exist on the optimal strategy of how to cure our patients. The key question is how to balance the risks and toxicities of chemotherapy and radiotherapy against the need for a definite treatment for early or advanced-stage HL patients. However, although many studies have been conducted and reported during the past decade, interpretation of their results and treatment recommendations might vary significantly in different countries. For example, early-stage HL might be divided into two different subgroups: early favorable and early unfavorable or not. Treatment of early-stage HL might include radiotherapy ("combined modality") or not. Depending on the extent of radiotherapy, the schedule and number of chemotherapy cycles are also questioned. For advanced-stage HL, the situation is not much different. Compared with ABVD (adriamycin, bleomycin, vinblastine, and dacarbazine), the more aggressive escalated BEACOPP regimen (bleomycin, etoposide, adriamycin, cyclophosphamide, vincristine, procarbazine, and prednisone) is highly effective, but also raises concern due to excessive toxicity. Thus, there is a controversy about the standard of care for advanced HL patients. Because no mature results comparing these approaches with each other are currently available, it remains our duty to share the preliminary information with our patients and to figure out the most appropriate individual treatment strategy. Of course, the discussion of these issues is influenced by experiences and preferences. In contrast, in this article, we will try to focus on the available scientific evidence regarding the first-line treatment of HL. Of course, focusing on the last decade necessarily exclude the most recent results from ongoing studies. Thus, even though this article comprises treatment recommendations for HL patients, the best treatment certainly still is within properly designed prospective clinical trials.