Posterior reversible encephalopathy syndrome (PRES) is a known but extremely rare side effect of bortezomib therapy. An unusual case of PRES possibly caused by bortezomib during induction treatment in a patient with multiple myeloma is reported. The patient experienced neither hypertensive crisis nor uremic encephalopathy at the onset of PRES, which are both well-known etiologies of PRES. The patient's PRESrelated symptoms resolved completely after discontinuation of bortezomib and administration of a bulk dose of corticosteroids. The importance of early recognition of this potential neurological complication must be emphasized because this new drug is being increasingly prescribed.
A 20-year-old man with a 5-year history of acute lymphoblastic leukemia (ALL) was admitted to our hospital for severe pains in his bilateral groin and right shoulder. He had experienced these pains for 16 months. He underwent allogeneic stem cell transplantation in his second complete remission 13 months prior to hospitalization. He had received corticosteroid therapy both for ALL and for graft versus host disease for a long period (more than 13 months in total), and the total dose of corticosteroids exceeded 20 g in prednisolone equivalent at the time of the hospitalization. X-ray films of the hip joints revealed collapse of bilateral femoral heads. In addition, a subarticular radiolucent line (''crescent sign'') was also observed in an X-ray film of the right shoulder joint (Fig. 1). He was diagnosed with osteonecrosis of the femoral and humeral heads. A magnetic resonance image (MRI) showed a geographical high-intensity area spread to diaphysis, suggesting necrotic changes affecting an extensive area (Fig. 2). He was treated with narcotics for pain. Corticosteroids were reduced as rapidly as possible and maintained at a low dose to treat his adrenal insufficiency. However, his range of motion gradually decreased. Longterm corticosteroid use has been reported to be a risk factor for osteonecrosis of the humeral head, as well as the hip joint. The pathogenesis of steroid-induced osteonecrosis remains unclear, but ischemia from lipocyte hypertrophy or fat embolism has been postulated. The interval between corticosteroid administration and onset of symptom has been reported as between 6 and 18 months. Although the humeral head is the second most commonly affected site in osteonecrosis, it is often unrecognized, and its initial symptoms are often nonspecific. Removal of risk factors can reduce the risk of osteonecrosis to other joints. Thus,
A 22-year-old woman was referred to our hospital with a 1-month history of recurrent fever, subacute onset of bilateral orbital pain, and diplopia. Physical examination revealed the limits of supraduction of her right eye and infraduction of her left eye. A bone marrow aspirate from the ilium showed scattered large immature-looking lymphocytes (15.8%) with pale cytoplasm, fine nuclear chromatin, and nucleoli (Fig. 1). These cells were stained positively with CD56, TIA-1, granzyme, and perforin, and were stained negatively with CD3. In situ hybridization for EBER demonstrated that the cells were EBV-positive. A diagnosis of aggressive NK-cell leukemia was made.Magnetic resonance imaging of orbital cavity showed marked enlargement, and diffuse high intensity signals in the right superior rectus muscle and left inferior rectus muscle on fat-saturated T2-weighted image (Fig. 1). These lesions were diffusely contrast-enhanced on fat-saturated T1-weighted image (Fig. 2).After two courses of dexamethasone, methotrexate, ifosfamide, L-asparaginase, and etoposide chemotherapy, she underwent cord blood transplantation with a preparative regimen comprised of etoposide, cyclophosphamide, and total body irradiation. She achieved complete remission, and her ocular manifestations completely resolved.We could not perform biopsy of the lesions due to the poor general condition of the patient, and the exact etiology
Objective To compare the findings of magnetic resonance imaging (MRI) with advanced protocols in patients with various types of acute sensorineural hearing loss (ASNHL). Study Design Retrospective case review. Setting Tertiary referral center. Patients Two hundred eighty-seven patients with ASNHL Interventions All patients underwent MRI scanning, including heavily T2-weighted three-dimensional fluid-attenuated inversion recovery before and 4 hours after the intravenous administration of gadolinium contrast medium (delayed 3D-FLAIR). A hybrid of the reversed image of the positive endolymph signal and the native image of the perilymph signal image was constructed to visualize the endolymphatic space. Results The detection rates of abnormal MRI findings vary significantly among different types of ASNHL. A hyperintense signal on delayed 3D-FLAIR was observed in all patients with intralabyrinthine schwannoma or vestibular schwannoma and 20.5% of patients with idiopathic sudden sensorineural hearing loss (ISSNHL) but was rarely observed in definite Ménière's disease (MD, 2.6%). In contrast, endolymphatic hydrops (EH) was frequently observed in patients with definite MD (79.5%) but was observed much less frequently in patients with ISSNHL (11.0%). In patients with cochlear MD and ALHL, detection rates of cochlear EH were similar to those with definite MD, whereas detection rates of vestibular EH were significantly lower than in patients with definite MD. Conclusions The significantly different detection rates of abnormal MRI findings among various types of ASNHL shed light on the distinct pathophysiology of each disorder. A diagnosis based on MRI findings with advanced protocols may help select treatment strategies and provide prognostic information for patients.
A 50-year-old woman received low dose lenalidomide for palliative treatment of advanced IgG myeloma. Despite a long and convoluted treatment history including second courses of autologous peripheral blood stem cell transplantation, bortezomib and thalidomide, the patient responded well to 2 courses of lenalidomide therapy, but developed severe thrombocytopenia. Therefore, lenalidomide treatment was temporally discontinued and the patient was given a platelet transfusion to maintain more than 20,000/μL. However, the patient suddenly developed severe left lower quadrant abdominal pain; physical findings and abdominal X-ray (Picture 1A) initially suggested strangulating intestinal obstruction, but subsequently abdominal CT disclosed a huge hematoma in the abdominal wall (Picture 1B, arrow), which permitted us to perform conservative management without surgical intervention. Spontaneous hematoma must be suspected in patients with advanced myeloma who are using lenalidomide and may present with acute abdominal pain.
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