A 59-year-old woman was diagnosed with symptomatic Bence Jones protein, lambda (λ) type, associated with multiple myeloma (BJP-λ MM). Considering her renal dysfunction, she initially received bortezomib and dexamethasone. After renal function improved, she received one cycle of bortezomib, lenalidomide, and dexamethasone (BLD) therapy and achieved stringent complete response. She presented with general fatigue and jaundice before the second cycle of BLD. Laboratory testing revealed: total bilirubin, 4.8 mg/dl; indirect bilirubin, 4.1 mg/dl; lactate dehydrogenase, 978 U/l; hemoglobin, 7.4 g/dl; haptoglobin, <10 mg/dl; platelet count, 23,000/µl; and creatinine, 0.96 mg/dl. A hemogram revealed 1% schistocytes. ADAMTS13 activity was undetectable and the ADAMTS13 inhibitor level was 1.8 Bethesda units. A diagnosis of acquired thrombotic thrombocytopenic purpura (aTTP) was made, and treatment was initiated with prednisolone and rituximab. Plasma exchange was not performed because thrombocytopenia did not progress. The first dose of rituximab restored platelet count, and ADAMTS13 inhibitor became undetectable. The clinical course in this case was consistent with drug-induced aTTP.
Spontaneous spinal epidural hematoma (SSEH) is a rare condition with an estimated incidence of 0.1 per 100,000 individuals. It is usually characterized by sudden spinal pain followed by rapidly progressive neurological deficits. Surgical treatment is generally indicated if a patient presents with neurological deficits. We report a case of SSEH presenting with neurological deficits relieved after position change, recovering without surgery. The patient was a 73-year-old woman developed sudden, severe pain in the neck, back, lumbar region, and abdomen while sitting after meals. Upon arrival at the emergency department, her vital signs were stable except for hypertension. The patient was placed supine on a stretcher and became agitated because of back pain, but no motor or sensory symptoms were noted in the extremities. Pain initially improved with acetaminophen but recurred, requiring diclofenac. When attempting to sit again, complete motor and sensory deficits were noted in both lower limbs extending from the femur to the soles of the feet (the trunk was not assessed). Lower limbs muscle strength was 1/1 by Manual Muscle Test. Perineal sensory deficits and incontinence were present, leading to a diagnosis of bladder and bowel dysfunction (ASIA Grade A). Imaging revealed an extensive posterior epidural hematoma from C6 to Th12 with maximal cord compression at Th10–12. No coagulopathy or vascular malformations were observed. The hospital was unable to provide emergency surgical decompression because of limited medical resources, including the unavailability of an on-call spine surgeon and refusal of the transfer request. The patient was managed conservatively with analgesia, blood pressure control, and hemostatic agents. Motor function recovered fully, and she was discharged independently on day 13 with only mild residual sensory impairment. This case demonstrates a unique position-induced course; symptoms improved when supine and worsened while sitting. Treatment of SSEH is generally initiated once neurological symptoms appear. A case report described lumbar SSEH with position-induced symptoms; however, it was the opposite of the present case. This discrepancy reflects differences in position related spinal alignment. Lumbar lordosis decreases while sitting, expanding the canal, whereas thoracic kyphosis flattens when supine and increases while seated, narrowing the canal. In this patient, maximal compression at Th10–12 was relieved when supine but exacerbated when sitting. In this case, conservative treatment was selected due to resource limitations, including the lack of an on-call spine surgeon and refusal of the transfer request. This approach ultimately resulted in the most favorable therapeutic outcome. When rapid improvement in position-induced symptoms is observed, conservative treatment may be a better option. These findings emphasize that SSEH presentation depends not only on hematoma size but also on lesion location and posture-related mechanics.
The creatinine muscle index (CMI) may reflect muscle mass or strength; however, simultaneous assessment of both in patients with chronic kidney disease (CKD) remains limited. We examined associations of CMI with handgrip strength (HGS) and bioimpedance analysis-estimated skeletal muscle index (SMI) in these patients. Patients with CKD had HGS and SMI measured at the initiation of dapagliflozin for CKD. Low muscle strength and mass were defined as HGS < 18 kg and SMI < 5.7 kg/m2 in women, and HGS < 28 kg and SMI < 7.0 kg/m2 in men. We included 97 patients with CKD (men: 73.2
Primary breast angiosarcoma is an exceptionally rare malignancy, particularly in elderly patients, and may closely resemble benign vascular lesions on imaging and core needle biopsy. We report a case of low-grade primary angiosarcoma in a woman in her late 70s, initially misdiagnosed as a haemangioma despite interval tumour growth. A definitive diagnosis was achieved only after wide local excision, which demonstrated well to intermediately differentiated angiosarcoma with clear margins. Given the limited evidence supporting adjuvant therapy in low-grade disease, surgery alone was appropriate, and the patient remains recurrence-free at 2.5 years. This case highlights the diagnostic challenges and importance of maintaining suspicion in older adults.
A 77-year-old man with unresectable advanced gastric cancer, complicated by multiple liver and distant lymph node metastases, began drug therapy. As a third-line treatment, nivolumab was administered for two courses;however, the patient developed destructive thyroiditis. Treatment with nivolumab was resumed after clinical improvement, but the patient developed interstitial pneumonia following a total of four courses, leading to discontinuation of treatment. Although nivolumab was discontinued and no further drug therapy was initiated, tumor shrinkage persisted for 15 months. Notably, the metastatic lesions remained stable and the tumor markers had not increased even 29 months later. The patient's clinical course differed from that typically observed in patients treated with conventional cytotoxic agents, as tumor shrinkage continued long after the discontinuation of nivolumab.
