Tumor lysis syndrome (TLS) is a potentially fatal oncological emergency caused by rapid tumor cell lysis, leading to metabolic abnormalities such as hyperuricemia, hyperkalemia, and hyperphosphatemia. While traditionally associated with hematologic malignancies, recent reports indicate its occurrence in solid tumors and under new treatments.

Management strategies include prophylactic hydration and pharmacotherapy. Allopurinol, a xanthine oxidase inhibitor, suppresses uric acid production but carries a risk of xanthine accumulation in renal impairment. Febuxostat, a non-purine xanthine oxidase inhibitor, demonstrates superiority in renal impairment and has proven efficacy in preventing TLS. Rasburicase, a recombinant uric acid oxidase, promotes rapid uric acid reduction and is recommended for high-risk cases. The role of febuxostat in TLS management, particularly in hematologic malignancy patients, was evaluated. Significant reductions in serum uric acid levels were observed without serious adverse events, leading to results reflected in insurance coverage for TLS and Japanese guidelines. For rasburicase, which has rapid onset of action, considerations regarding TLS administration strategies were explored, including proposals for combination therapy for optimized treatment.

Further research is needed to evaluate long-term prognosis, enhance understanding of the disease, and develop treatments.

Urinary stone formation is closely associated with abnormal excretion and secretion of organic anions, including uric acid and dicarboxylates such as oxalate and citrate. Hyperuricemia contributes to stone formation by increasing urinary uric acid concentrations, and urinary stones are frequently observed in patients with gout. Urinary levels of these organic acids are primarily determined by transporters expressed in renal proximal tubules. In this review, we provide an overview of key organic anion transporters (OAT1, OAT3, and OAT4), which mediate the exchange of organic anions driven by intracellular dicarboxylates. These dicarboxylates are supplied by Na⁺-dependent dicarboxylate cotransporters, such as NaDC1 and NaDC3. Additionally, we describe other relevant transporters, including CFEX and Sat-1, which are involved in the transport of oxalate, a key factor in calcium stone formation. Urinary stones are considered to result from imbalances in the reabsorption and secretion of various compounds, including organic anions, regulated by renal tubular transporters. Further investigation of such transport mechanisms may contribute to the development of novel therapeutic strategies targeting these transporters.

高尿酸血症・痛風の治療において，生活習慣の改善，特に運動習慣は血清尿酸値のコントロールに重要である．高強度の無酸素運動はアデノシン三リン酸（ATP）の分解亢進と，乳酸の蓄積による尿酸排泄低下により，血清尿酸値を上昇させる．一方で，適度な有酸素運動，継続的な運動習慣は，肥満の予防やインスリン抵抗性の改善にも寄与し，長期的な血清尿酸値の低下につながると考えられている．我々は，JMDCの健診データベースを用いた研究を行い，男性では，運動習慣や日常運動があることと，血清尿酸値が低いことが関係することを示し，肥満者ほどその効果が大きい可能性を示した．また女性でも，特に肥満者において，運動習慣と血清尿酸値が低いことが関係する可能性を示した．運動指導においては，患者の背景，関節症状，合併症を考慮し，有酸素運動を中心に行うことが勧められる．高強度の運動を行う際には水分摂取を推奨し，痛風発作時や関節症状のある場合は，関節に負担のかからないような指導も重要である．高尿酸血症・痛風の患者に対して，定期的な血清尿酸値の確認と共に，個々の患者に適した運動指導を行うことが，コンプライアンス維持の観点からも大切である．

Recent studies have highlighted that xanthine oxidoreductase (XOR) inhibitors, widely used as therapeutic agents for gout, have effects beyond urate-lowering, notably impacting cellular energy metabolism. Beneficial effects on the brain and cardiovascular system have been reported following administration of allopurinol or febuxostat. Conversely, clinical observations suggest that discontinuation of XOR inhibitors may be associated with an increased risk of cardiovascular events. These findings indicate that XOR inhibition not only suppresses uric acid production but also markedly influences purine metabolism, particularly the salvage pathway-mediated ATP production mechanism. This review outlines the relevance of impaired energy metabolism in the pathophysiology of neurodegenerative diseases, and significance of the purine salvage pathway in the human brain. Furthermore, we discuss combination strategies, focusing on XOR inhibitors, which aim to enhance intracellular ATP levels.

患者は48歳女性．右手第3・4指，左手第4指の腫脹・疼痛に対し近医にて痛風・高尿酸血症と診断されたが，腎機能が低下していたため当院紹介となり精査加療入院となった．問診にて，約10年前より下肢の浮腫に対し自己判断により大量のトラセミド（20〜40mg/日）を内服していたことが判明した．トラセミドを漸減中止し血清クレアチニン値は改善傾向を示したが，血清尿酸値は依然高値であったためトピロキソスタット40mg/日を開始し退院となった．しかし15日後，両足背部の腫脹と疼痛（右＞左）が再燃し来院した．来院時検査ではCRP高値だが，尿酸値5.1mg/dlと正常範囲内であった．その他の所見に異常なかったため，下肢血管超音波検査と関節超音波検査を施行したところ，右拇趾MTP関節，右足外踝に結晶沈着と血流シグナルを認めたため，痛風関節炎と診断された．浮腫との鑑別に超音波検査が有用であった症例を報告する．

Spinal gout is a rare clinical presentation of gout; its diagnosis is challenging. Dual-energy CT (DECT) enables the detection of monosodium urate (MSU) deposition in the spine as well as in the extremities. A young man with hyperuricemia and no history of gout complained of pain around his sternum, which worsened during work. DECT revealed significant MSU deposition around his first thoracic vertebra as compared to the spine of a patient with severe hyperuricemia, as well as multiple tophi in the extremities. His hyperuricemia was caused by a decrease in the urinary excretion of uric acid. The patient was then treated with a selective urate resorption inhibitor (SURI), dotinurad. His serum uric acid level was within normal limits, and MSU deposition was reduced as observed on DECT images after six months. Treatment with the SURI reduced MSU deposition in the vertebrae, as confirmed on DECT images, as well as serum uric acid levels.