痛風
簡介
痛風是一種常見且痛苦的炎症性關節炎，通常由於血中尿酸水平異常高導致關節和周圍組織中單鈉尿酸晶體的沉積。全球大約1-4％人受痛風困擾。男性比女性更容易患痛風，比例為3:1到10:1。年長人士更大機會患上痛風，80歲以上的人群中，患病人數可達11-13％。痛風由於尿酸水平過高導致關節和周圍組織中單鈉尿酸晶體的沉積。排出的尿酸形成晶體，觸發炎症反應。
臨床表現
痛風通常表現為急性，劇烈疼痛和關節腫脹，周圍的皮膚也會出現炎症。最常受影響的是第一跖趾關節（大腳趾）。其他關節，如腳踝，膝蓋，手腕和肘部，也可能受到影響。急性痛風攻擊可以由尿酸水平的急性變化引起，例如飲酒或食用高嘌呤食物，創傷，脫水。如果未經治療，痛風攻擊常常突然發生，並可以持續數天到數周。某些患者可能存在痛風結節，這是皮膚中尿酸晶體沉積形成的結節。
診斷
痛風的診斷基於臨床表現，驗血和醫學影像檢查。如要百分百確診，就需要在關節抽取物中驗出單鈉尿酸晶體或結節（尿酸沉積物）。血液檢測可能顯示血清尿酸水平增高，但這並不能單獨作為診斷，因為某些高尿酸血症者可能不會患痛風。醫學影像檢查，如X光，超聲波可以幫助見到關節損傷和晶體沉積。
治療
痛風的治療包括緩解急性攻擊並防止未來的發作。急性發作通常使用非類固醇抗炎藥（NSAIDs），秋水仙素或皮質類固醇來減輕炎症和疼痛。長期管理包括使用藥物降低尿酸尿，如別嘌醇或費布醇，以防止晶體形成。
假性痛風
假性痛風，也稱為二磷酸氫鈣二水合物（CPPD）晶體沉積病，是一種類似痛風的情況，但其原因是由於關節和周圍組織中的二磷酸氫鈣晶體沉積。假性痛風的臨床表現，診斷和治療與痛風類似，但其潛在的病理生理學和晶體組成是不同的。
併發症
痛風的併發症包括關節損傷，腎結石。此外，痛風還可能引起眼疾，包括視網膜並發症以及增加黃斑變性的風險。在罕見的情況下，痛風結節也可能在不尋常的部位形成，例如腳背骨窩，舟跡關節甚至視網膜，使人誤診成其他疾病。
生活方式改變
生活方式改變可以幫助降低痛風發作的風險並提高整體健康水平。這些包括戒酒，保持足夠的水分，以及減少高嘌呤食物（例如紅肉，海鮮和內臟）。
以下是一些飲食要點：
通過改善飲食，患者可以更好地控制其痛風並降低痛風發作的可能性。
常見誤解
關於痛風，一些常見的誤解包括認為它只影響大腳趾。事實上，痛風可以影響各種關節。另一個常見的誤解是血液中高尿酸水平即表示患有痛風，但並非所有高尿酸血症者都會患上痛風。此外，血液測試的尿酸水平並不能作為診斷痛風的依據。若要百分百確診，就需要在關節抽取物中驗出單鈉尿酸晶體或結節（尿酸沉積物）。
結論
儘管痛風係一種常見且令人不快的關節炎，但透過正確的診斷和治療以及生活方式改變，患者可以有效地改善其症狀並減少未來發作的風險。
摘要
痛風是一種關節炎，主要由於尿酸水平過高導致關節及周邊組織形成單鈉尿酸晶體沉積。痛風的臨床表現為急性，嚴重疼痛和關節腫脹，最常見於大腳趾，但也可能影響腳踝，膝蓋，手腕和肘部。痛風的確診需要透過臨床表現，驗血和醫學影像檢查，並在關節抽取物中驗出單鈉尿酸晶體，血液檢測血清尿酸水平增高並不能單獨作為診斷。治療痛風包括緩解急性發作，預防未來發作，包含使用非類固醇抗炎藥，秋水仙素，皮質類固醇，以及長期使用藥物降低尿酸如別嘌醇或費布醇。生活方式改變，包括限制酒精，保持充足的水分，以及減少高嘌呤食物可幫助減少痛風報發作。痛風的常見誤解包括認為痛風只影響大腳趾，以及高尿酸血症者一定會患痛風，這些觀念皆是不正確的。儘管痛風是一種常見的疾病，但透過適當的診斷和治療，以及生活方式的改變，病患可以有效地管理自己的病情，並降低未來痛風發作的風險。
Gout
Introduction
Gout is a common and painful inflammatory arthritis caused by the deposition of monosodium urate crystals in joints and surrounding tissues usually associated with hyperuricemia, which is an abnormally high level of uric acid in the blood. The prevalence of gout ranges from 1-4% worldwide. Gout is more common in men than women, with a ratio of 3:1 to 10:1. The prevalence of gout increase with age, reaching up to 11-13% prevalence in people older than 80 years. Gout is caused by the deposition of monosodium urate crystals in joints and surrounding tissues due to hyperuricemia. The excreted uric acid form crystals that trigger an inflammatory response.
Clinical Presentation
Gout typically presents as an acute, severely painful, and swollen joint, and overlying skin inflammation. It most commonly affects the first metatarsophalangeal joint (big toe). Other joints, such as the ankles, knees, wrists, and elbows, can also be affected. Acute gout attacks can be triggered by acute changes in uric acid levels, such as the consumption of alcohol or high-purine foods, trauma, dehydration. Gout attacks often occur suddenly and can last for several days to weeks if left untreated. Gouty tophi, which are nodules formed by the deposition of urate crystals in the skin, can also be present in some patient.
Diagnosis
Diagnosis of gout is based on clinical presentation, laboratory tests, and imaging studies. The gold standard for diagnosis is the identification of monosodium urate crystals in synovial fluid or tophi (urate deposits) obtained from the affected joint. Laboratory tests may show elevated serum uric acid levels, but this alone is not diagnostic, as some individuals with hyperuricemia may not develop gout. Imaging studies, such as X-rays, ultrasound can help visualize joint damage and crystal deposits.
Treatment
The treatment of gout involves managing acute attacks and preventing future episodes. Acute attacks are treated with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids to reduce inflammation and pain. Long-term management includes urate-lowering therapy (ULT), such as allopurinol or febuxostat, to reduce serum uric acid levels and prevent crystal formation.
Pseudo Gout
Pseudo gout, also known as calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, is a condition that can mimic gout but is caused by the deposition of calcium pyrophosphate crystals in joints and surrounding tissues. The clinical presentation, diagnosis, and management of pseudo gout are similar to those of gout, but the underlying pathophysiology and crystal composition are different.
Complications
Complications of gout can include joint damage, kidney stones. Gout has also been associated with ocular abnormalities, including retinal complications and an increased risk of macular degeneration. In rare cases, gouty tophi can form in unusual locations, such as the sinus tarsi, subtalar joint, or even the retina, mimicking other pathologic conditions.
Lifestyle Modification
Lifestyle modifications can help reduce the risk of gout attacks and improve overall health. These include limiting alcohol consumption, staying well-hydrated, and consuming a balanced diet low in purine-rich foods (e.g., red meat, seafood, and organ meats).
Here are some key points to consider when educating patients about dietary modifications for gout:
1. Limit purine-rich foods: High-purine foods can increase uric acid levels, leading to gout attacks. Patients should avoid or limit their intake of organ meats (e.g., liver, kidney, sweetbreads), certain seafood (e.g., anchovies, shellfish, sardines, tuna), and high-purine vegetables (e.g., asparagus, spinach).
2. Alcohol consumption: Alcohol, particularly beer and grain liquors, can increase the risk of gout attacks.
3. Hydration: Staying well-hydrated can help flush out uric acid and prevent kidney stones, which are potential complications of gout
By following these dietary modifications, patients can better manage their gout and reduce the risk of gout attacks.
Common Misunderstandings
Some common misunderstandings about gout include the belief that it only affects the big toe. In reality, gout can affect various joints. Another common misunderstanding is that high uric acid levels in the blood always indicate gout, but not all individuals with hyperuricemia develop gout. Additionally, blood tests for uric acid levels are not diagnostic tests for gout, as the gold standard for diagnosis is the identification of monosodium urate crystals in synovial fluid or tophi.
資料由疼痛醫學專科醫生
李旭明醫生提供