This document provides information on the management of acute gout. It begins by defining gout as a chronic inflammatory disease caused by deposition of uric acid crystals in the joints. The first symptom is usually pain and swelling in the big toe. Treatment of acute gout flares involves the use of NSAIDs and colchicine to relieve symptoms, while long-term management requires urate-lowering therapy (ULT) like allopurinol or febuxostat to lower uric acid levels and prevent future flares. Dietary and lifestyle factors that can trigger flares are also addressed.
The document discusses gout, including its causes, symptoms, diagnosis and treatment. It is a metabolic disorder caused by elevated uric acid levels (hyperuricemia) which can be due to overproduction or underexcretion of uric acid. Gout causes sudden, severe attacks of pain and inflammation in joints due to urate crystals depositing in the joints. Treatment involves drugs to relieve acute attacks like NSAIDs or colchicine, and long term drugs like allopurinol or probenecid to lower uric acid levels and prevent future attacks.
The document discusses gout, including its causes, symptoms, diagnosis and treatment. It is a metabolic disorder caused by elevated uric acid levels (hyperuricemia) which can be due to overproduction or underexcretion of uric acid. Gout causes sudden, severe attacks of pain and inflammation in joints due to urate crystals depositing in the joints. Treatment involves drugs to relieve acute attacks like NSAIDs or colchicine, and long term drugs like allopurinol or probenecid to lower uric acid levels and prevent future attacks.
There are over 127 types of arthritis. This document discusses gout, which is caused by uric acid crystals forming in the joints due to abnormally high levels of uric acid in the blood (hyperuricemia). Gout can cause acute attacks of severe pain and inflammation. Treatment involves drugs to terminate attacks, prevent complications, and manage chronic gout through reducing uric acid production or increasing excretion. Key drugs discussed are colchicine, NSAIDs, corticosteroids for acute gout and allopurinol, probenecid, sulfinpyrazone for chronic management and uric acid control.
There are over 127 types of arthritis. This document discusses gout, which is caused by uric acid crystals forming in the joints due to abnormally high levels of uric acid in the blood (hyperuricemia). Gout can cause acute attacks of severe pain and inflammation. Treatment involves drugs to terminate attacks, prevent complications, and manage chronic gout through reducing uric acid production or increasing excretion. Key drugs discussed are colchicine, NSAIDs, corticosteroids for acute gout and allopurinol, probenecid, sulfinpyrazone for chronic management and uric acid control.
- Gout is caused by elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
- Gout is caused by elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
The document discusses gout, including its causes, symptoms, diagnosis and treatment. It is a metabolic disorder caused by elevated uric acid levels (hyperuricemia) which can be due to overproduction or underexcretion of uric acid. Gout causes sudden, severe attacks of pain and inflammation in joints due to urate crystals depositing in the joints. Treatment involves drugs to relieve acute attacks like NSAIDs or colchicine, and long term drugs like allopurinol or probenecid to lower uric acid levels and prevent future attacks.
The document discusses gout, including its causes, symptoms, diagnosis and treatment. It is a metabolic disorder caused by elevated uric acid levels (hyperuricemia) which can be due to overproduction or underexcretion of uric acid. Gout causes sudden, severe attacks of pain and inflammation in joints due to urate crystals depositing in the joints. Treatment involves drugs to relieve acute attacks like NSAIDs or colchicine, and long term drugs like allopurinol or probenecid to lower uric acid levels and prevent future attacks.
There are over 127 types of arthritis. This document discusses gout, which is caused by uric acid crystals forming in the joints due to abnormally high levels of uric acid in the blood (hyperuricemia). Gout can cause acute attacks of severe pain and inflammation. Treatment involves drugs to terminate attacks, prevent complications, and manage chronic gout through reducing uric acid production or increasing excretion. Key drugs discussed are colchicine, NSAIDs, corticosteroids for acute gout and allopurinol, probenecid, sulfinpyrazone for chronic management and uric acid control.
There are over 127 types of arthritis. This document discusses gout, which is caused by uric acid crystals forming in the joints due to abnormally high levels of uric acid in the blood (hyperuricemia). Gout can cause acute attacks of severe pain and inflammation. Treatment involves drugs to terminate attacks, prevent complications, and manage chronic gout through reducing uric acid production or increasing excretion. Key drugs discussed are colchicine, NSAIDs, corticosteroids for acute gout and allopurinol, probenecid, sulfinpyrazone for chronic management and uric acid control.
- Gout is caused by elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
- Gout is caused by elevated uric acid levels in the blood (hyperuricemia) which can lead to the deposition of urate crystals in the joints, causing inflammation and pain.
- There are different treatments for the acute attacks and long-term management. For acute attacks, NSAIDs or corticosteroids can be used to reduce pain and inflammation. Colchicine may also be used.
- For long-term management and prevention of recurrent attacks, allopurinol is commonly prescribed to lower uric acid levels by inhibiting its production. Probenecid or other uricosuric
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
This document discusses gout and hyperuricemia. It defines gout as a type of inflammatory arthritis caused by uric acid crystals depositing in joints. Gout is associated with hyperuricemia, an elevated uric acid level. The document reviews risk factors, pathophysiology, clinical presentation, diagnosis, and treatment approaches including lifestyle changes, medications to treat acute attacks, and long-term urate-lowering therapy. It provides details on medications commonly used to treat gout such as allopurinol, febuxostat, colchicine, NSAIDs, and corticosteroids.
The patient is experiencing recurrent acute attacks of severe joint pain characteristic of gout. For the acute attacks, the GP should prescribe a potent non-steroidal anti-inflammatory drug (NSAID) or corticosteroid to reduce pain and inflammation. The rheumatologist can test the patient's blood and joint fluid for uric acid crystals to confirm a diagnosis of gout. Gout is caused by elevated uric acid levels leading to urate crystal deposition in joints. NSAIDs, colchicine, or corticosteroids can treat acute gout attacks, while allopurinol or probenecid given long-term can prevent recurrent attacks by lowering uric acid levels.
The patient is experiencing recurrent acute attacks of severe joint pain characteristic of gout. For the acute attacks, the GP should prescribe a potent non-steroidal anti-inflammatory drug (NSAID) or corticosteroid to reduce pain and inflammation. The rheumatologist can test the patient's blood and joint fluid for uric acid crystals to confirm a diagnosis of gout. Gout is caused by elevated uric acid levels leading to urate crystal deposition in joints. NSAIDs, colchicine, or corticosteroids can treat acute gout attacks, while allopurinol or probenecid given long-term can prevent recurrent attacks by lowering uric acid levels.
Steroids are hormones that have wide-ranging effects in the body. Common types include mineralocorticoids like aldosterone, glucocorticoids like cortisol and prednisone, and androgens. They work by binding to intracellular receptors and acting as transcription factors to influence gene expression. Glucocorticoids are commonly prescribed for their anti-inflammatory and immunosuppressive effects to treat conditions like asthma, arthritis, and IBD. Their use can cause adverse effects like fluid retention, hypertension, immunosuppression, and HPA axis suppression requiring tapering of treatment. Dexamethasone and prednisone are potent synthetic glucocorticoids often used orally or parenterally
Steroids are hormones that have wide-ranging effects in the body. Common types include mineralocorticoids like aldosterone, glucocorticoids like cortisol and prednisone, and androgens. They work by binding to intracellular receptors and acting as transcription factors to influence gene expression. Glucocorticoids are commonly prescribed for their anti-inflammatory and immunosuppressive effects to treat conditions like asthma, arthritis, and IBD. Their use can cause adverse effects like fluid retention, hypertension, immunosuppression, and HPA axis suppression requiring tapering of treatment. Dexamethasone and prednisone are potent synthetic glucocorticoids often used orally or parenterally
Gout - what should I be doing in Primary Care?pcsciences
Dr Ed Roddy, Reader in Rheumatology (Keele University) and Consultant Rheumatologist (Haywood Hospital) presented at this year's 'Musculoskeletal Education Day'. Here Ed advises what health care professionals should be be doing when dealing with patients suffering with gout based on recent research findings.
Gout - what should I be doing in Primary Care?pcsciences
Dr Ed Roddy, Reader in Rheumatology (Keele University) and Consultant Rheumatologist (Haywood Hospital) presented at this year's 'Musculoskeletal Education Day'. Here Ed advises what health care professionals should be be doing when dealing with patients suffering with gout based on recent research findings.
This document provides information on gout and hyperuricemia. It discusses the pathophysiology of gout, including how uric acid crystals form in the joints and cause inflammation. It also covers risk factors, clinical presentation, diagnosis, and treatment approaches. Treatment involves acute relief of gout attacks with medications like NSAIDs or colchicine, as well as long-term urate-lowering therapy with drugs like allopurinol or febuxostat to prevent future attacks by lowering uric acid levels.
Pancreatitis is an inflammation of the pancreas. The pancreas produces enzymes that help digest food and hormones that regulate blood sugar. Pancreatitis occurs when these digestive enzymes are activated within the pancreas itself, causing the pancreas to digest itself. There are two types - acute pancreatitis, which is a sudden but short-term inflammation, and chronic pancreatitis, which involves long-lasting and recurring inflammation that can permanently damage the pancreas over many years. Pancreatitis has various causes including gallstones, heavy alcohol use, certain medications, and genetic factors. Symptoms include abdominal pain, nausea, vomiting and weight loss in chronic cases. Treatment focuses on relieving pain and addressing the underlying cause through medications, lifestyle
This document provides information on gout and hyperuricemia. It discusses the pathophysiology of gout, including how uric acid crystals form in the joints and cause inflammation. It also covers risk factors, clinical presentation, diagnosis, and treatment approaches. Treatment involves acute relief of gout attacks with medications like NSAIDs or colchicine, as well as long-term urate-lowering therapy with drugs like allopurinol or febuxostat to prevent future attacks by lowering uric acid levels.
Pancreatitis is an inflammation of the pancreas. The pancreas produces enzymes that help digest food and hormones that regulate blood sugar. Pancreatitis occurs when these digestive enzymes are activated within the pancreas itself, causing the pancreas to digest itself. There are two types - acute pancreatitis, which is a sudden but short-term inflammation, and chronic pancreatitis, which involves long-lasting and recurring inflammation that can permanently damage the pancreas over many years. Pancreatitis has various causes including gallstones, heavy alcohol use, certain medications, and genetic factors. Symptoms include abdominal pain, nausea, vomiting and weight loss in chronic cases. Treatment focuses on relieving pain and addressing the underlying cause through medications, lifestyle
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
Gout is a disorder caused by elevated uric acid levels that leads to painful arthritis attacks. It occurs when uric acid crystallizes and deposits in joints. The most common initial attack affects the big toe joint. Treatment focuses on relieving pain and inflammation during attacks using NSAIDs, colchicine, or corticosteroids. Long term management involves lowering uric acid levels with medications like allopurinol or probenecid to prevent recurrent attacks. Gout diagnosis requires identifying urate crystals in joint fluid or addressing other criteria when fluid cannot be obtained.
Gout is a disorder caused by elevated uric acid levels that leads to painful arthritis attacks. It occurs when uric acid crystallizes and deposits in joints. The most common initial attack affects the big toe joint. Treatment focuses on relieving pain and inflammation during attacks using NSAIDs, colchicine, or corticosteroids. Long term management involves lowering uric acid levels with medications like allopurinol or probenecid to prevent recurrent attacks. Gout diagnosis requires identifying urate crystals in joint fluid or addressing other criteria when fluid cannot be obtained.
The patient is experiencing recurrent acute attacks of severe joint pain characteristic of gout. For the acute attacks, the GP should prescribe a potent non-steroidal anti-inflammatory drug (NSAID) or corticosteroid to reduce pain and inflammation. The rheumatologist can test the patient's blood and joint fluid for uric acid crystals to confirm a diagnosis of gout. Gout is caused by elevated uric acid levels leading to urate crystal deposition in joints. NSAIDs, colchicine, or corticosteroids can treat acute gout attacks, while allopurinol or probenecid given long-term can prevent recurrent attacks by lowering uric acid levels.
The patient is experiencing recurrent acute attacks of severe joint pain characteristic of gout. For the acute attacks, the GP should prescribe a potent non-steroidal anti-inflammatory drug (NSAID) or corticosteroid to reduce pain and inflammation. The rheumatologist can test the patient's blood and joint fluid for uric acid crystals to confirm a diagnosis of gout. Gout is caused by elevated uric acid levels leading to urate crystal deposition in joints. NSAIDs, colchicine, or corticosteroids can treat acute gout attacks, while allopurinol or probenecid given long-term can prevent recurrent attacks by lowering uric acid levels.
Steroids are hormones that have wide-ranging effects in the body. Common types include mineralocorticoids like aldosterone, glucocorticoids like cortisol and prednisone, and androgens. They work by binding to intracellular receptors and acting as transcription factors to influence gene expression. Glucocorticoids are commonly prescribed for their anti-inflammatory and immunosuppressive effects to treat conditions like asthma, arthritis, and IBD. Their use can cause adverse effects like fluid retention, hypertension, immunosuppression, and HPA axis suppression requiring tapering of treatment. Dexamethasone and prednisone are potent synthetic glucocorticoids often used orally or parenterally
Steroids are hormones that have wide-ranging effects in the body. Common types include mineralocorticoids like aldosterone, glucocorticoids like cortisol and prednisone, and androgens. They work by binding to intracellular receptors and acting as transcription factors to influence gene expression. Glucocorticoids are commonly prescribed for their anti-inflammatory and immunosuppressive effects to treat conditions like asthma, arthritis, and IBD. Their use can cause adverse effects like fluid retention, hypertension, immunosuppression, and HPA axis suppression requiring tapering of treatment. Dexamethasone and prednisone are potent synthetic glucocorticoids often used orally or parenterally
Gout - what should I be doing in Primary Care?pcsciences
Dr Ed Roddy, Reader in Rheumatology (Keele University) and Consultant Rheumatologist (Haywood Hospital) presented at this year's 'Musculoskeletal Education Day'. Here Ed advises what health care professionals should be be doing when dealing with patients suffering with gout based on recent research findings.
Gout - what should I be doing in Primary Care?pcsciences
Dr Ed Roddy, Reader in Rheumatology (Keele University) and Consultant Rheumatologist (Haywood Hospital) presented at this year's 'Musculoskeletal Education Day'. Here Ed advises what health care professionals should be be doing when dealing with patients suffering with gout based on recent research findings.
This document provides information on gout and hyperuricemia. It discusses the pathophysiology of gout, including how uric acid crystals form in the joints and cause inflammation. It also covers risk factors, clinical presentation, diagnosis, and treatment approaches. Treatment involves acute relief of gout attacks with medications like NSAIDs or colchicine, as well as long-term urate-lowering therapy with drugs like allopurinol or febuxostat to prevent future attacks by lowering uric acid levels.
Pancreatitis is an inflammation of the pancreas. The pancreas produces enzymes that help digest food and hormones that regulate blood sugar. Pancreatitis occurs when these digestive enzymes are activated within the pancreas itself, causing the pancreas to digest itself. There are two types - acute pancreatitis, which is a sudden but short-term inflammation, and chronic pancreatitis, which involves long-lasting and recurring inflammation that can permanently damage the pancreas over many years. Pancreatitis has various causes including gallstones, heavy alcohol use, certain medications, and genetic factors. Symptoms include abdominal pain, nausea, vomiting and weight loss in chronic cases. Treatment focuses on relieving pain and addressing the underlying cause through medications, lifestyle
This document provides information on gout and hyperuricemia. It discusses the pathophysiology of gout, including how uric acid crystals form in the joints and cause inflammation. It also covers risk factors, clinical presentation, diagnosis, and treatment approaches. Treatment involves acute relief of gout attacks with medications like NSAIDs or colchicine, as well as long-term urate-lowering therapy with drugs like allopurinol or febuxostat to prevent future attacks by lowering uric acid levels.
Pancreatitis is an inflammation of the pancreas. The pancreas produces enzymes that help digest food and hormones that regulate blood sugar. Pancreatitis occurs when these digestive enzymes are activated within the pancreas itself, causing the pancreas to digest itself. There are two types - acute pancreatitis, which is a sudden but short-term inflammation, and chronic pancreatitis, which involves long-lasting and recurring inflammation that can permanently damage the pancreas over many years. Pancreatitis has various causes including gallstones, heavy alcohol use, certain medications, and genetic factors. Symptoms include abdominal pain, nausea, vomiting and weight loss in chronic cases. Treatment focuses on relieving pain and addressing the underlying cause through medications, lifestyle
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
Gout is caused by deposits of sodium urate crystals in joints and tissues. It can be primary, due to a hereditary purine metabolism disorder, or secondary to drugs or other conditions that inhibit uric acid excretion. The document discusses the incidence, risk factors, pathophysiology, clinical manifestations, complications, diagnosis, and collaborative care of gout including treatments for acute attacks and chronic management. Tests like serum uric acid levels and synovial fluid analysis are used to monitor therapy for this metabolic disorder characterized by hyperuricemia and acute or chronic arthritis.
Gout is a disorder caused by elevated uric acid levels that leads to painful arthritis attacks. It occurs when uric acid crystallizes and deposits in joints. The most common initial attack affects the big toe joint. Treatment focuses on relieving pain and inflammation during attacks using NSAIDs, colchicine, or corticosteroids. Long term management involves lowering uric acid levels with medications like allopurinol or probenecid to prevent recurrent attacks. Gout diagnosis requires identifying urate crystals in joint fluid or addressing other criteria when fluid cannot be obtained.
Gout is a disorder caused by elevated uric acid levels that leads to painful arthritis attacks. It occurs when uric acid crystallizes and deposits in joints. The most common initial attack affects the big toe joint. Treatment focuses on relieving pain and inflammation during attacks using NSAIDs, colchicine, or corticosteroids. Long term management involves lowering uric acid levels with medications like allopurinol or probenecid to prevent recurrent attacks. Gout diagnosis requires identifying urate crystals in joint fluid or addressing other criteria when fluid cannot be obtained.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
2. What is gout?
• Chronic progressive inflammatory disease
• Persistent hyperuricaemia (serum urate >0.42mmol/L)
• Deposition of uric acid crystals in the joint, soft tissues and kidneys
• Onset 40-60 years old
• Very treatable: adherence to lifelong ULT
• Untreated complication: Tophaceous gout
3. Symptoms
• First attack usually monoarticular (big toe)
• Affect other parts of body: ankle, heel, knee, wrist, elbow and fingers
• Episodic pain (night) with redness, warmth, swelling and disability
• If not treated, usually subside within a week
4. Risk factors
• Male > Female
• Genetical defects in enzyme (HPRT)
• Uric acid is formed in liver from dietary & endogenous purines
• Purine-rich diet (meat & seafood)
• Excessive alcohol consumption (beer & spirits)
• Fructose-sweetened drinks
• Disorders of high cell turnover (eg severe psoriasis)
• Concurrent medication that inhibits excretion of uric acid (eg
thiazide)
• Recent initiation of urate-lowering therapy (ULT)
6. Management of ACUTE gout
• Provide symptom relief, but do not reduce serum urate
concentration or prevent progressive joint damage
• NSAID +/- Colchicine
• NSAID +/- intra-articular corticosteroids
7. NSAID
• Drug choice & dosage: Indomethacin 50mg TDS, Diclofenac 50mg TID,
Ibuprofen 800mg TDS. Most effective when initiated within 48 hours of
symptom onset
• If flare occurs during ULT flare prophylaxis with an NSAID, increase to full
dose of NSAID until flare solves
• Stop treatment 2 to 3 days after symptoms resolved
• Adverse effects: GI discomfort, hypertension, hypersensitivity reaction
• Contraindication: Renal impairment, active GI disorder, asthma, CV
disease and known NSAID allergy
• DDI: Anticoagulants, Antiplatelets, Triple whammy (ACE inhibitors +
NSAID + thiazide diuretics)
8. Colchicine
• Indication
• To reduce pain & inflammation in acute gout
• As flare prophylaxis when starting or increasing ULT (different
regimen)
• Dosage: Colchicine 1.2mg ASAP, then 0.6mg 1 hour later on day 1.
Continue with 0.6mg OD or BD as tolerated for the duration of gout.
• Resume prophylactic colchicine with a gap of at least 12 hours
• Adverse effects: Diarrhea, vomiting, abdominal pain
• DDI: P-gp inhibitors (macrolide antibiotics), CYP3A4 inhibitors
(antifungals)
• Contraindication: severe renal or hepatic impairment, concurrent
medication of strong CYP34A or P-gp inhibitors
9. Corticosteroid (Oral/IM/IV)
• When NSAID or colchicine are inappropriate (pt taking coagulation)
• Oral dosage: Prednisolone 15mg to 30mg daily, typically 3 to 5 days
until symptoms resolved
• Joint injection: A single dose of intramuscular corticosteroid
injection, triamcinolone acetonide 40/30/10mg at up to a maximum
of two affected sites
• Adverse effect: Diabetes, hypertension, weight gain
10. Long-term management of gout with ULT
• Allopurinol 50mg for 4 weeks; increase up to 900mg daily
• Febuxostat 40mg daily for 4 weeks; increase up to 120mg daily
• Probenecid 250mg BD for 1 week; increase up to 2g daily
• Rationale: lower serum urate below target concentration to dissolve
crystals, so stopping acute flares, joint destruction and resolve tophi
• Optimal time to start ULT is delayed until flare has resolved;
Appropriate to start ULT concurrently with gout flare treatment provided
flare treatment is adequate and risk of flare is well informed
• Need to be taken for lifelong
• Starting or increasing ULT is associated with high risk of gout flare
therefore given together with NSAID or colchicine
11. • Adjunct treatment for gout
• Relieve painful symptoms of gout by
breaking up the uric acid crystals that
accumulate in the joints
• Ingredient: Sodium bicarbonate 1760mg,
sodium citrate 630mg, citric acid 720mg,
tartaric acid 890mg
• Dosage: Take 1-2 sachets, 4 times daily
[Total of 4-8 sachets]
• Drink plenty of water
Adjunct treatment: Urinary alkaliniser
12. Dietary supplement:
Tart cherry extract & bromelain
• Lower serum uric acid by flushing out uric acid to
prevent build-up
• Inhibit COX-1 & COX-2 to provide inflammatory
effect
• Therefore quickly stop gout attacks in progress
while preventing future attacks from occurring
• Dosage for acute gout attack: 1 sachet 3 times a day
• Dosage for maintenance: 1 sachet 2 times a day
• Can safely be taken with gout medication
• Other benefit: exercise recovery, cardiovascular
health, enhance sleep quality
13. Counselling point
• Avoid purine-rich food (Meat, seafoods, and sweet drinks)
• Limit alcohol consumption
• Advise resting & apply ice pack on affected joint until onset of drug’s effect
• Review concurrent medication that decreases uric acid excretion (Thiazide can
cause hyperuricemia and should be substituted with other diuretics)
• Stay hydrated
• Check uric acid level twice a year
• Emphasize the importance of being adherence to ULT (even flare up occurs)
Editor's Notes
The topic im going to talking about is the management of gout, specifically focus on acute gout management
Gout is a type of arthritis – often call as crystal arthritis because of the deposition of urate crystal in joints, soft titssues and kidneys
Gout happen when the serum uric acid is persistently elevated more than 0.42mmol/L//7mg/dL (milligram per deciliter)
The incidence of gout is usually increased with age from 40yo but gout is very treatable if patient has good adherence to lifelong urate lowering therapy (ULT)
If the gout is not treated promptly, the collection of solid urate can cause destructive changes in surrounding tissue – we call it tophaceous gout
Therefore it’s important to emphasize importance of being adhere to ULT to patients
Talking about the symptoms: the first attack of gout is usually monoarticular (usually the big toe)
But it can also affect other part of body such as ankle, heel, knee and wrist
It can be very painful, red, swollen & the pain typically throughout the night
However, symptoms usually subside within 1 week if not treated but patient usually seek medical advice, so our aim of management is to provide rapid symptom relief
Taking about the risk factors of gout
Gout is more common in male
Deficiency in the HPRT enzyme can also lead to overproduction of uric acid – it can be the genetical risk factor
Other risk factors include:
Purine-rich diet, high alcohol consumption, fructose-sweetened drinks which can breakdown into uric acid in the blood
Concurrent medication that inhibit uric acid excretion such as thiazide
Reason behind: uric acid is eliminated by kidney (2/3) – drugs that inhibit renal excretion of uric acid can increase serum uric acid concentration.
Recent initiation of ULT can also precipitate gout flare but beneficial in long-term
How does gout happens?
Patients with risk factors mentioned just now will experience increased uric acid production/ decreased excretion of uric acid
Therefore the uric acid accumulate in the body leading to formation of urate crystal. When the urate crystal is accumulated then it will deposit in the joints
The formation of urate crystal will interact with inflammatory system releasing inflammatory mediators. Therefore inflammatory reaction (pain, swelling) seen in the joints
If they are treated promptly with treatment it can help to prevent complication such as renal damage and formation of tophi
Talking about the management of flare up in gout
Our main focus is to provide symptomatic relief
The treatment can be either NSAID alone, NSAID + colchicine/ addition of corticosteroid
NSAID is routinely given for patient without contraindication
Common drug of choice include: diclofenac 50mg TID. It’s most effective when given within 48h of symptom onset
NSAID shouldn’t be taking long term. Therefore must inform patient to stop taking it after symptoms has resolved
There are some adverse effect of NSAID need to take note of: they can cause GI discomfort, hypertension, hypersensitivity reaction (if patient has previous allergic reaction reported)
NSAID is contraindicated in those with severe renal impair, active GI disorder, asthma, pt with cardiovascular disease and known severe NSAID allergy
It can interact with other medication as well, such as anticoagulants, antiplatelet, and will cause AKI due to triple whammy effect if pt taking ACEi & diuretics together with NSAID
Therefore, proper medication history taking should be done
Colchicine is another medication can be use to reduce pain & inflammation during acute gout
It can also be given as flare prophylaxis when starting or increasing ULT
The usual dosage for acute flare is: 1.2mg ASAP, then 0.6mg 1 hour later on day 1. Continue with 0.6mg OD or BD as tolerated for the duration of gout
For those patient has been taking colchicine as prophylactic therapy, resume it for a least a gap of 12 hours to avoid toxicity
The adverse effect of colchicine include: diarrhea, vomiting, abdominal pain. Therefore patient should stop taking it whenever they experience these
One thing to take note about colchicine is that is has many DDI. Take note if patient taking p-gp inhibitors (macrolide antibiotics), CYP3A4 inhibitors (antifungals) because concurrent use of them can cause toxicity.
Prophylaxis dose: 0.6mg OD or BD according response & GI symptoms. Usually use during the first 6 months of ULT.
Colchicine may be used instead of NSAID in heart failure as it doesn’t cause fluid retention
Corticosteroid is usually reserve for candidate that cannot tolerate NSAID or colchicine or they are unable to tolerate orally
Will not talk much on this because corticosteroid require prescription from doctor
The long-term management of gout is slightly different from flare up management
Drugs that usually given as ULT are allopurinol, febuxostat, probenecid
Their principle of action is to lower serum urate below target concentration to dissolve the crystal. Therefore stopping acute flares, joint destruction & resolve tophi – it should be taken for lifelong and adherence is the crucial to manage the symptoms
For the very first episode of gout, the optimal time to start ULT is usually delayed until flare has resolved. But practically, it’s not wrong to start ULT concurrently while having gout flare treatment provided that risk of having 2nd flare is well informed
Starting during flare is thought to worsen the existing flare
Next, urinary alkaliniser can also be recommended as adjunct treatment for gout
The ingredient in urinary alkaliniser increase excretion of acid element in urine and raises the pH value of urine.
Raising urinary pH makes urine become more alkaline & will promote dissolution of uric acid crystals. Therefore relieve painful symptoms of gout.
Dosage recommended for gout patient is usually 1-2 sachets 4 times daily. Advise patient to drink plenty of water and stay hydrate so that it can flush out the uric acid from body.
Tart cherry is good for gout because contains a high amount of antioxidant & anthocyanins 1 and 2 to block cox enzyme – therefore can that help to relieve pain & inflammation
It can help to stop gout attack in progress and prevent future attacks
Dosage for gout attack is 1 sachet 3 times daily; while if it’s use as maintenance then 1 sachet 2 times daily
Improve CV health: reduce c-reactive protein & lower total cholesterol
Bromelain best known for its enzymes (proteases) to help break down foods for healthy digestion. These enzymes also contribute to joint health. Work to foster absorption of certain nutrients include glucosamine, sulfur, both present in joints & crucial for ongoing joint comfort.
These are some important counselling point we should take note when counselling patient with acute gout
If we identified that diet is the trigger factor of the gout: advise pt to cut down intake of purine-rich food such as meat, seaffods, sweet drinks
Sudden high alcohol consumption can sometimes be the risk factor also
We can advise patient to rest & apply ice pack on affected joint while waiting the drug to be effect
Most importantly, we should make use of the medication history taking session to find out if pt taking other medication that cause uric acid build up in the body. Consider to substitute to other class of drug or contact GP if required
Advise patient to stay hydrated & routinely checkup on uric acid level
Last but not least, we should highlight the importance of being adherence to ULT & reassure the flare up happen when initiating ULT is normal as it indicated that the treatment is working.