Amlodipine versus Felodipine

A student wanted to know why some doctors prescribed Amlodipine while others prescribed Felodipine as the calcium channel blocker for treating hypertension. This is what I found in the published literature:

Amlodipine seems to be more effective than felodipine when these drugs are compared in the same dose, with regard to the effect on BP measured in the clinic 24 hours after dosing, and to ambulatory BP during the night. The longer elimination half-life of amlodipine as compared to felodipine is the probable reason for this finding. (1998) (reference). 

However another side to the story is this: Felodipine decreased BP sooner than amlodipine. Amlodipine and felodipine are similar antihypertensive agents and have comparable BP profiles during the day and night following 8 weeks of therapy in patients with mild to moderate hypertension.  (2001) (reference).

Current advice from NICE recommends calcium channel blockers as potential first line agents in older patients (over 55 years) or black patients of any age and as potential second line adjunctive agent in younger non-black patients. No specific calcium channel blocker is recommended.  The choice of calcium channel blocker may depend on local recommendations, with the least expensive one being preferred. For patients with both hypertension and angina, amlodipine or felodipine are suitable choices. (2012) (reference).

A patient with pernicious anemia

A young man with anemia had paresthesiae of his feet and difficulty in walking. Investigations revealed that he had a macrocytic anemia due to Vitamin B12 deficiency. 

Pernicious anemia is due to Vit B12 deficiency. This is a macrocytic anemia with a megaloblastic reaction in the bone marrow. Patients with pernicious anemia can also have pancytopenia because of defective cell formation in the bone marrow. Neurological disorders involving the spinal cord, peripheral nerves and sometimes the brain are what gives this anemia the adjective 'pernicious' which means dangerous. The neurological complications of Vit B12 deficiency can occur without the anemia and anemia can be present without the neurological complications.

Pernicious anemia is often associated with gastric atrophy and hypochlorhydria which leads to poor iron absorption and associated iron deficiency. Gastric atrophy increases the risk of gastric adenocarcinoma in patients with pernicious anemia.

Autoantibodies directed against the gastric parietal cells and the intrinsic factor produced by these parietal cells are the usual cause of pernicious anemia. These patients are therefore at increased risk of other autoimmune diseases involving the thyroid, pancreas and adrenal glands.

Serum LDH levels are useful in diagnosis because they are elevated in patients with haemolytic anemia. Once the diagnosis is made, treatment is started with either cyanocobalamin or hydroxocobalamin. These are given as injections subcutaneously or intramuscularly until the desired response is achieved. Maintenance doses of Vit B12 need only be given once a month because the body requires very low amounts of Vit B12 per day (1ug per day). It may also be possible for maintenance doses of Vit B12 to be given orally in high daily doses because, even without intrinsic factor, about 1 percent of Vit B12 is absorbed from the gut.

People at risk of pernicious anemia are those who do not consume either meat or milk because the natural source of Vit B12 is from these two dietary products.

Data published by the Institute of Medical Research in 1994 (article) gives us an idea of the prevalence of Vitamin B12 deficiency in Malaysia. In the year 1993 to 1994 it was around 8.2 percent (based on a sample of around 9000 patients who were suspected to have Vit B12 deficiency). 

Macrocytic anemia can also be due to folic acid deficiency. Folic acid deficiency can cause cognitive changes, depression, dementia and rarely the spinal cord and peripheral nerve damage of Vitamin B12 deficiency. Both folic acid and Vitamin B12 are therefore important vitamins for the blood and nervous system (article). 

A patient with rheumatoid arthritis on methotrexate

A patient with rheumatoid arthritis was prescribed Tab Methotrexate 5mg per week and Tab Folic acid 5mg per day. I know that methotrexate blocks the conversion of folic acid to folinic acid and hence can inhibit the action of certain important enzymes in the body.  

I asked myself two questions: 

1. Is folic acid really necessary when prescribing low dose long term methotrexate? 
2. Will folic acid reduce the efficacy of methotrexate? 

A Medscape article provided the answers. Low dose methotrexate refers to the use of less than 20mg of methotrexate per week. Studies have shown that folic acid supplementation has a beneficial effect in reducing the side effects of methotrexate like stomatitis, gastrointestinal upsets, liver dysfunction and bone marrow suppression. Folinic acid too has the same benefit but it is more expensive. It is not entirely clear whether folic acid supplementation will reduce the efficacy of methotrexate in rheumatoid arthritis but it probably will not. The beneficial effect of low dose methotrexate in rheumatoid arthritis appears not to be related to its inhibition of folic acid metabolism. 

A cardiovascular benefit in providing supplementation with folic acid is also present. Methotrexate tends to increase homocysteine levels (a cardiovascular risk factor) in the blood. This will be prevented by folic acid. 

A patient with pericardial effusion and an endocrine problem

An elderly man with diabetes and chronic renal failure was diagnosed with a pericardial effusion a few months ago. He underwent pericardial aspiration and analysis of the pericardial fluid at another hospital before coming to us. The cardiologist in that hospital felt that the pericardial effusion was due to his renal failure. This patient presented to us because of a feeling of extreme tiredness and a history of hypoglycemic episodes. We initially attributed his tiredness to his hypoglycemic episodes. He was on oral Glibeclamide for diabetes and we stopped that drug. When his blood reports showed a severe degree of hyponatremia and his physical examination showed pigmentation of the palms, palate and lips, we considered another diagnosis.

Discussion

The pigmentation over the skin and mucosa along with the hyponatremia and hypoglycemia are suggestive of adrenal insufficiency or Addison's disease. Since this patient has chronic renal failure and is on a long acting sulphonylurea - Glibenclamide - the hypoglycemic episodes can also be blamed on the inappropriate use of glibenclamide. The suspicion of Addison's disease can be tested by doing a random plasma cortisol level. If the random plasma cortisol value is more than 25mcg/dL in a patient whose serum albumin is normal, Addison's disease is unlikely. Confirmation of diagnosis of Addison's disease can be done by doing the ACTH stimulation tests to see if the adrenal cortex responds appropriately by producing glucocorticoids and mineralocorticoids to an injection of ACTH. Treatment of Adrenal insufficiency for this patient can be initiated with a higher than usual replacement doses of hydrocortisone (for example, 100mg three times a day for one day followed by 50mg three times a day for one day and tapering thereafter). Maintenance doses of hydrocortisone for Addison's disease is usually between 15 and 20mg per day: a larger portion of hydrocortisone (10 -15mg) is given in the morning and a smaller portion (5 -10mg) is given in the late afternoon. When hydrocortisone is given at night, it may cause insomnia and that is why it is preferable to give the evening dose in the late afternoon. One thing to remember is that the adrenal gland produces both glucocorticoids and mineralocorticoids and replacement for both is needed. However, since hydrocortisone has a slight degree of mineralocorticoid activity, it is not necessary to add a separate mineralocorticoid drug (fludrocortisone) if more than 100mg per day of hydrocortisone is being given. When maintenance doses of hydrocortisone are being used, fludrocortisone is needed.

The following facts are nice to know:

1. Cortisol is the name of the glucocorticoid produced by the adrenal gland. This is the same as hydrocortisone.

2. Cortisone is the inactive form of cortisol. When given as a tablet, it is converted to cortisol in the body.

3. Prednisolone is the active form of prednisone. This is a synthetic glucocorticoid. Prednisolone is preferred over prednisone in patients with liver disease.

4. All glucocorticoid hormones have anti-inflammatory activity. These are graded as:

5mg of prednisolone being equivalent to 20mg of hydrocortisone / 25mg cortisone / 0.75mg dexamethasone /4mg methylprednisolone.

14 lessons from HIV Update 2014

HIV update 2014 was held in Seremban on 22nd May 2014. 

1. As of 2011, there were approximately 34 million people living with HIV infection in the world.

2. In 2011, the incidence of new HIV cases in Malaysia was 12.2 per 100000 people. The state of Johor had reported the greatest number of new cases that year. 

3. Antiretroviral therapy should be started according to the CD4 cell count or when there is “double trouble” (HIV infection plus another condition). If we decide to start antiretroviral therapy based on the CD4 count, then for practical purposes, in Malaysia, we start when the CD4 count is below 350 cells per cubic mm. The ideal is probably to start when the count is below 500 cells per cubic mm. Conditions that constitute double trouble include: HIV plus active tuberculosis infection; HIV plus HBV infection; when an HIV patient has a sexual partner who is not positive; when a woman with HIV is pregnant or breastfeeding; when the patient with HIV is a child below 5 years of age.

4. A template for initiating antiretroviral therapy is: Efavirenz plus Tenofovir plus Lamivudine or Efavirenz plus Tenofovir plus Emtricitabine. Other combinations involving the cheaper drug zidovudine are also possible. An important update is that Efavirenz is no longer considered teratogenic now. Important points to remember are: Efavirenz causes CNS toxicity and skin rashes.

5. The HIV viral load (HIV RNA count) is more important for decision making than the CD4 count. This is because the CD4 count is subject to variations caused by factors other than HIV infection.

6. The gold standard for the diagnosis of HIV used to be the ELISA test (for detection of antibodies) and the Western Blot test (for detection of antigens).  Nowadays different methods (rapid assay tests) are used to detect antibodies and antigens.

7. One quarter of new deaths from HIV infection are due to tuberculosis in the world. The WHO recommendation is to give co-trimoxazole (Bactrim) for all patients who have both tuberculosis and advanced HIV infection because co-trimoxazole protects against infections that such people with advanced immunosuppression are also susceptible to. The drug should be given for at least six months.

8. Diagnosing tuberculosis can be difficult when resources to do so are not easily available. A useful aphorism to remember is: If patients do not have all these 4 symptoms of cough, fever, night sweats and loss of weight, they are unlikely to have tuberculosis. Conversely if they have one or more of these symptoms, the diagnosis of tuberculosis should be suspected and options to confirm or rule out the diagnosis should be explored.

9. It has been found that 57 percent of all people being treated for tuberculosis develop hepatitis. In this regard, pyrazinamide and isoniazid are more likely than rifampicin to be the cause of the hepatitis. Ethambutol and Streptomycin are very unlikely to cause hepatitis.

10. When Efavirenz is used along with Ethambutol, the serum levels of Efavirenz will decrease.

11. Efavirenz should be avoided in people prone to depression.

12. When a patient on antiretroviral therapy develops proteinuria or acute kidney injury, suspect Tenofovir induced damage to the proximal convoluted tubules of the kidney.

13. When a patient on antiretroviral therapy develops anemia, suspect zidovudine as a cause.

14. Failure of antiretroviral therapy can be defined thus: Virological failure is said to be present when the viral load is more than 1000 copies per millilitre on 2 occasions, more than 3 months apart. Immunological failure is said to be present when the CD4 count remains less than the baseline (before treatment) or remains less than 100 cells per millilitre persistently. Clinical failure is said to be present when a new illness due to immunosuppression occurs after 6 months of treatment. 

Using rubrics for decision making

Daniel Kahneman, the Nobel Prize winning Professor of Psychology from Princeton University, has written a book titled “Thinking, fast and slow”. In this book there is a chapter called “Intuitions versus Formulas”.  He explains that our evaluation of complex problems can sometimes be standardised by the use of algorithms or formulas with numerical values attached to them.  There are two examples that I wish to quote from that book because I feel it is relevant to how we can use rubrics (or formulas with scores) for standardising the evaluation of student portfolios.

1. How do you evaluate the stability of a marriage?

The formula (frequency of lovemaking – frequency of quarrels) will give a fair idea of marital stability. If the answer is not a negative number, the marriage is probably stable. 

2. How do you evaluate the chances of survival in a new born child?

Obstetricians have always known that infants who do not breathe well within a few minutes of birth are at high risk of brain damage or death. But until the anaesthetist Virginia Apgar wrote a simple algorithm incorporating five variables to observe in all new born infants, with a score assigned to each variable, doctors and midwives used their clinical judgement to determine whether babies were in distress. Some watched for breathing problems while others focused on how soon the baby cried. Without a standardised procedure, danger signs were often missed and many new born infants died. The Apgar scoring system gave everyone a consistent standard for determining risk and helped everyone evaluate this risk in the same way as experienced obstetricians. The Apgar test is credited with helping to reduce infant mortality.

A patient with hypernatremia

A 75 year old man with a history of chronic alcohol abuse presented with bleeding per rectum. He was diagnosed to have bleeding haemorrhoids and was admitted in the hospital and given intravenous fluids. A day later he became confused and agitated. He was suspected to have delirium tremens and was treated with parenteral Thiamine. His agitated behaviour subsided but he became drowsy and lethargic. At this point his serum sodium was noted to be 168mmol/L. His blood urea was elevated but his serum creatinine was within normal limits.

About hypernatremia

Hypernatremia should be considered a water-problem and not a salt-problem. People develop hypernatremia only when there is an impairment of the thirst mechanism or when there is limited access to water. This elderly man developed hypernatremia in the hospital in the setting of an alcohol-related change in behaviour and sensorium. We can assume that his hypernatremia reflects impaired release of vasopressin from the brain (diabetes insipidus) along with insufficient fluid intake. There is evidence that alcohol can damage the supraoptic and paraventricular nuclei in the brain. (Reference) 

The diagnosis of diabetes insipidus is suspected when a person has polyuria (more than 3 litres of urine in a day) with hypotonic urine (urine osmolality less than 300mOsm/kg). As a general rule, in all patients who have polyuria with hypotonic urine, we must suspect three possibilities: compulsive polydipsia, central diabetes insipidus and nephrogenic diabetes insipidus. The fluid deprivation test can help us confirm or rule out compulsive polydipsia. The desmopressin stimulation test will help us identify nephrogenic diabetes insipidus. 

Treating hypernatremia

Hypernatremia is dangerous because it dehydrates brain cells and damages them. Before treating hypernatremia, we should know the duration of hypernatremia. If the condition has been present for less than 24 hours, rapid correction is safe. In this patient we have to assume that the hypernatremia was present for more than 24 hours. Hence his hypernatremia should be corrected slowly. Rapid correction can lead to cerebral edema. Slow correction means reducing the sodium levels by not more than 10 to 12 mmol/L per day.

Correcting elevated serum sodium

In correcting hypernatremia we use 5 percent dextrose which does not contain any sodium at all. To know how much the serum sodium will fall by giving 1 litre of 5 percent dextrose, there is a formula:

(Amount of sodium in the infusate minus the serum sodium) divided by (total body water plus 1) is equal to the amount by which the serum sodium will fall. 

His total body water = 50 percent of body weight = 30 litres because his body weight was estimated to be 60kg.

The calculated fall in serum sodium by infusing one litre of 5 percent dextrose will be: (0 – 168) divided by (30+1) = 5.4mmol/L

A fall of 10mmol/L in serum sodium needs: 10 divided by 5.4 = 1.85 litres of 5 percent dextrose.

Now we must add in the insensible and obligatory losses of fluid from the body per day. This depends on factors like urine output, body temperature, ambient temperature and respiratory rate. As an approximation, if his urine output is 900 ml per day, and insensible losses are 600ml per day, we have to add (900+600) = 1.5 L to the daily fluid requirement.

Hence he should be given (1.85 + 1.5) = 3.15 L of 5 percent dextrose per day in order to reduce serum sodium by 10mmol/day. 

This means infusing the fluid at the rate of approximately 130ml per hour. This is a rough guide only. We must check the serum sodium every 1 to 2 hours and adjust our infusion rate accordingly. At all costs, we must avoid a rapid fall in serum sodium.

What predisposed this patient to develop a confusional state in hospital?

There are two possibilities. Delirium tremens and acute onset of beriberi.

Delirium tremens is a severe clinical manifestation of alcohol withdrawal and shows itself as a confusional state with features of sympathetic over-activity. It generally occurs 3 to 10 days after stopping alcohol intake. It is important to treat it urgently because cardiovascular collapse can occur. Benzodiazepines in adequate doses should always be used. Beta blockers can be added if necessary. Attention must be paid to fluid and electrolyte balance and management of other medical / surgical conditions in the patient.

Beriberi can present as a confusional state – Wernicke’s encephalopathy and Korsakoff psychosis. People who chronically abuse alcohol may have low levels of Vitamin B1 or thiamine in their bodies. When such people are given dextrose containing fluids, they can develop acute thiamine deficiency because whatever little thiamine is present in them is used up for the metabolism of glucose.

 How should diabetes insipidus be treated?

If this patient is confirmed to have central diabetes insipidus, he will need replacement doses of vasopressin. Vasopressin (trade name Pitressin) can be given intramuscularly or subcutaneously twice or thrice a day. There is also a form of vasopressin that can be given as a nasal spray or as a tablet.

References:

1. Diabetes insipidus. http://emedicine.medscape.com/article/117648-overview

2. Delirium tremens. http://emedicine.medscape.com/article/166032-overview

3. Beriberi. http://emedicine.medscape.com/article/116930-overview

Prescribing statins - current concepts

What is the dose of statin that should be prescribed to patients who have clinically evident coronary artery disease?

When a patient below the age of 75 years has evidence of coronary artery disease, statins in appropriately high doses should be prescribed irrespective of their serum cholesterol values. A high dose (or intensive dose) for Atorvastatin refers to 40 to 80mg per day; a similar dose for Simvastatin is 40mg per day.

Is the dose of statin prescribed to a patient determined by the LDL - cholesterol value?
The new 2013 cholesterol lowering guidelines tell us that the decision to start a statin can be determined, in part, by the LDL cholesterol level. But the dose (high intensity versus moderate intensity) is determined by parameters other than the LDL cholesterol value. 

When should serum creatine kinase (CK) be tested when patients are on statins?

CK needs to be tested only when patients on statins complain of muscle pain or muscle weakness.

How can muscle pain due to statins be differentiated from other causes of myalgia?

Myalgia due to statins will resolve within 2 weeks of stopping the drug. When muscle pain persists beyond 2 weeks after discontinuing statins, other causes of myalgia must be considered.

Should liver function tests be done routinely when patients are on statins?

No. It is not necessary.

Should all patients with diabetes be prescribed with a statin?

All diabetic patients between the ages of 40 and 75 years should generally receive a statin unless their LDL cholesterol level is unusually low (below 1.8mmol/L). Whether low dose (moderate intensity) or high dose (high intensity) statins are needed should be decided by their 10-year risk of developing atherosclerotic coronary artery disease.

Is there any role for the combination of a statin with a non-statin (fenofibrate / gemfibrosil / nicotinic acid)?

Yes. There is definite evidence for doing so in patients with familial hypercholesterolemia because the reduction in cardiovascular risk is proportional to the degree of lowering of LDL cholesterol. The diagnosis of familial hypercholesterolemia should be suspected in patients with LDL cholesterol levels more than 4.9mmol/L (190mg/dL). Whether there is a benefit in combining a statin with a non-statin for those with diabetes and coronary artery disease is still not clear. When a statin is combined with a fibrate, it is better to use fenofibrate (and not gemfibrosil) because it is safer.

Can statins be continued during pregnancy?
Statins and non-statin cholesterol lowering drugs are classified as pregnancy category X and should not be taken during pregnancy and while breast feeding. Those who are on statins should discontinue them 2 to 3 months before becoming pregnant. 

Is there an increased risk of new-onset diabetes due to statin therapy?
Yes, but the risk is modest. With low dose statin therapy, 1 out of 1000 will develop diabetes per year. With high dose statin therapy, 3 out of 1000 will develop diabetes per year according to available evidence. On the other hand, appropriately used statin therapy prevents 5 to 6 cases of atherosclerosis induced vascular disease per 1000 population per year. 

Is there any role for using statins for primary prevention in individuals who are younger than 40 years of age if they do not have diabetes or heart disease?
Yes, in selected individuals. Young people who have risk factors like: a strong family history of premature coronary artery disease, an LDL cholesterol more than 4.1mmol/L (160mg/dL), a high sensitivity CRP level more than 2mg/L, or a coronary calcium score more than 300units can be considered for statin therapy as primary prevention. Moderate intensity (lower dose) statins are recommended if their calculated lifetime risk of developing coronary artery disease is not high. High intensity statin therapy is recommended if the calculated lifetime risk is high.

How are the statins different from each other in their LDL- cholesterol lowering ability?
When statins are evaluated based on their ability to lower LDL cholesterol, we note that 5mg of Rosuvastatin is equal to 10mg of Atrovastatin is equal to 20mg of Simvastatin is equal to 40mg of Lovastatin. The relationship between dose of statin and degree of LDL-cholesterol lowering is not linear: doubling of a statin dose does not double the fall in LDL cholesterol, but only an extra 6 percent fall will be seen.

Based on the 2013 cholesterol lowering guidelines from the American Heart Association and the prevention guidelines clinical vignettes . 

Acute and chronic gout

The following is based on the Malaysian Clinical Practice Guidelines for Management of Gout (Published in October 2008)

1. The first line treatment for acute gouty arthritis is non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, diclofenac and indomethacin. Aspirin is not recommended because it increases uric acid levels in the blood unless given in very high doses.

Question: A patient with acute gouty arthritis has peptic ulcer disease and hence cannot be prescribed any of the traditional NSAIDs. What can be done for pain relief in this situation?

Answer: We can use either COX-2 (cyclooxygenase 2) inhibitors like Celecoxib or Etoricoxib. We can also use Colchicine. A third option for pain relief, particularly in elderly people and in those who have renal disease, is the use of glucocorticoids. Short courses of oral prednisolone are effective in providing pain relief. Intra-articular injections of corticosteroids are also helpful.

2. Long term therapy with Allopurinol to reduce serum uric acid levels should be initiated in those who have chronic gout – that is, those who have experienced 3 or more episodes of acute gouty arthritis in a year, those who have erosive gouty arthritis, those who have tophi, and those who have uric acid nephropathy or uric acid stones.

Question: How is Allopurinol prescribed?

Answer: Allopurinol should be started in a low dose of 100 to 150mg once a day. After 3 to 4 weeks, the dose can be increased to usual maximum dose of 300mg per day. In those who have renal impairment, the dose of Allopurinol should be appropriately reduced. For example, if a patient with gout has end stage renal failure, the dose of allopurinol should not exceed 100mg once in 2 to 3 days. If a patient with gout has Stage 3 CKD, the maximum dose should not exceed 200mg per day. The usual dose of 300mg per day should only be prescribed for those with normal renal function.

Question: Can Allopurinol be prescribed for those with asymptomatic hyperuricemia?

Answer: It is not necessary to prescribe Allopurinol for all asymptomatic people with elevated uric acid levels because most of them will never suffer from gout. However, if the uric acid level is very high (about twice the upper limit of normal), it is better to prescribe allopurinol to reduce the risk of developing nephropathy. Prophylactic use of allopurinol is also recommended when a rapid increase in serum uric acid  is anticipated – as in treatment of leukemias and lymphomas.

Question: Since allopurinol has the potential to cause severe allergic reactions and bone marrow depression, is there an alternative drug for reducing serum uric acid?

Answer: Probenecid is also a uric acid lowering drug. Unlike allopurinol, probenecid increases the excretion of uric acid in the urine. Hence probenecid is not recommended for those who have uric acid nephropathy or uric acid nephrolithiasis. Ideally, urinary excretion of uric acid should be measured and probenecid should be prescribed only for those who do not have elevated urinary uric acid levels. 

Question: Will allopurinol therapy increase the risk of acute gouty arthritis?

Answer: Yes, there is an increased risk of acute arthritis during the initial period after allopurinol is initiated. That is why one should not prescribe allopurinol during an acute episode. To minimise acute episodes while initiating allopurinol therapy, low doses of colchicine (0.5mg twice a day) can be given. Colchicine can be stopped when the patient has not suffered acute arthritis for 6 months or when serum uric acid levels are normal for one month.

Question: Should allopurinol be stopped when a person, who is already on allopurinol, develops acute gouty arthritis?

Answer: No. Allopurinol need not be stopped in this situation. 

Question: What is risk when Allopurinol is prescribed along with Ampicillin?

Answer: There is an increased risk of developing a skin rash due to allopurinol.

Question: What is the risk of prescribing allopurinol with warfarin?

Answer: There is the risk of bleeding because allopurinol reduces the metabolism of warfarin and increases its half-life.

3. Polyarticular gout mimics rheumatoid arthritis. Gouty arthritis can lead to osteoarthritis.

Question: How do the subcutaneous tophi in gout differ from the subcutaneous nodules of rheumatoid arthritis?

Answer: Tophi are painless while rheumatoid nodules are generally painful.

Question: Is it possible to differentiate gouty arthritis from osteoarthritis with an x-ray of a painful joint?

Answer: Yes. The joint space is preserved in acute gouty arthritis while the joint space is narrowed in osteoarthritis.

4. A normal serum uric acid in a person with acute arthritis does not exclude gout.

Question: Can a therapeutic response to colchicine be used to diagnose gout?

Answer: Yes. Acute gouty arthritis responds within 48 hours to colchicine.

5. Alcohol should be restricted or avoided in all patients with gout.

Question: Why is alcohol restriction necessary in gout?

Answer: Alcohol reduces the excretion of purines. Uric acid is the result of purine metabolism.

6. Drugs that increase uric acid levels can provoke acute gouty arthritis.

Question: A patient with diabetes, hypertension and ischemic heart disease experiences frequent gouty arthritis. Which of her medications may need to be changed?

Answer: Is she on thiazide diuretics for hypertension and low dose aspirin for heart disease? If yes, these should be changed.

7. Food that is high in purine content should be avoided by those who have gout.

Question: Should eggs be avoided by those who have gout?

Answer: No. Eggs have low purine content.

Question: Should mushrooms, beans and peas be avoided by those who have gout?

Answer: These foods have moderate purine content and should be eaten less frequently than usual.

Question: Can those with gout eat red meat, anchovies and sardines?

Answer: These are food items with high purine content and should be avoided.