Recently I saw an elderly patient with episodic hypertension. The pheo markers were mildly elevated at times but normal at others. Before I saw the patient, abdominal and pelvic CT had already been done and some thickening of left adrenal gland was noted. No tumors were identified. MIBG scan had also been done, and there was a slight uptake in the left adrenal area. A few of those involved in the patient’s care believed that she/he had pheo. The patient also firmly accepted the pheo diagnosis after reading about pheo. Once again, I was the pain-in-the-neck doctor and told the patient that it was very unlikely that she/he had pheo. Then someone brought up the issue of “adrenal medulla hyperplasia” and wondered if it was not pheo, it might be “adrenal medulla hyperplasia”. I have followed the literature on this alleged condition for a while and would like to share my thoughts here with you.
Adrenal medulla, the inner part of adrenal gland where pheo is derived from, is part of the sympathetic nervous system (the “fight-and-flight” system). The exact role of adrenal medulla in blood pressure control is still not so clear. For example, most patients with bilateral adrenalectomy do not have low blood pressure. In the earlier part of last century, adrenalectomy was used to treat hypertension with mixed results. The adrenal medulla has a very small mass of less than 1 gram. The adrenal medulla of some patients indeed becomes bigger with more cells (“hyperplasia”). In patients with multiple endocrine neoplasia type 2 (MEN2), adrenal medulla hyperplasia occurs before pheo develops. In patients with long-standing hypertension, the adrenal gland tends to be bigger and both cortex and medulla are bigger.
In the literature, there are a handful of reports claiming adrenal medulla hyperplasia can cause symptoms very similar to that of pheo. In these reports, usually the patients have labile hypertension and pheo is suspected. The pheo markers are either normal or mildly elevated. The adrenal glands are either normal or mildly enlarged but clearly without a tumor on CT or MRI. MIBG scan typically is borderline positive. These reports then claim the patients immediately get better after unilateral or bilateral adrenalectomy. The pathology exam of course shows adrenal medulla hyperplasia.
Based on my own experience, my discussion with other experts on pheo, and review of literature, I simply think there are no adequate evidence and no need to consider the so-called adrenal medulla hyperplasia as a disease in clinical practice. My reasoning is as follows:
1. Adrenal medulla hyperplasia is either a pre-tumor lesion or a secondary change caused by hypertension rather than causing hypertension.
2. Nowadays most patients with labile hypertension can be satisfactorily controlled by medications.
3. There are no universal criteria accepted by pathologists to diagnose adrenal medulla hyperplasia.
4. Most patients with “adrenal medulla hyperplasia” do not have labile hypertension.
5. The diagnosis of “adrenal medulla hyperplasia” is often a hindsight after pheo is not found in the adrenal.
6. Most patients continue to experience the same symptoms after adrenalectomy.
As medicine is ever-developing, I can imagine that adrenal medulla hyperplasia may indeed cause symptoms in a small number of patients. The problem is that many patients will undergo unnecessary and ineffective adrenalectomy if we allow “adrenal medulla hyperplasia” to be in the differential diagnosis of hypertension. The proponents of “adrenal medulla hyperplasia” need to establish a clear set of diagnostic criteria to identify the few patients who might benefit from adrenalectomy.
Dr. Pheo
Friday, January 1, 2010
Monday, December 7, 2009
Interferences with pheo tests
The 5 pheo tests are subjected to interferences by quite a few factors. I list those factors here according to their significance. The most important message, however, is that these factors are usually not a big deal and can be rather easily figured out by an expert. Reaching a pheo diagnosis requires all things considered, rather than any evidence in isolation.
Major interferences:
1. In many diseases, catecholamines and metanephrines levels are indeed genuinely elevated, and can be rather high. About 30 such diseases are known. Obstructive sleep apnea, severe anxiety, and essential hypertension are the most common ones.
2. Any major stress, such as stroke, severe infection, and bad pain, elevate catecholamines and metanephrines levels.
3. Some drugs such as cocaine, phenoxybenzamine, tricyclic antidepressants, and monoamine oxidase inhibitors can also elevate catecholamines and metanephrines levels. Sinemet elevates dopamine levels tremendously.
Minor interferences:
Eating, standing, the stress of venipuncture, and old age. These conditions usually elevate catecholamines and metanephrines levels only slightly.
Variable interferences:
These are caused by drugs (usually beta blockers) and they are assay-dependent. The clinicians and the lab should communicate about them.
Errors:
Clerical and lab errors are also realistic possibilities. They are rare but can happen.
When I order pheo tests, I actually tell the patients initially not to worry about any interferences. If the results are normal (which is the case in most patients), the patient does not have pheo. If the results are elevated (usually in 20% of cases), I will then decide on a case-by-case basis.
This will be the last post this year. Happy holidays! I will continue posting next year.
Dr. Pheo
Major interferences:
1. In many diseases, catecholamines and metanephrines levels are indeed genuinely elevated, and can be rather high. About 30 such diseases are known. Obstructive sleep apnea, severe anxiety, and essential hypertension are the most common ones.
2. Any major stress, such as stroke, severe infection, and bad pain, elevate catecholamines and metanephrines levels.
3. Some drugs such as cocaine, phenoxybenzamine, tricyclic antidepressants, and monoamine oxidase inhibitors can also elevate catecholamines and metanephrines levels. Sinemet elevates dopamine levels tremendously.
Minor interferences:
Eating, standing, the stress of venipuncture, and old age. These conditions usually elevate catecholamines and metanephrines levels only slightly.
Variable interferences:
These are caused by drugs (usually beta blockers) and they are assay-dependent. The clinicians and the lab should communicate about them.
Errors:
Clerical and lab errors are also realistic possibilities. They are rare but can happen.
When I order pheo tests, I actually tell the patients initially not to worry about any interferences. If the results are normal (which is the case in most patients), the patient does not have pheo. If the results are elevated (usually in 20% of cases), I will then decide on a case-by-case basis.
This will be the last post this year. Happy holidays! I will continue posting next year.
Dr. Pheo
Sunday, November 22, 2009
Happy Holidays
Dear readers,
The Dr. Pheo's blog has been running for 8 months. Since the very beginning, readers have been giving me very positive feedbacks. Up to now, the blog has covered almost all aspects of pheo and I hope that patients and families benefit from reading these posts.
As the holiday season is approaching, I want to take this opportunity to wish all patients, their families and friends, and all those interested in this disease a very happy holiday season.
Dr. Pheo
The Dr. Pheo's blog has been running for 8 months. Since the very beginning, readers have been giving me very positive feedbacks. Up to now, the blog has covered almost all aspects of pheo and I hope that patients and families benefit from reading these posts.
As the holiday season is approaching, I want to take this opportunity to wish all patients, their families and friends, and all those interested in this disease a very happy holiday season.
Dr. Pheo
Thursday, October 1, 2009
Pheo tests in the real world
Whenever a new test is reported, its performance is always great (why report it if not?). There are multiple reasons why the test performs well in the original reports. The diagnosis criteria are strict and clear, the tests are run by experts with strict quality control measures, the clerical errors are minimized, etc. When the test is used by more people, it usually becomes not as great. One example is the pheo test "plasma metanephrines."
In the first few studies of this test, the sensitivity (if you have pheo, the test will be positive) and specificity (if you don't have pheo, the test will be negative) both approach 100%. In a very well-designed, definitive study (published in 2002), the sensitivity and specificity are indeed close to 100% but only in people with family history of pheo. In patients without family history of pheo, the sensitivity is also nearly 100%, but the specificity is about 85%. That means, if you do not have a family history of pheo and if your doctors suspect you have pheo but you do not actually have pheo, the chance that the test will still be positive is 15% (false positive). In most cases, it is the normetanephrine that is false positive rather than metanephrine. I am sure you know what I am talking about if you have ever read a plasma metanephrines test report. The metanephrines test gives two values, metanephrine and normetanephrine.
How does the plasma metanephrines test perform in the real world? Earlier this year, a report was published comparing the performances of all 5 tests for pheo in a large US hospital. The 5 tests are plasma metanephrines, plasma catecholamines, urine metanephrines, urine catecholamines, and urine VMA. The study has quite a few limits; the major one being that not a lot of patients eventually prove to have pheo (which is also a strength because it reflects the fact that pheo is rare). With these limits, this study shows that the sensitivity and specificity of all 5 tests are about the same. The nicest thing about the study is that it gives positive predictive value (PPV) and negative predictive value (NPV) of the 5 tests in the real world.
The PPV and NPV are different from sensitivity and specificity because they depend on how the ordering physician selects patients to be tested. Let's not get entangled in technicality but the PPV of a test means that if you have a positive test for pheo, what the chance is that you actually have pheo. The NPV means that if your test result is negative, what the chance is that you actually do not have pheo. In this community-based study, the PPVs of all these tests range from 15-30%. That means if you have a pheo test at this hospital and it is positive, the chance that you indeed have pheo is about 15-30%. If the test is only moderately elevated, the PPVs are even much lower and range from 2-15%. The NPVs of all these tests are excellent: close to 100%. That means if you have a normal test result (from just any of the 5 tests) at this hospital, you are pretty sure that you do not have pheo.
Make no mistake. I do think that the plasma metanephrines is the best test for pheo. It is scientifically sound, highly reproducible, and not as interfered by medications as some other tests. I can also do clonidine suppression test based on the plasma metanephrines. I use it as the main test to diagnose pheo. It is just that the test results need to be interpreted by an expert.
Dr. Pheo
In the first few studies of this test, the sensitivity (if you have pheo, the test will be positive) and specificity (if you don't have pheo, the test will be negative) both approach 100%. In a very well-designed, definitive study (published in 2002), the sensitivity and specificity are indeed close to 100% but only in people with family history of pheo. In patients without family history of pheo, the sensitivity is also nearly 100%, but the specificity is about 85%. That means, if you do not have a family history of pheo and if your doctors suspect you have pheo but you do not actually have pheo, the chance that the test will still be positive is 15% (false positive). In most cases, it is the normetanephrine that is false positive rather than metanephrine. I am sure you know what I am talking about if you have ever read a plasma metanephrines test report. The metanephrines test gives two values, metanephrine and normetanephrine.
How does the plasma metanephrines test perform in the real world? Earlier this year, a report was published comparing the performances of all 5 tests for pheo in a large US hospital. The 5 tests are plasma metanephrines, plasma catecholamines, urine metanephrines, urine catecholamines, and urine VMA. The study has quite a few limits; the major one being that not a lot of patients eventually prove to have pheo (which is also a strength because it reflects the fact that pheo is rare). With these limits, this study shows that the sensitivity and specificity of all 5 tests are about the same. The nicest thing about the study is that it gives positive predictive value (PPV) and negative predictive value (NPV) of the 5 tests in the real world.
The PPV and NPV are different from sensitivity and specificity because they depend on how the ordering physician selects patients to be tested. Let's not get entangled in technicality but the PPV of a test means that if you have a positive test for pheo, what the chance is that you actually have pheo. The NPV means that if your test result is negative, what the chance is that you actually do not have pheo. In this community-based study, the PPVs of all these tests range from 15-30%. That means if you have a pheo test at this hospital and it is positive, the chance that you indeed have pheo is about 15-30%. If the test is only moderately elevated, the PPVs are even much lower and range from 2-15%. The NPVs of all these tests are excellent: close to 100%. That means if you have a normal test result (from just any of the 5 tests) at this hospital, you are pretty sure that you do not have pheo.
Make no mistake. I do think that the plasma metanephrines is the best test for pheo. It is scientifically sound, highly reproducible, and not as interfered by medications as some other tests. I can also do clonidine suppression test based on the plasma metanephrines. I use it as the main test to diagnose pheo. It is just that the test results need to be interpreted by an expert.
Dr. Pheo
Tuesday, September 1, 2009
Dr. Pheo's musings on health care cost
I usually do not pay much attention to political arguments. In these days, however, I cannot go a single day without hearing discussions on health care or health insurance reform. A lot of discussions, I feel, are not on the really important issues. Today, I'd like to share my thoughts on one of the key issues in health insurance reform: health care cost.
The one thing everyone seems to agree upon is that the health care cost is too high for our society to afford and "we" spend way too much money on health care in America but only to achieve the same levels of health that other developed countries achieve with much less cost. But who are "we"? Am I one of the "we"? Are the readers of this blog some of the "we"? Who are responsible for the high cost in health care? How do we cut down the cost?
I, as a physician, may contribute to the high cost. For example, although I know that the MIBG scan probably does not add much to the localization of pheo if CT or MRI already finds a clear adrenal tumor in a middle-aged patient with high markers, I order the MIBG scan anyway for this patient because I worry about the small possibility that there may be a second pheo somewhere that I may miss otherwise. Although the literature and my own research show that ordering multiple tests for pheo is not necessary, I sometimes do order 2 markers because there is a small chance that there may be a lab error.
As a patient, you may also contribute to the high cost. Yearly follow-up of pheo markers is sufficient after pheo resection; some patients, though, insist on testing every 3 months because they worry about the small chance that they may have a fast-growing pheo. Some patients demand to have an MRI even after CT shows clear results because MRI does have a small advantage over CT in describing the pheo.
All medically justified costs are not waste. But who determines if a test or a treatment is justified? In reality and in theory, the physicians are the ones who eventually determine if a cost is justified. The insurance clerk who declined the coverage of your MRI just acted on the recommendations made by physicians hired by the insurance company. Although physicians have the intellectual capacity to perform this function, the society as a whole has to decide on a few key issues to make physicians exercise their best judgment on cost justification.
1. Do we trust physicians to do this job at the first place? If we don't, who else do we trust?
2. If we trust physicians, how do we make sure that physicians always exercise their best judgment without playing favoritism?
3. What is the maximal acceptable risk? If there is a 1/million chance a pheo may be missed, most reasonable people don't worry about it. What if the chance is 1/1,000, or 1/100, or 1/10?
4. How much do we want to pay for "peace of mind" and how much physical discomfort is intolerable?
5. Who is responsible for the risk? If I do not order an MIBG on a patient who I feel rather sure only has a solitary pheo but it turns out that the patient does have metastasis, whose fault is it? Am I free of blame because I exercised my best judgment?
6. What is the appropriate mechanism to reward physicians so that physicians are motivated both to avoid unnecessary tests and treatments and to use all necessary tests and treatments?
7. Do the answers to the above questions depend on whether a patient pays everything by her/himself, has private insurance, has public insurance, or has no insurance at all?
Our society has to be reasonable and responsible to achieve an efficient, equitable, and satisfying health care system.
Dr. Pheo
The one thing everyone seems to agree upon is that the health care cost is too high for our society to afford and "we" spend way too much money on health care in America but only to achieve the same levels of health that other developed countries achieve with much less cost. But who are "we"? Am I one of the "we"? Are the readers of this blog some of the "we"? Who are responsible for the high cost in health care? How do we cut down the cost?
I, as a physician, may contribute to the high cost. For example, although I know that the MIBG scan probably does not add much to the localization of pheo if CT or MRI already finds a clear adrenal tumor in a middle-aged patient with high markers, I order the MIBG scan anyway for this patient because I worry about the small possibility that there may be a second pheo somewhere that I may miss otherwise. Although the literature and my own research show that ordering multiple tests for pheo is not necessary, I sometimes do order 2 markers because there is a small chance that there may be a lab error.
As a patient, you may also contribute to the high cost. Yearly follow-up of pheo markers is sufficient after pheo resection; some patients, though, insist on testing every 3 months because they worry about the small chance that they may have a fast-growing pheo. Some patients demand to have an MRI even after CT shows clear results because MRI does have a small advantage over CT in describing the pheo.
All medically justified costs are not waste. But who determines if a test or a treatment is justified? In reality and in theory, the physicians are the ones who eventually determine if a cost is justified. The insurance clerk who declined the coverage of your MRI just acted on the recommendations made by physicians hired by the insurance company. Although physicians have the intellectual capacity to perform this function, the society as a whole has to decide on a few key issues to make physicians exercise their best judgment on cost justification.
1. Do we trust physicians to do this job at the first place? If we don't, who else do we trust?
2. If we trust physicians, how do we make sure that physicians always exercise their best judgment without playing favoritism?
3. What is the maximal acceptable risk? If there is a 1/million chance a pheo may be missed, most reasonable people don't worry about it. What if the chance is 1/1,000, or 1/100, or 1/10?
4. How much do we want to pay for "peace of mind" and how much physical discomfort is intolerable?
5. Who is responsible for the risk? If I do not order an MIBG on a patient who I feel rather sure only has a solitary pheo but it turns out that the patient does have metastasis, whose fault is it? Am I free of blame because I exercised my best judgment?
6. What is the appropriate mechanism to reward physicians so that physicians are motivated both to avoid unnecessary tests and treatments and to use all necessary tests and treatments?
7. Do the answers to the above questions depend on whether a patient pays everything by her/himself, has private insurance, has public insurance, or has no insurance at all?
Our society has to be reasonable and responsible to achieve an efficient, equitable, and satisfying health care system.
Dr. Pheo
Saturday, August 1, 2009
Chromogranin A
Chromogranin A (CGA) is one of the most important tests in the diagnosis of neuroendocrine tumors. Unfortunately, it is also one of the trickiest tests to interpret. I am asked very frequently by patients and colleagues on interpretation of CGA.
CGA is a protein. It is produced in neuroendocrine cells and released into the circulation. CGA is metabolized to fragments and cleared by the kidney. CGA is actually a hardy protein. It is very stable in serum at long incubation at 37°C, or even after repeated freezing and thawing. It reflects the cumulative secretory activity of all those cells. So CGA can be elevated by any of the many types of neuroendocrine cells. CGA indirectly reflects tissue or tumor mass. CGA is elevated in most patients with pheochromocytoma or paraganglioma.
Several issues need to be considered when interpreting the CGA results. One problem is that the reference range differs among labs. In Quest, the upper limit of normal is 36 ng/mL, while in Labcorp, it is 5 nmol/L (equivalent to 245 ng/mL). The Quest test is more useful. (Note added on July 26, 2010: One reader contests this point. Please see comment 25 and others.)
CGA can be elevated in benign and reversible conditions. In a type of gastritis (atrophic gastritis), acid production is decreased, which in turn stimulates CGA production from the stomach.
The most common cause of elevated CGA in clinical practice is anti-acid treatment, especially proton pump inhibitors for acid reflux. CGA will increase even after days of PPI in healthy volunteers. The prevalence of elevated CGA is common in patients on PPI, and more than 60% patients on PPI have elevated CGA after 4 years.
Because CGA is cleared by the kidney, CGA is elevated in kidney failure.
CGA can be elevated in several other diseases: hepatocellular carcinoma, prostate cancer, adrenal incidentaloma, pituitary tumors, and rheumatoid arthritis.
In summary, CGA is an important marker for neuroendocrine tumors. In routine clinical practice, the most common cause of high CGA is anti-acid treatment. Kidney failure and atrophic gastritis are also causes of high CGA. In a patient is not taking anti-acids or has chronic kidney failure, high CGA levels raise suspicion of neuroendocrine tumor or other tumors, including pheochromocytoma.
Obviously, CGA is not specific for pheochromocytoma and is less important than metanephrines in the diagnosis of pheochromocytoma. CGA can be used in combination with metanephrines to increase diagnostic accuracy for pheochromocytoma.
Dr. Pheo
CGA is a protein. It is produced in neuroendocrine cells and released into the circulation. CGA is metabolized to fragments and cleared by the kidney. CGA is actually a hardy protein. It is very stable in serum at long incubation at 37°C, or even after repeated freezing and thawing. It reflects the cumulative secretory activity of all those cells. So CGA can be elevated by any of the many types of neuroendocrine cells. CGA indirectly reflects tissue or tumor mass. CGA is elevated in most patients with pheochromocytoma or paraganglioma.
Several issues need to be considered when interpreting the CGA results. One problem is that the reference range differs among labs. In Quest, the upper limit of normal is 36 ng/mL, while in Labcorp, it is 5 nmol/L (equivalent to 245 ng/mL). The Quest test is more useful. (Note added on July 26, 2010: One reader contests this point. Please see comment 25 and others.)
CGA can be elevated in benign and reversible conditions. In a type of gastritis (atrophic gastritis), acid production is decreased, which in turn stimulates CGA production from the stomach.
The most common cause of elevated CGA in clinical practice is anti-acid treatment, especially proton pump inhibitors for acid reflux. CGA will increase even after days of PPI in healthy volunteers. The prevalence of elevated CGA is common in patients on PPI, and more than 60% patients on PPI have elevated CGA after 4 years.
Because CGA is cleared by the kidney, CGA is elevated in kidney failure.
CGA can be elevated in several other diseases: hepatocellular carcinoma, prostate cancer, adrenal incidentaloma, pituitary tumors, and rheumatoid arthritis.
In summary, CGA is an important marker for neuroendocrine tumors. In routine clinical practice, the most common cause of high CGA is anti-acid treatment. Kidney failure and atrophic gastritis are also causes of high CGA. In a patient is not taking anti-acids or has chronic kidney failure, high CGA levels raise suspicion of neuroendocrine tumor or other tumors, including pheochromocytoma.
Obviously, CGA is not specific for pheochromocytoma and is less important than metanephrines in the diagnosis of pheochromocytoma. CGA can be used in combination with metanephrines to increase diagnostic accuracy for pheochromocytoma.
Dr. Pheo
Wednesday, July 1, 2009
A sexual side effect of phenoxybenzamine
As the cliché goes, the best teacher of a doctor is the patient. There is nothing more true about it, especially on side effects of a drug.
Years ago, I had the opportunity of seeing a very pleasant 30-something male patient. He had been diagnosed with pheo by another doctor and saw me for a second opinion. He had been on phenoxybenzamine for the alleged specific anti-pheo effects for more than a year. His blood pressure was well controlled by phenoxybenzamine. After reviewing the numerous tests and imaging studies, I determined that he did not have pheo. I recommended using a diuretic medication for blood pressure control, instead of using the expensive phenoxybenzamine. He was so relieved once he learned that he would not absolutely need phenoxybenzamine—but not due to financial reasons. He told me that he could not have children while on the drug but his wife and he so much wanted to start a family. An inquisitive soul, I asked him to elaborate. The patient shyly told me that he had not had ejaculates after he was on phenoxybenzamine.
That was the first time I learned this very common side effect of phenoxybenzamine in men. We all know the standard common side effects such as nasal stuffiness, orthostatic hypotension, and fatigue. Ejaculatory failure happens in almost every man taking phenoxybenzamine. Most men do not complain of this side effect, probably because the treatment is usually short-term and patients have anxiety before operation so that they do not attempt sexual activity. Men may also be embarrassed to talk about this what is perceived by some as a sensitive but trivial symptom.
The mechanism of ejaculatory failure is not retrograde ejaculation, rather, patients simply do not transfer seminal fluid (the bulk of ejaculates) to be ejaculated. The good news is that this sexual side effect is completely reversible in 1-2 days after discontinuing phenoxybenzamine. And phenoxybenzamine does NOT affect libido, potency, or orgasm.
Prazosin and doxazosin usually do not cause ejaculatory problems but sometimes they do.
After I learned this side effect from that patient, I always inform my male patients of this unique side effect of phenoxybenzamine. Most of them appreciate my warning. Some would say “Doc, sex is the last thing I am thinking of now.” Hey, you never know. Sexual activity is generally not contraindicated in patients with pheo, provided that it is not particularly violent.
Dr. Pheo
Years ago, I had the opportunity of seeing a very pleasant 30-something male patient. He had been diagnosed with pheo by another doctor and saw me for a second opinion. He had been on phenoxybenzamine for the alleged specific anti-pheo effects for more than a year. His blood pressure was well controlled by phenoxybenzamine. After reviewing the numerous tests and imaging studies, I determined that he did not have pheo. I recommended using a diuretic medication for blood pressure control, instead of using the expensive phenoxybenzamine. He was so relieved once he learned that he would not absolutely need phenoxybenzamine—but not due to financial reasons. He told me that he could not have children while on the drug but his wife and he so much wanted to start a family. An inquisitive soul, I asked him to elaborate. The patient shyly told me that he had not had ejaculates after he was on phenoxybenzamine.
That was the first time I learned this very common side effect of phenoxybenzamine in men. We all know the standard common side effects such as nasal stuffiness, orthostatic hypotension, and fatigue. Ejaculatory failure happens in almost every man taking phenoxybenzamine. Most men do not complain of this side effect, probably because the treatment is usually short-term and patients have anxiety before operation so that they do not attempt sexual activity. Men may also be embarrassed to talk about this what is perceived by some as a sensitive but trivial symptom.
The mechanism of ejaculatory failure is not retrograde ejaculation, rather, patients simply do not transfer seminal fluid (the bulk of ejaculates) to be ejaculated. The good news is that this sexual side effect is completely reversible in 1-2 days after discontinuing phenoxybenzamine. And phenoxybenzamine does NOT affect libido, potency, or orgasm.
Prazosin and doxazosin usually do not cause ejaculatory problems but sometimes they do.
After I learned this side effect from that patient, I always inform my male patients of this unique side effect of phenoxybenzamine. Most of them appreciate my warning. Some would say “Doc, sex is the last thing I am thinking of now.” Hey, you never know. Sexual activity is generally not contraindicated in patients with pheo, provided that it is not particularly violent.
Dr. Pheo
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