CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.

The genus Yersinia includes 11 species. Three species are generally associated with human disease; Y. enterocolitica, Y. pestis, and Y. pseudotuberculosis. Yersinia pestis is the causative agent of plague. Yersinia pseudotuberculosis can manifest with fever, abdominal pain, and scarlatiniform rash. Additional symptoms include diarrhea, sterile joint effusions, erythema nodosum, and septicemia; these symptoms can be indistinguishable from Kawasaki Disease. By report, almost 10 % of cases of Kawasaki Disease in Japan have serologic or bacteriologic evidence of Y. pseudotuberculosis infection [Redbook: 2012 Report of the Committee on Infectious Diseases, 795-7]. Y. enterocolitica is most often associated with yersiniosis.

Although Y. enterocolitica is not the most common cause of diarrheal illness in the United States, it is one of the nine pathogens that have been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In the United States, it is estimated that Y. enterocolitica causes slightly over 115,000 infections annually (Emerg. Infect. Dis. 2011;17:7-15). The disease is more common in cooler months. It is transmitted by consumption of contaminated food, especially raw or undercooked pork products.

Only a few outbreaks have been reported in the United States, and these were usually associated with consumption of pork, specifically chitterlings (pig intestines), a winter holiday dish prepared most frequently in black households in the South (MMWR 1990;39:819-20). Transmission to infants and young children is thought to occur from caretakers preparing chitterlings who have not adequately cleaned their hands prior to touching objects subsequently handled by the child.

The incubation period is usually 4-6 days (range, 1-14 days). The duration of diarrhea is variable and can persist up to 3 weeks. Organisms can be excreted an average of 6 weeks. Clinical manifestations vary by age. Younger children usually present with fever and diarrhea. Stools frequently contain blood and leucocytes. Vomiting is also reported in most series. In contrast, older children and adults often present with a pseudoappendicitis syndrome with right-sided abdominal pain and fever. Leukocytosis is often present. At surgery, mesenteric adenitis is observed, and the appendix generally is normal.

Bacteremia can occur and is usually associated with infection in children less than 1 year of age and in those with iron-overloaded states, including persons with sickle cell disease, beta-thalassemia, and those receiving deferoxamine therapy. While uncommon, focal manifestations including pharyngitis, osteomyelitis, pyomyositis, pneumonia, empyema, and meningitis may occur.

Courtesy CDC

Diagnosis is confirmed by isolation of the organism from stool, blood, peritoneal fluid, lymph nodes, and throat cultures. Most laboratories do not routinely test for Yersinia in stool cultures. If Y. enterocolitica is suspected, you should notify the laboratory so the stool can be plated on appropriate media (CIN agar). Serologic tests to detect a rise in serum antibody titers to confirm infection are available in reference and research laboratories, but are not generally used for diagnosis. Cross reactivity with Brucella, Salmonella, Vibrio, and Rickettsia may lead to false positive titer results. Y. enterocolitica antibodies also have antigenic similarity with thyroid tissue. You may see persistent elevation of titers in patients with thyroid disease.

Benefit of antimicrobial therapy for isolated Y. enterocolitica gastrointestinal disease and Y. pseudotuberculosis has not been established. Therapy may decrease the duration of fecal shedding. Treatment is indicated for immunocompromised hosts and persons with septicemia and focal infections. Y. enterocolitica and Y. pseudotuberculosis are usually sensitive to trimethoprim-sulfamethoxazole, aminoglycosides, cefotaxime, fluoroquinolones (persons greater than 18 years of age or older), and tetracycline or doxycycline (for children at least 8 years of age and older).

So what is the actual incidence and when should the practitioner be concerned? Initial population based surveillance data for Y. enterocolitica infections in FoodNet sites between 1996 and 1999 reported an overall incidence of 0.9 cases per 100,000 population. The highest incidence was among black and Asian individuals and was 3.2 cases and 1.5 cases per 100,000 population, respectively. The incidence in Hispanics and whites was 0.6 and 0.4 cases per 100,000 respectively. Incidence increased with decreasing age in all racial/ethnic groups. Blacks infants had the highest incidence, 141.9 cases/100,000 population, and the highest incidence in infants was reported from Georgia (207 cases/100,000). Seasonal variation in incidence was noted only in black individuals with peak activity occurring in December (Clin. Infect. Dis. 2004;38[Suppl 3]:S181-9).

A.Currell/Flickr Creative Commons

The most recent data from FoodNet (1996-2009) reveals an overall incidence of 0.5/100,000. There was a decline in incidence in all racial and ethnic groups. The highest incidence is still observed in black and Asians (0.9 and 0.7 per 100,000). The most dramatic decline occurred in black individuals (3.2 vs. 0.9 per 100,000). In 1998, an educational campaign was initiated in Georgia that targeted high-risk individuals and provided information on the safe handling and preparation of chitterlings. The state of Georgia reported the greatest decline to 0.4/100,000, which has almost eliminated the racial disparity reported in 2009. It is unclear if this campaign was the only reason for the decline in Georgia. The incidence in whites is 0.2/100,000. Since 2007, the incidence in Asian children less than 5 years of ages has been the highest amongst all racial and ethnic groups. Pork consumption is still assumed to be the major source. Seasonal variability persists amongst Black children less 5 years of age, implying that chitterlings may still be the source of infection for individuals in this group (Clin. Infect. Dis. 2012:54 [Suppl 5]:S385-S90).

In general, yersiniosis should be included in the differential of a febrile diarrheal illness, particularly during the cooler months and holiday season. It is prudent to determine if consumption and/or preparation of chitterlings or other pork products by the patient or caretakers has occurred. This will enable you to alert the laboratory so stool specimens can be cultured on the appropriate medium (CIN agar). Consumption of chitterlings is not limited to any specific racial or ethnic group. Individuals from rural and farming areas may also consume this product.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures. Write to Dr. Word at [email protected].

The genus Yersinia includes 11 species. Three species are generally associated with human disease; Y. enterocolitica, Y. pestis, and Y. pseudotuberculosis. Yersinia pestis is the causative agent of plague. Yersinia pseudotuberculosis can manifest with fever, abdominal pain, and scarlatiniform rash. Additional symptoms include diarrhea, sterile joint effusions, erythema nodosum, and septicemia; these symptoms can be indistinguishable from Kawasaki Disease. By report, almost 10 % of cases of Kawasaki Disease in Japan have serologic or bacteriologic evidence of Y. pseudotuberculosis infection [Redbook: 2012 Report of the Committee on Infectious Diseases, 795-7]. Y. enterocolitica is most often associated with yersiniosis.

Although Y. enterocolitica is not the most common cause of diarrheal illness in the United States, it is one of the nine pathogens that have been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In the United States, it is estimated that Y. enterocolitica causes slightly over 115,000 infections annually (Emerg. Infect. Dis. 2011;17:7-15). The disease is more common in cooler months. It is transmitted by consumption of contaminated food, especially raw or undercooked pork products.

Only a few outbreaks have been reported in the United States, and these were usually associated with consumption of pork, specifically chitterlings (pig intestines), a winter holiday dish prepared most frequently in black households in the South (MMWR 1990;39:819-20). Transmission to infants and young children is thought to occur from caretakers preparing chitterlings who have not adequately cleaned their hands prior to touching objects subsequently handled by the child.

The incubation period is usually 4-6 days (range, 1-14 days). The duration of diarrhea is variable and can persist up to 3 weeks. Organisms can be excreted an average of 6 weeks. Clinical manifestations vary by age. Younger children usually present with fever and diarrhea. Stools frequently contain blood and leucocytes. Vomiting is also reported in most series. In contrast, older children and adults often present with a pseudoappendicitis syndrome with right-sided abdominal pain and fever. Leukocytosis is often present. At surgery, mesenteric adenitis is observed, and the appendix generally is normal.

Bacteremia can occur and is usually associated with infection in children less than 1 year of age and in those with iron-overloaded states, including persons with sickle cell disease, beta-thalassemia, and those receiving deferoxamine therapy. While uncommon, focal manifestations including pharyngitis, osteomyelitis, pyomyositis, pneumonia, empyema, and meningitis may occur.

Courtesy CDC

Diagnosis is confirmed by isolation of the organism from stool, blood, peritoneal fluid, lymph nodes, and throat cultures. Most laboratories do not routinely test for Yersinia in stool cultures. If Y. enterocolitica is suspected, you should notify the laboratory so the stool can be plated on appropriate media (CIN agar). Serologic tests to detect a rise in serum antibody titers to confirm infection are available in reference and research laboratories, but are not generally used for diagnosis. Cross reactivity with Brucella, Salmonella, Vibrio, and Rickettsia may lead to false positive titer results. Y. enterocolitica antibodies also have antigenic similarity with thyroid tissue. You may see persistent elevation of titers in patients with thyroid disease.

Benefit of antimicrobial therapy for isolated Y. enterocolitica gastrointestinal disease and Y. pseudotuberculosis has not been established. Therapy may decrease the duration of fecal shedding. Treatment is indicated for immunocompromised hosts and persons with septicemia and focal infections. Y. enterocolitica and Y. pseudotuberculosis are usually sensitive to trimethoprim-sulfamethoxazole, aminoglycosides, cefotaxime, fluoroquinolones (persons greater than 18 years of age or older), and tetracycline or doxycycline (for children at least 8 years of age and older).

So what is the actual incidence and when should the practitioner be concerned? Initial population based surveillance data for Y. enterocolitica infections in FoodNet sites between 1996 and 1999 reported an overall incidence of 0.9 cases per 100,000 population. The highest incidence was among black and Asian individuals and was 3.2 cases and 1.5 cases per 100,000 population, respectively. The incidence in Hispanics and whites was 0.6 and 0.4 cases per 100,000 respectively. Incidence increased with decreasing age in all racial/ethnic groups. Blacks infants had the highest incidence, 141.9 cases/100,000 population, and the highest incidence in infants was reported from Georgia (207 cases/100,000). Seasonal variation in incidence was noted only in black individuals with peak activity occurring in December (Clin. Infect. Dis. 2004;38[Suppl 3]:S181-9).

A.Currell/Flickr Creative Commons

The most recent data from FoodNet (1996-2009) reveals an overall incidence of 0.5/100,000. There was a decline in incidence in all racial and ethnic groups. The highest incidence is still observed in black and Asians (0.9 and 0.7 per 100,000). The most dramatic decline occurred in black individuals (3.2 vs. 0.9 per 100,000). In 1998, an educational campaign was initiated in Georgia that targeted high-risk individuals and provided information on the safe handling and preparation of chitterlings. The state of Georgia reported the greatest decline to 0.4/100,000, which has almost eliminated the racial disparity reported in 2009. It is unclear if this campaign was the only reason for the decline in Georgia. The incidence in whites is 0.2/100,000. Since 2007, the incidence in Asian children less than 5 years of ages has been the highest amongst all racial and ethnic groups. Pork consumption is still assumed to be the major source. Seasonal variability persists amongst Black children less 5 years of age, implying that chitterlings may still be the source of infection for individuals in this group (Clin. Infect. Dis. 2012:54 [Suppl 5]:S385-S90).

In general, yersiniosis should be included in the differential of a febrile diarrheal illness, particularly during the cooler months and holiday season. It is prudent to determine if consumption and/or preparation of chitterlings or other pork products by the patient or caretakers has occurred. This will enable you to alert the laboratory so stool specimens can be cultured on the appropriate medium (CIN agar). Consumption of chitterlings is not limited to any specific racial or ethnic group. Individuals from rural and farming areas may also consume this product.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures. Write to Dr. Word at [email protected].

The genus Yersinia includes 11 species. Three species are generally associated with human disease; Y. enterocolitica, Y. pestis, and Y. pseudotuberculosis. Yersinia pestis is the causative agent of plague. Yersinia pseudotuberculosis can manifest with fever, abdominal pain, and scarlatiniform rash. Additional symptoms include diarrhea, sterile joint effusions, erythema nodosum, and septicemia; these symptoms can be indistinguishable from Kawasaki Disease. By report, almost 10 % of cases of Kawasaki Disease in Japan have serologic or bacteriologic evidence of Y. pseudotuberculosis infection [Redbook: 2012 Report of the Committee on Infectious Diseases, 795-7]. Y. enterocolitica is most often associated with yersiniosis.

Although Y. enterocolitica is not the most common cause of diarrheal illness in the United States, it is one of the nine pathogens that have been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In the United States, it is estimated that Y. enterocolitica causes slightly over 115,000 infections annually (Emerg. Infect. Dis. 2011;17:7-15). The disease is more common in cooler months. It is transmitted by consumption of contaminated food, especially raw or undercooked pork products.

Only a few outbreaks have been reported in the United States, and these were usually associated with consumption of pork, specifically chitterlings (pig intestines), a winter holiday dish prepared most frequently in black households in the South (MMWR 1990;39:819-20). Transmission to infants and young children is thought to occur from caretakers preparing chitterlings who have not adequately cleaned their hands prior to touching objects subsequently handled by the child.

The incubation period is usually 4-6 days (range, 1-14 days). The duration of diarrhea is variable and can persist up to 3 weeks. Organisms can be excreted an average of 6 weeks. Clinical manifestations vary by age. Younger children usually present with fever and diarrhea. Stools frequently contain blood and leucocytes. Vomiting is also reported in most series. In contrast, older children and adults often present with a pseudoappendicitis syndrome with right-sided abdominal pain and fever. Leukocytosis is often present. At surgery, mesenteric adenitis is observed, and the appendix generally is normal.

Bacteremia can occur and is usually associated with infection in children less than 1 year of age and in those with iron-overloaded states, including persons with sickle cell disease, beta-thalassemia, and those receiving deferoxamine therapy. While uncommon, focal manifestations including pharyngitis, osteomyelitis, pyomyositis, pneumonia, empyema, and meningitis may occur.

Courtesy CDC

Diagnosis is confirmed by isolation of the organism from stool, blood, peritoneal fluid, lymph nodes, and throat cultures. Most laboratories do not routinely test for Yersinia in stool cultures. If Y. enterocolitica is suspected, you should notify the laboratory so the stool can be plated on appropriate media (CIN agar). Serologic tests to detect a rise in serum antibody titers to confirm infection are available in reference and research laboratories, but are not generally used for diagnosis. Cross reactivity with Brucella, Salmonella, Vibrio, and Rickettsia may lead to false positive titer results. Y. enterocolitica antibodies also have antigenic similarity with thyroid tissue. You may see persistent elevation of titers in patients with thyroid disease.

Benefit of antimicrobial therapy for isolated Y. enterocolitica gastrointestinal disease and Y. pseudotuberculosis has not been established. Therapy may decrease the duration of fecal shedding. Treatment is indicated for immunocompromised hosts and persons with septicemia and focal infections. Y. enterocolitica and Y. pseudotuberculosis are usually sensitive to trimethoprim-sulfamethoxazole, aminoglycosides, cefotaxime, fluoroquinolones (persons greater than 18 years of age or older), and tetracycline or doxycycline (for children at least 8 years of age and older).

So what is the actual incidence and when should the practitioner be concerned? Initial population based surveillance data for Y. enterocolitica infections in FoodNet sites between 1996 and 1999 reported an overall incidence of 0.9 cases per 100,000 population. The highest incidence was among black and Asian individuals and was 3.2 cases and 1.5 cases per 100,000 population, respectively. The incidence in Hispanics and whites was 0.6 and 0.4 cases per 100,000 respectively. Incidence increased with decreasing age in all racial/ethnic groups. Blacks infants had the highest incidence, 141.9 cases/100,000 population, and the highest incidence in infants was reported from Georgia (207 cases/100,000). Seasonal variation in incidence was noted only in black individuals with peak activity occurring in December (Clin. Infect. Dis. 2004;38[Suppl 3]:S181-9).

A.Currell/Flickr Creative Commons

The most recent data from FoodNet (1996-2009) reveals an overall incidence of 0.5/100,000. There was a decline in incidence in all racial and ethnic groups. The highest incidence is still observed in black and Asians (0.9 and 0.7 per 100,000). The most dramatic decline occurred in black individuals (3.2 vs. 0.9 per 100,000). In 1998, an educational campaign was initiated in Georgia that targeted high-risk individuals and provided information on the safe handling and preparation of chitterlings. The state of Georgia reported the greatest decline to 0.4/100,000, which has almost eliminated the racial disparity reported in 2009. It is unclear if this campaign was the only reason for the decline in Georgia. The incidence in whites is 0.2/100,000. Since 2007, the incidence in Asian children less than 5 years of ages has been the highest amongst all racial and ethnic groups. Pork consumption is still assumed to be the major source. Seasonal variability persists amongst Black children less 5 years of age, implying that chitterlings may still be the source of infection for individuals in this group (Clin. Infect. Dis. 2012:54 [Suppl 5]:S385-S90).

In general, yersiniosis should be included in the differential of a febrile diarrheal illness, particularly during the cooler months and holiday season. It is prudent to determine if consumption and/or preparation of chitterlings or other pork products by the patient or caretakers has occurred. This will enable you to alert the laboratory so stool specimens can be cultured on the appropriate medium (CIN agar). Consumption of chitterlings is not limited to any specific racial or ethnic group. Individuals from rural and farming areas may also consume this product.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures. Write to Dr. Word at [email protected].

The American Family Therapy Academy recently issued a policy statement protesting the DSM-5, and asks the American Psychiatric Association to consider the importance of relational and family context to psychiatric diagnoses.

AFTA, a multidisciplinary group, does not support the current revision of the DSM, stating that it "continues a long history of ignoring research and excluding vital contributions of nonpsychiatric mental health disciplines." This statement refers to the substantial body of research concerning the role of relational factors in mental health and mental illness, and also refers to the large number of effective family treatments, including, but not limited to, family therapy.

The academy criticizes the DSM’s use of the biomedical model and its omission of the role of family and sociocultural contexts on well-being. AFTA states that the DSM "delegitimizes the focus on relationship, life stage, community, and access to power and resources." AFTA points out that the DSM fails to take into account culture, class and ‘destructive unjust social factors,’ such as poverty, hunger, homelessness, violence, racism, and other forms of oppression. AFTA considers these factors to be important in reaching a diagnosis that accurately describes patients.

Many psychiatrists, especially family, social, and cultural psychiatrists, agree with AFTA’s position. Several family researchers and family psychiatrists have been pushing for many years to get relational diagnoses included in the DSM-IV and the DSM-5 (J. Fam. Psychol. 2006;20:359-68), citing decades of excellent research into relational diagnoses. Their attempts are supported by nonmedical health care professionals who complain that they cannot get paid by insurance companies for treating families. However, putting any diagnosis in the DSM so the insurance companies get paid is a backward way of thinking. Any diagnostic system of American psychiatry should not be framed or influenced by financial organizations that want to ration health care.

Some psychiatrists who contributed to the DSM offer the disclaimer that "they do not mean this to be a bible." However, the DSM is frequently used "as a bible," for example, in the courts. More importantly, reductionist diagnostic descriptions in the DSM narrow the public’s and the professionals’ thinking about psychological difficulties, and, by extrapolation, limit the conceptualization of what types of interventions might be helpful.

For example, describing psychiatric illnesses as biological leads to the assumption that biological interventions are needed. If an illness is defined using a biopsychosocial explanation, however, this broader understanding leads to a wider array of possible treatments. A psychiatric diagnostic system should recognize all the factors that are known to contribute to psychological health and illness to be of most use in patient care.

There is also a strong argument for not including relational diagnoses in the DSM. The argument is this: Relational factors are process factors, rather than static factors. For example, expressed emotion (EE) is not a characteristic of a family but rather a description of family distress that arises as a result of living with a disease. It is a description of a family process. Providing psychoeducation to a distressed family substantially reduces the level of EE and the subsequent risk of patient relapse. EE is a measure of relational process. If EE is entered into the DSM, there is a danger of its being seen as a static entity.

A delicate balance exists between the utilitarian need for a system of diagnoses and the risk of overdefining people and their relationships as "pathological." It was not that long ago that we pathologized homosexuality and described the entity of the "schizophrenogenic mother."

Dr. Larry Freeman, a member of the Association of Family Psychiatrists, adds: "Be wary of a pressure beyond medical circles to utilize psychiatry as a force for social control. I do a great deal of workers’ [compensation], and so-called ‘preexisting conditions’ are commonly framed as the "cause" of a worker’s emotional response to injury, and therefore, [the worker’s] current psychiatric conditions are not accepted as a consequence of the original injury event.

"Be careful that we do not enable this distortion further in our efforts to include context and history."

How should we include patient contexts such as violence, abuse, trauma, poverty, injustice, or relational dysfunction? How do we acknowledge that these factors play a significant role in the lives of our patients? For children, this is especially important as treatment often focuses on changing or stabilizing their environment, and ensuring that there is adequate attachment and nurturance.

How do we ensure that these relationships and contexts are adequately defined so we can monitor the effectiveness (or not) of interventions? AFTA supports the creation of a work group that will focus on developing an alternative to the DSM for the conceptualization of emotional distress. David Elkins, Ph.D., is planning an international summit in 2013 with representatives from all therapist groups to discuss the feasibility of such a system.

Another way forward is to develop a diagnostic system that focuses on health. The Global Assessment of Functioning (GAF), describes with reasonable accuracy a person’s individual level of functioning on a scale of 1 to 100. The Global Assessment of Relational Functioning (GARF) describes the health of a relationship on a scale of 1-100. Using these scales, pathology and health coexist on a continuum, with anchors throughout the scale. These systems are currently crude instruments, but imagine how much better they could become if they were the focus of research, clinical trials, etc.

There will always be the need for individual diagnoses, where the melancholic continues to suffer despite having an excellent social and family context, and there will always be cases where we cannot decide if the patient is ill unto himself or if his illness is informed by the context of his life.

But consider the inverse, the person who is optimistic and functional in spite of the dire context of his life, people who hold beliefs, convictions, and so on that raise them above their life circumstances. (Think of visionaries like Gandhi or Mandela). In the same way, there are relationships that function well, despite the presence of adversity. How do we develop a system that aspires to "health" instead of pathology? The American health care system (or rather its illness care system) needs to morph into true health care with a focus on prevention on both an individual and relational front.

For additional information, see Relational Processes and DSM-V: Neuroscience, Assessment, Prevention, and Treatment (Washington: American Psychiatric Association Publishing, 2006).

Dr. Alison Heru is with the department of psychiatry at the University of Colorado at Denver, Aurora. She has been a member of the Association of Family Psychiatrists since 2002 and currently serves as the organization’s treasurer. In addition, she is the coauthor of two books on working with families and is the author of numerous articles on this topic.

The American Family Therapy Academy recently issued a policy statement protesting the DSM-5, and asks the American Psychiatric Association to consider the importance of relational and family context to psychiatric diagnoses.

AFTA, a multidisciplinary group, does not support the current revision of the DSM, stating that it "continues a long history of ignoring research and excluding vital contributions of nonpsychiatric mental health disciplines." This statement refers to the substantial body of research concerning the role of relational factors in mental health and mental illness, and also refers to the large number of effective family treatments, including, but not limited to, family therapy.

The academy criticizes the DSM’s use of the biomedical model and its omission of the role of family and sociocultural contexts on well-being. AFTA states that the DSM "delegitimizes the focus on relationship, life stage, community, and access to power and resources." AFTA points out that the DSM fails to take into account culture, class and ‘destructive unjust social factors,’ such as poverty, hunger, homelessness, violence, racism, and other forms of oppression. AFTA considers these factors to be important in reaching a diagnosis that accurately describes patients.

Many psychiatrists, especially family, social, and cultural psychiatrists, agree with AFTA’s position. Several family researchers and family psychiatrists have been pushing for many years to get relational diagnoses included in the DSM-IV and the DSM-5 (J. Fam. Psychol. 2006;20:359-68), citing decades of excellent research into relational diagnoses. Their attempts are supported by nonmedical health care professionals who complain that they cannot get paid by insurance companies for treating families. However, putting any diagnosis in the DSM so the insurance companies get paid is a backward way of thinking. Any diagnostic system of American psychiatry should not be framed or influenced by financial organizations that want to ration health care.

Some psychiatrists who contributed to the DSM offer the disclaimer that "they do not mean this to be a bible." However, the DSM is frequently used "as a bible," for example, in the courts. More importantly, reductionist diagnostic descriptions in the DSM narrow the public’s and the professionals’ thinking about psychological difficulties, and, by extrapolation, limit the conceptualization of what types of interventions might be helpful.

For example, describing psychiatric illnesses as biological leads to the assumption that biological interventions are needed. If an illness is defined using a biopsychosocial explanation, however, this broader understanding leads to a wider array of possible treatments. A psychiatric diagnostic system should recognize all the factors that are known to contribute to psychological health and illness to be of most use in patient care.

There is also a strong argument for not including relational diagnoses in the DSM. The argument is this: Relational factors are process factors, rather than static factors. For example, expressed emotion (EE) is not a characteristic of a family but rather a description of family distress that arises as a result of living with a disease. It is a description of a family process. Providing psychoeducation to a distressed family substantially reduces the level of EE and the subsequent risk of patient relapse. EE is a measure of relational process. If EE is entered into the DSM, there is a danger of its being seen as a static entity.

A delicate balance exists between the utilitarian need for a system of diagnoses and the risk of overdefining people and their relationships as "pathological." It was not that long ago that we pathologized homosexuality and described the entity of the "schizophrenogenic mother."

Dr. Larry Freeman, a member of the Association of Family Psychiatrists, adds: "Be wary of a pressure beyond medical circles to utilize psychiatry as a force for social control. I do a great deal of workers’ [compensation], and so-called ‘preexisting conditions’ are commonly framed as the "cause" of a worker’s emotional response to injury, and therefore, [the worker’s] current psychiatric conditions are not accepted as a consequence of the original injury event.

"Be careful that we do not enable this distortion further in our efforts to include context and history."

How should we include patient contexts such as violence, abuse, trauma, poverty, injustice, or relational dysfunction? How do we acknowledge that these factors play a significant role in the lives of our patients? For children, this is especially important as treatment often focuses on changing or stabilizing their environment, and ensuring that there is adequate attachment and nurturance.

How do we ensure that these relationships and contexts are adequately defined so we can monitor the effectiveness (or not) of interventions? AFTA supports the creation of a work group that will focus on developing an alternative to the DSM for the conceptualization of emotional distress. David Elkins, Ph.D., is planning an international summit in 2013 with representatives from all therapist groups to discuss the feasibility of such a system.

Another way forward is to develop a diagnostic system that focuses on health. The Global Assessment of Functioning (GAF), describes with reasonable accuracy a person’s individual level of functioning on a scale of 1 to 100. The Global Assessment of Relational Functioning (GARF) describes the health of a relationship on a scale of 1-100. Using these scales, pathology and health coexist on a continuum, with anchors throughout the scale. These systems are currently crude instruments, but imagine how much better they could become if they were the focus of research, clinical trials, etc.

There will always be the need for individual diagnoses, where the melancholic continues to suffer despite having an excellent social and family context, and there will always be cases where we cannot decide if the patient is ill unto himself or if his illness is informed by the context of his life.

But consider the inverse, the person who is optimistic and functional in spite of the dire context of his life, people who hold beliefs, convictions, and so on that raise them above their life circumstances. (Think of visionaries like Gandhi or Mandela). In the same way, there are relationships that function well, despite the presence of adversity. How do we develop a system that aspires to "health" instead of pathology? The American health care system (or rather its illness care system) needs to morph into true health care with a focus on prevention on both an individual and relational front.

For additional information, see Relational Processes and DSM-V: Neuroscience, Assessment, Prevention, and Treatment (Washington: American Psychiatric Association Publishing, 2006).

Dr. Alison Heru is with the department of psychiatry at the University of Colorado at Denver, Aurora. She has been a member of the Association of Family Psychiatrists since 2002 and currently serves as the organization’s treasurer. In addition, she is the coauthor of two books on working with families and is the author of numerous articles on this topic.

The American Family Therapy Academy recently issued a policy statement protesting the DSM-5, and asks the American Psychiatric Association to consider the importance of relational and family context to psychiatric diagnoses.

AFTA, a multidisciplinary group, does not support the current revision of the DSM, stating that it "continues a long history of ignoring research and excluding vital contributions of nonpsychiatric mental health disciplines." This statement refers to the substantial body of research concerning the role of relational factors in mental health and mental illness, and also refers to the large number of effective family treatments, including, but not limited to, family therapy.

The academy criticizes the DSM’s use of the biomedical model and its omission of the role of family and sociocultural contexts on well-being. AFTA states that the DSM "delegitimizes the focus on relationship, life stage, community, and access to power and resources." AFTA points out that the DSM fails to take into account culture, class and ‘destructive unjust social factors,’ such as poverty, hunger, homelessness, violence, racism, and other forms of oppression. AFTA considers these factors to be important in reaching a diagnosis that accurately describes patients.

Many psychiatrists, especially family, social, and cultural psychiatrists, agree with AFTA’s position. Several family researchers and family psychiatrists have been pushing for many years to get relational diagnoses included in the DSM-IV and the DSM-5 (J. Fam. Psychol. 2006;20:359-68), citing decades of excellent research into relational diagnoses. Their attempts are supported by nonmedical health care professionals who complain that they cannot get paid by insurance companies for treating families. However, putting any diagnosis in the DSM so the insurance companies get paid is a backward way of thinking. Any diagnostic system of American psychiatry should not be framed or influenced by financial organizations that want to ration health care.

Some psychiatrists who contributed to the DSM offer the disclaimer that "they do not mean this to be a bible." However, the DSM is frequently used "as a bible," for example, in the courts. More importantly, reductionist diagnostic descriptions in the DSM narrow the public’s and the professionals’ thinking about psychological difficulties, and, by extrapolation, limit the conceptualization of what types of interventions might be helpful.

For example, describing psychiatric illnesses as biological leads to the assumption that biological interventions are needed. If an illness is defined using a biopsychosocial explanation, however, this broader understanding leads to a wider array of possible treatments. A psychiatric diagnostic system should recognize all the factors that are known to contribute to psychological health and illness to be of most use in patient care.

There is also a strong argument for not including relational diagnoses in the DSM. The argument is this: Relational factors are process factors, rather than static factors. For example, expressed emotion (EE) is not a characteristic of a family but rather a description of family distress that arises as a result of living with a disease. It is a description of a family process. Providing psychoeducation to a distressed family substantially reduces the level of EE and the subsequent risk of patient relapse. EE is a measure of relational process. If EE is entered into the DSM, there is a danger of its being seen as a static entity.

A delicate balance exists between the utilitarian need for a system of diagnoses and the risk of overdefining people and their relationships as "pathological." It was not that long ago that we pathologized homosexuality and described the entity of the "schizophrenogenic mother."

Dr. Larry Freeman, a member of the Association of Family Psychiatrists, adds: "Be wary of a pressure beyond medical circles to utilize psychiatry as a force for social control. I do a great deal of workers’ [compensation], and so-called ‘preexisting conditions’ are commonly framed as the "cause" of a worker’s emotional response to injury, and therefore, [the worker’s] current psychiatric conditions are not accepted as a consequence of the original injury event.

"Be careful that we do not enable this distortion further in our efforts to include context and history."

How should we include patient contexts such as violence, abuse, trauma, poverty, injustice, or relational dysfunction? How do we acknowledge that these factors play a significant role in the lives of our patients? For children, this is especially important as treatment often focuses on changing or stabilizing their environment, and ensuring that there is adequate attachment and nurturance.

How do we ensure that these relationships and contexts are adequately defined so we can monitor the effectiveness (or not) of interventions? AFTA supports the creation of a work group that will focus on developing an alternative to the DSM for the conceptualization of emotional distress. David Elkins, Ph.D., is planning an international summit in 2013 with representatives from all therapist groups to discuss the feasibility of such a system.

Another way forward is to develop a diagnostic system that focuses on health. The Global Assessment of Functioning (GAF), describes with reasonable accuracy a person’s individual level of functioning on a scale of 1 to 100. The Global Assessment of Relational Functioning (GARF) describes the health of a relationship on a scale of 1-100. Using these scales, pathology and health coexist on a continuum, with anchors throughout the scale. These systems are currently crude instruments, but imagine how much better they could become if they were the focus of research, clinical trials, etc.

There will always be the need for individual diagnoses, where the melancholic continues to suffer despite having an excellent social and family context, and there will always be cases where we cannot decide if the patient is ill unto himself or if his illness is informed by the context of his life.

But consider the inverse, the person who is optimistic and functional in spite of the dire context of his life, people who hold beliefs, convictions, and so on that raise them above their life circumstances. (Think of visionaries like Gandhi or Mandela). In the same way, there are relationships that function well, despite the presence of adversity. How do we develop a system that aspires to "health" instead of pathology? The American health care system (or rather its illness care system) needs to morph into true health care with a focus on prevention on both an individual and relational front.

For additional information, see Relational Processes and DSM-V: Neuroscience, Assessment, Prevention, and Treatment (Washington: American Psychiatric Association Publishing, 2006).

Dr. Alison Heru is with the department of psychiatry at the University of Colorado at Denver, Aurora. She has been a member of the Association of Family Psychiatrists since 2002 and currently serves as the organization’s treasurer. In addition, she is the coauthor of two books on working with families and is the author of numerous articles on this topic.