The Journal of Family Practice

The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.¹ Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.² Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.³ And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.⁴

I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.

Zvi Weizman, MD
Beer-Sheva, Israel

The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.¹ Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.² Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.³ And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.⁴

I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.

Zvi Weizman, MD
Beer-Sheva, Israel

The average American consumes about 3400 mg/d of sodium, which is more than double the 1500 mg recommended by the American Heart Association.¹ Excess sodium added to foods during commercial processing and preparation represents the main source of sodium intake in American diets.² Nevertheless, adding salt at the table is still very common, and people who add salt at the table have 1.5 g higher salt intakes than those who do not add salt.³ And as we know, high sodium intake has been associated with elevated blood pressure and an increased rate of cardiovascular disease.⁴

I have designed a self-produced “Salt Awareness—Limit Today” (SALT) label (FIGURE). This label is attached to the cap of a salt shaker in such a way that less salt flows through the openings of the cap. Moreover, the label serves as a reminder to limit salt intake in general. The feedback I have received from my patients has been extremely positive; they report increased awareness and decreased sodium intake. I mention it here so that others may benefit.

Zvi Weizman, MD
Beer-Sheva, Israel

In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).

It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.¹ This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”

POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.² The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.

I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.

Todd Fredricks, DO
Athens, Ohio

In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).

It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.¹ This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”

POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.² The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.

I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.

Todd Fredricks, DO
Athens, Ohio

In his August editorial, Dr. Hickner noted that an article in the issue prompted him to “wonder whether ultrasound might become the stethoscope of the future” (J Fam Pract. 2016;65:516). To that I say that we need to avoid conflating the stethoscope with point-of-care ultrasound (POCUS).

It is well documented that auscultation skills rapidly deteriorate (specifically in the cardiology realm) in clinical practice.¹ This may occur because many physicians already think ultrasound can replace actually listening to their patients’ hearts. The motto has become, “I’ll just order an echo.”

POCUS is an imaging modality. Period. It can be used to auscultate, but Doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.² The stethoscope remains an outstanding, inexpensive, and convenient screening tool and its use needs to be emphasized.

I strongly believe in training all medical students in POCUS—but as a complementary and adjunctive tool—not as something to replace a perfectly functional piece of equipment used around the world to provide good care.

Todd Fredricks, DO
Athens, Ohio

The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.

Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.¹

The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.² We consider it important to discuss challenges and limitations with each patient.

For example, a more lenient A1C goal may be appropriate when:

• the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
• new medications with undesirable metabolic effects are prescribed or titrated
• social support is poor
• patients have limited confidence in their ability to accomplish tasks and goals
• patients have cognitive limitations
• patients abuse substances.

We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.

There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.

Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio

The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.

Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.¹

The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.² We consider it important to discuss challenges and limitations with each patient.

For example, a more lenient A1C goal may be appropriate when:

• the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
• new medications with undesirable metabolic effects are prescribed or titrated
• social support is poor
• patients have limited confidence in their ability to accomplish tasks and goals
• patients have cognitive limitations
• patients abuse substances.

We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.

There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.

Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio

The article, “Diabetes update: Your guide to the latest ADA standards,” by Shubrook, et al (J Fam Pract. 2016;65:310-318) is a precise review of current recommendations for diabetes. We would like to draw attention, however, to comorbid diabetes and mental illness.

Diabetes and serious mental illness often coincide, making the treatment of both conditions difficult and leading to higher rates of complications.¹

The American Diabetes Association (ADA)’s “Standards of Medical Care in Diabetes” recognizes that hemoglobin A1C targets for patients should be individualized.² We consider it important to discuss challenges and limitations with each patient.

For example, a more lenient A1C goal may be appropriate when:

• the assessment of the patient shows that he or she is struggling with active symptoms of mental illness
• new medications with undesirable metabolic effects are prescribed or titrated
• social support is poor
• patients have limited confidence in their ability to accomplish tasks and goals
• patients have cognitive limitations
• patients abuse substances.

We suggest that when factors are favorable (eg, younger patient, well-controlled serious mental illness, adequate support, good cognitive skills, no hazardous use of substances, good level of confidence in the ability to control diabetes), the A1C target can be set lower. When the factors are less favorable (eg, older patient, poorly controlled mental illness, abusing substances, cognitive impairment), the target should be set higher and incrementally reduced as care engagement, circumstances, and symptom control improve.

There is a need for further research to investigate the factors that can impact diabetes self-management in patients with comorbid mental illness.

Corinna Falck-Ytter, MD
Stephanie W. Kanuch, MEd
Richard McCormick, PhD
Michael Purdum, PhD
Neal V. Dawson, MD
Shari D. Bolen, MD, MPH
Martha Sajatovic, MD
Cleveland, Ohio

An 88-year-old woman presented to our primary care clinic with recurrent right upper quadrant abdominal pain. Her history was negative for nausea, fever, vomiting, chest pain, heartburn, back pain, or changes in bowel movement patterns. There was no association between the pain and her eating patterns. She described the pain as dull, and rated it as a 4 to 5 out of 10. A physical examination was unremarkable except for a minimally tender mass in the right upper quadrant that was detected during palpation of the abdomen. A Murphy’s test was negative. A comprehensive metabolic panel, complete blood count, lipase test, amylase test, abdominal ultrasound, and abdominal x-ray (FIGURE) were ordered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

Diagnosis: Porcelain gallbladder

We diagnosed this patient with porcelain gallbladder based on her history, physical exam, and x-ray, which revealed a well-defined air gas bubble encased in a calcified pouch. (The patient’s lab work was unremarkable and the ultrasound revealed the same findings as seen on the x-ray.)

Porcelain gallbladder is a rare condition.¹ It is characterized by intramural calcifications of the gallbladder wall, which is rarely seen with chronic cholecystitis.²

One theory suggests that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.

There are a few theories behind the etiology of porcelain gallbladder. One theory is that gallstones can irritate the gallbladder wall, leading to inflammation and then calcification. Others believe that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.³

Patients may present with biliary pain or a firm palpable mass in the right upper quadrant. However, patients are often asymptomatic.⁴

Cancer risk. There is about a 2% to 3% risk of gallbladder cancer in patients with porcelain gallbladder.⁵ The nature of the calcification has been linked to the probability that a patient will develop gallbladder cancer. Specifically, there is a higher probability of gallbladder cancer if discontinuous calcification is noted, or if only some portion of the gallbladder wall has calcified.⁶ About 80% of all gallbladder cancers are adenocarcinomas.⁶

Differential diagnosis includes GERD, cholecystitis

Right upper quadrant pain is associated with acute hepatitis, acute cholecystitis, acute pancreatitis, gastroesophageal reflex disease (GERD), ulcers, and umbilical hernias. In this patient’s case, her history and physical examination made a number of diagnoses less likely, including acute cholecystitis, GERD, ulcers, and an umbilical hernia. In addition, normal values on the patient’s lipase and amylase tests ruled out pancreatitis.

Imaging brought things into focus. The most significant finding in this case was the abdominal x-ray, which showed a well-defined air gas bubble encased in a calcified pouch.

In addition to an x-ray or an ultrasound, a computed tomography scan can confirm the diagnosis of porcelain gallbladder.

For most patients, cholecystectomy is recommended

Treatment and management is based on the pattern of calcification and the patient’s current health status. If there is incomplete calcification, cholecystectomy is warranted. Cholecystectomy may also be warranted when a patient is symptomatic and has complete calcification of the gallbladder. Regardless of the pattern of calcification, imaging surveillance of the patient is necessary. Moreover, cholecystectomy is preferred regardless of the status of the calcification if the patient is a good surgical candidate.⁷

It is important to send the gallbladder for histopathological examination after it is removed to determine the likelihood of malignancy.⁷ If cancer is ruled out, then no further work-up is necessary. If cancer is detected, then further evaluation, including additional surgery, may be necessary.

Our patient was a good surgical candidate, so we recommended cholecystectomy. The patient underwent surgery and the pathology report was negative for cancer.

CORRESPONDENCE
Pradeepa Vimalachandran, MD, MPH, 601 North 30th Street, Suite 6720, Omaha, NE 68131; [email protected].

An 88-year-old woman presented to our primary care clinic with recurrent right upper quadrant abdominal pain. Her history was negative for nausea, fever, vomiting, chest pain, heartburn, back pain, or changes in bowel movement patterns. There was no association between the pain and her eating patterns. She described the pain as dull, and rated it as a 4 to 5 out of 10. A physical examination was unremarkable except for a minimally tender mass in the right upper quadrant that was detected during palpation of the abdomen. A Murphy’s test was negative. A comprehensive metabolic panel, complete blood count, lipase test, amylase test, abdominal ultrasound, and abdominal x-ray (FIGURE) were ordered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

Diagnosis: Porcelain gallbladder

We diagnosed this patient with porcelain gallbladder based on her history, physical exam, and x-ray, which revealed a well-defined air gas bubble encased in a calcified pouch. (The patient’s lab work was unremarkable and the ultrasound revealed the same findings as seen on the x-ray.)

Porcelain gallbladder is a rare condition.¹ It is characterized by intramural calcifications of the gallbladder wall, which is rarely seen with chronic cholecystitis.²

One theory suggests that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.

There are a few theories behind the etiology of porcelain gallbladder. One theory is that gallstones can irritate the gallbladder wall, leading to inflammation and then calcification. Others believe that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.³

Patients may present with biliary pain or a firm palpable mass in the right upper quadrant. However, patients are often asymptomatic.⁴

Cancer risk. There is about a 2% to 3% risk of gallbladder cancer in patients with porcelain gallbladder.⁵ The nature of the calcification has been linked to the probability that a patient will develop gallbladder cancer. Specifically, there is a higher probability of gallbladder cancer if discontinuous calcification is noted, or if only some portion of the gallbladder wall has calcified.⁶ About 80% of all gallbladder cancers are adenocarcinomas.⁶

Differential diagnosis includes GERD, cholecystitis

Right upper quadrant pain is associated with acute hepatitis, acute cholecystitis, acute pancreatitis, gastroesophageal reflex disease (GERD), ulcers, and umbilical hernias. In this patient’s case, her history and physical examination made a number of diagnoses less likely, including acute cholecystitis, GERD, ulcers, and an umbilical hernia. In addition, normal values on the patient’s lipase and amylase tests ruled out pancreatitis.

Imaging brought things into focus. The most significant finding in this case was the abdominal x-ray, which showed a well-defined air gas bubble encased in a calcified pouch.

In addition to an x-ray or an ultrasound, a computed tomography scan can confirm the diagnosis of porcelain gallbladder.

For most patients, cholecystectomy is recommended

Treatment and management is based on the pattern of calcification and the patient’s current health status. If there is incomplete calcification, cholecystectomy is warranted. Cholecystectomy may also be warranted when a patient is symptomatic and has complete calcification of the gallbladder. Regardless of the pattern of calcification, imaging surveillance of the patient is necessary. Moreover, cholecystectomy is preferred regardless of the status of the calcification if the patient is a good surgical candidate.⁷

It is important to send the gallbladder for histopathological examination after it is removed to determine the likelihood of malignancy.⁷ If cancer is ruled out, then no further work-up is necessary. If cancer is detected, then further evaluation, including additional surgery, may be necessary.

Our patient was a good surgical candidate, so we recommended cholecystectomy. The patient underwent surgery and the pathology report was negative for cancer.

CORRESPONDENCE
Pradeepa Vimalachandran, MD, MPH, 601 North 30th Street, Suite 6720, Omaha, NE 68131; [email protected].

An 88-year-old woman presented to our primary care clinic with recurrent right upper quadrant abdominal pain. Her history was negative for nausea, fever, vomiting, chest pain, heartburn, back pain, or changes in bowel movement patterns. There was no association between the pain and her eating patterns. She described the pain as dull, and rated it as a 4 to 5 out of 10. A physical examination was unremarkable except for a minimally tender mass in the right upper quadrant that was detected during palpation of the abdomen. A Murphy’s test was negative. A comprehensive metabolic panel, complete blood count, lipase test, amylase test, abdominal ultrasound, and abdominal x-ray (FIGURE) were ordered.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

Diagnosis: Porcelain gallbladder

We diagnosed this patient with porcelain gallbladder based on her history, physical exam, and x-ray, which revealed a well-defined air gas bubble encased in a calcified pouch. (The patient’s lab work was unremarkable and the ultrasound revealed the same findings as seen on the x-ray.)

Porcelain gallbladder is a rare condition.¹ It is characterized by intramural calcifications of the gallbladder wall, which is rarely seen with chronic cholecystitis.²

One theory suggests that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.

There are a few theories behind the etiology of porcelain gallbladder. One theory is that gallstones can irritate the gallbladder wall, leading to inflammation and then calcification. Others believe that porcelain gallbladder is due to the obstruction of cystic ducts, which leads to bile stasis in the gallbladder, followed by the accumulation of calcium carbonate salts.³

Patients may present with biliary pain or a firm palpable mass in the right upper quadrant. However, patients are often asymptomatic.⁴

Cancer risk. There is about a 2% to 3% risk of gallbladder cancer in patients with porcelain gallbladder.⁵ The nature of the calcification has been linked to the probability that a patient will develop gallbladder cancer. Specifically, there is a higher probability of gallbladder cancer if discontinuous calcification is noted, or if only some portion of the gallbladder wall has calcified.⁶ About 80% of all gallbladder cancers are adenocarcinomas.⁶

Differential diagnosis includes GERD, cholecystitis

Right upper quadrant pain is associated with acute hepatitis, acute cholecystitis, acute pancreatitis, gastroesophageal reflex disease (GERD), ulcers, and umbilical hernias. In this patient’s case, her history and physical examination made a number of diagnoses less likely, including acute cholecystitis, GERD, ulcers, and an umbilical hernia. In addition, normal values on the patient’s lipase and amylase tests ruled out pancreatitis.

Imaging brought things into focus. The most significant finding in this case was the abdominal x-ray, which showed a well-defined air gas bubble encased in a calcified pouch.

In addition to an x-ray or an ultrasound, a computed tomography scan can confirm the diagnosis of porcelain gallbladder.

For most patients, cholecystectomy is recommended

Treatment and management is based on the pattern of calcification and the patient’s current health status. If there is incomplete calcification, cholecystectomy is warranted. Cholecystectomy may also be warranted when a patient is symptomatic and has complete calcification of the gallbladder. Regardless of the pattern of calcification, imaging surveillance of the patient is necessary. Moreover, cholecystectomy is preferred regardless of the status of the calcification if the patient is a good surgical candidate.⁷

It is important to send the gallbladder for histopathological examination after it is removed to determine the likelihood of malignancy.⁷ If cancer is ruled out, then no further work-up is necessary. If cancer is detected, then further evaluation, including additional surgery, may be necessary.

Our patient was a good surgical candidate, so we recommended cholecystectomy. The patient underwent surgery and the pathology report was negative for cancer.

CORRESPONDENCE
Pradeepa Vimalachandran, MD, MPH, 601 North 30th Street, Suite 6720, Omaha, NE 68131; [email protected].

Evidence summary

A cross-sectional study found no correlation between knuckle popping and osteoarthritis (OA) of the hand.¹ Investigators recruited 300 consecutive patients (ages 45 years and older, mean age 63 years) and evaluated them for a history of habitual knuckle popping (74 of 300 patients, mean duration 35 years) and hand arthritis or dysfunction. Investigators excluded patients with neuromuscular, inflammatory, or malignant diseases.

Investigators found OA equally in both patients who did and didn’t pop their knuckles (12 of 74 vs 36 of 226, respectively; P nonsignificant); joint swelling was more common in participants with a history of knuckle popping (84% vs 6%; P<.01). Investigators didn’t describe how OA was diagnosed or specify which joints were affected.

Another cross-sectional study also found no correlation between habitual knuckle popping of the metacarpal phalangeal joint and the prevalence of OA in that joint.² Investigators recruited 28 patients (mean age 78.5 years; 23 women and 5 men) from a Jewish home for the aged and asked them whether they had habitually cracked their knuckles during their lifetime. They then performed clinical and radiographic hand examinations (excluding patients with a history of ­traumatic injury, rheumatoid arthritis, gout, chondrocalcinosis, and hemochromatosis).

Knuckle popping didn’t correlate with OA of the metacarpal phalanges (1 of 15 knuckle popping patients vs 5 of 13 patients who didn’t pop their knuckles; P=.06). All 6 patients with radiographic evidence of OA showed involvement at the metacarpal phalangeal and distal interphalangeal joints, whether or not they popped their knuckles.

A case control study found no correlation between OA in the hands and habitual knuckle popping.³ Investigators recruited 215 patients 50 to 89 years old who had received a radiograph of their right hand during the previous 5 years and divided them into cases with OA (135 patients), and controls without OA (80 patients). Patients completed questionnaires assessing the prevalence (20%), frequency (1 to 20 times per day), and duration (26 to 36 years) of knuckle popping.

Patients most commonly popped proximal interphalangeal joints (15.9%) followed by metacarpal phalangeal joints (13.5%), distal interphalangeal joints (6.1%), and first carpal metacarpal joints (2.3%). OA most often affected the distal interphalangeal joint (68.4%), followed by the first carpal metacarpal (57.1%), proximal interphalangeal (54.1%), and metacarpal phalangeal joints (28.6%). Investigators found no difference in the prevalence of knuckle popping between cases and controls (18% in cases vs 23.2% in controls; P=.361).

When investigators evaluated total knuckle popping exposure in “crack years” (number of times per day multiplied by years) in the distal interphalangeal or metacarpal phalangeal joints, they found no significant association between crack years and OA (distal interphalangeal joint, mean 108 crack years; metacarpal phalangeal joint, mean 75 crack years).

50 years of knuckle popping without ill effects

An n-of-1 case control study found similar results.⁴ The researcher, a physician, popped only the knuckles of his left hand, twice a day, for 50 years. He compared his hands at the end of the trial and found no arthritis in either hand and no visible differences.

But knuckle popping does have a downside

A paper described 2 case reports of acute injuries sustained during attempted knuckle popping—a partial tear of the ulnar collateral ligament of the thumb and subluxation of the extensor tendon of the fifth digit.⁵ Both injuries were associated with forceful manipulation of the digits, and both resolved with conservative management within 4 weeks.

Evidence summary

A cross-sectional study found no correlation between knuckle popping and osteoarthritis (OA) of the hand.¹ Investigators recruited 300 consecutive patients (ages 45 years and older, mean age 63 years) and evaluated them for a history of habitual knuckle popping (74 of 300 patients, mean duration 35 years) and hand arthritis or dysfunction. Investigators excluded patients with neuromuscular, inflammatory, or malignant diseases.

Investigators found OA equally in both patients who did and didn’t pop their knuckles (12 of 74 vs 36 of 226, respectively; P nonsignificant); joint swelling was more common in participants with a history of knuckle popping (84% vs 6%; P<.01). Investigators didn’t describe how OA was diagnosed or specify which joints were affected.

Another cross-sectional study also found no correlation between habitual knuckle popping of the metacarpal phalangeal joint and the prevalence of OA in that joint.² Investigators recruited 28 patients (mean age 78.5 years; 23 women and 5 men) from a Jewish home for the aged and asked them whether they had habitually cracked their knuckles during their lifetime. They then performed clinical and radiographic hand examinations (excluding patients with a history of ­traumatic injury, rheumatoid arthritis, gout, chondrocalcinosis, and hemochromatosis).

Knuckle popping didn’t correlate with OA of the metacarpal phalanges (1 of 15 knuckle popping patients vs 5 of 13 patients who didn’t pop their knuckles; P=.06). All 6 patients with radiographic evidence of OA showed involvement at the metacarpal phalangeal and distal interphalangeal joints, whether or not they popped their knuckles.

A case control study found no correlation between OA in the hands and habitual knuckle popping.³ Investigators recruited 215 patients 50 to 89 years old who had received a radiograph of their right hand during the previous 5 years and divided them into cases with OA (135 patients), and controls without OA (80 patients). Patients completed questionnaires assessing the prevalence (20%), frequency (1 to 20 times per day), and duration (26 to 36 years) of knuckle popping.

Patients most commonly popped proximal interphalangeal joints (15.9%) followed by metacarpal phalangeal joints (13.5%), distal interphalangeal joints (6.1%), and first carpal metacarpal joints (2.3%). OA most often affected the distal interphalangeal joint (68.4%), followed by the first carpal metacarpal (57.1%), proximal interphalangeal (54.1%), and metacarpal phalangeal joints (28.6%). Investigators found no difference in the prevalence of knuckle popping between cases and controls (18% in cases vs 23.2% in controls; P=.361).

When investigators evaluated total knuckle popping exposure in “crack years” (number of times per day multiplied by years) in the distal interphalangeal or metacarpal phalangeal joints, they found no significant association between crack years and OA (distal interphalangeal joint, mean 108 crack years; metacarpal phalangeal joint, mean 75 crack years).

50 years of knuckle popping without ill effects

An n-of-1 case control study found similar results.⁴ The researcher, a physician, popped only the knuckles of his left hand, twice a day, for 50 years. He compared his hands at the end of the trial and found no arthritis in either hand and no visible differences.

But knuckle popping does have a downside

A paper described 2 case reports of acute injuries sustained during attempted knuckle popping—a partial tear of the ulnar collateral ligament of the thumb and subluxation of the extensor tendon of the fifth digit.⁵ Both injuries were associated with forceful manipulation of the digits, and both resolved with conservative management within 4 weeks.

Evidence summary

A cross-sectional study found no correlation between knuckle popping and osteoarthritis (OA) of the hand.¹ Investigators recruited 300 consecutive patients (ages 45 years and older, mean age 63 years) and evaluated them for a history of habitual knuckle popping (74 of 300 patients, mean duration 35 years) and hand arthritis or dysfunction. Investigators excluded patients with neuromuscular, inflammatory, or malignant diseases.

Investigators found OA equally in both patients who did and didn’t pop their knuckles (12 of 74 vs 36 of 226, respectively; P nonsignificant); joint swelling was more common in participants with a history of knuckle popping (84% vs 6%; P<.01). Investigators didn’t describe how OA was diagnosed or specify which joints were affected.

Another cross-sectional study also found no correlation between habitual knuckle popping of the metacarpal phalangeal joint and the prevalence of OA in that joint.² Investigators recruited 28 patients (mean age 78.5 years; 23 women and 5 men) from a Jewish home for the aged and asked them whether they had habitually cracked their knuckles during their lifetime. They then performed clinical and radiographic hand examinations (excluding patients with a history of ­traumatic injury, rheumatoid arthritis, gout, chondrocalcinosis, and hemochromatosis).

Knuckle popping didn’t correlate with OA of the metacarpal phalanges (1 of 15 knuckle popping patients vs 5 of 13 patients who didn’t pop their knuckles; P=.06). All 6 patients with radiographic evidence of OA showed involvement at the metacarpal phalangeal and distal interphalangeal joints, whether or not they popped their knuckles.

A case control study found no correlation between OA in the hands and habitual knuckle popping.³ Investigators recruited 215 patients 50 to 89 years old who had received a radiograph of their right hand during the previous 5 years and divided them into cases with OA (135 patients), and controls without OA (80 patients). Patients completed questionnaires assessing the prevalence (20%), frequency (1 to 20 times per day), and duration (26 to 36 years) of knuckle popping.

Patients most commonly popped proximal interphalangeal joints (15.9%) followed by metacarpal phalangeal joints (13.5%), distal interphalangeal joints (6.1%), and first carpal metacarpal joints (2.3%). OA most often affected the distal interphalangeal joint (68.4%), followed by the first carpal metacarpal (57.1%), proximal interphalangeal (54.1%), and metacarpal phalangeal joints (28.6%). Investigators found no difference in the prevalence of knuckle popping between cases and controls (18% in cases vs 23.2% in controls; P=.361).

When investigators evaluated total knuckle popping exposure in “crack years” (number of times per day multiplied by years) in the distal interphalangeal or metacarpal phalangeal joints, they found no significant association between crack years and OA (distal interphalangeal joint, mean 108 crack years; metacarpal phalangeal joint, mean 75 crack years).

50 years of knuckle popping without ill effects

An n-of-1 case control study found similar results.⁴ The researcher, a physician, popped only the knuckles of his left hand, twice a day, for 50 years. He compared his hands at the end of the trial and found no arthritis in either hand and no visible differences.

But knuckle popping does have a downside

A paper described 2 case reports of acute injuries sustained during attempted knuckle popping—a partial tear of the ulnar collateral ligament of the thumb and subluxation of the extensor tendon of the fifth digit.⁵ Both injuries were associated with forceful manipulation of the digits, and both resolved with conservative management within 4 weeks.

THE CASE

A 49-year-old woman visited our family medicine clinic because she’d had 3 episodes of epistaxis during the previous month. She’d already visited the emergency department, and the doctor there had treated her symptomatically and referred her to our clinic.

On physical examination, we noted a whitish mass in the patient’s right nostril that was attached to the nasal septum. The patient’s vital signs were within normal limits. She had a history of hypertension, depression, anxiety, gastroesophageal reflux disease, and post-traumatic stress disorder. Her medications included amlodipine-benazepril, atenolol-chlorthalidone, citalopram, clonazepam, prazosin, and omeprazole. The patient lived alone and denied using tobacco or illicit drugs, but she drank one to 2 glasses of brandy every day. She denied any past medical or family history of similar complaints, autoimmune disorders, or skin rashes.

A complete blood count, international normalized ratio, sedimentation rate, anti-nuclear antibody test, and an anti-neutrophil cytoplasmic antibody panel were normal.

THE DIAGNOSIS

We referred the patient to an ear, nose, and throat doctor for a nasal endoscopy and a biopsy, which showed granulation tissue. A maxillofacial computed tomography (CT) scan revealed a 1.44 cm x 0.8 cm polypoid soft tissue mass in the right nasal cavity adherent to the nasal septum with no posterior extension (FIGURE 1).

Pyogenic granuloma (PG) is a benign vascular tumor of the skin and mucous membranes that is not associated with an infection. Rather, it is a hyperplastic, neovascular, inflammatory response to an angiogenic stimulus. Several enhancers and inhibitors of angiogenesis have been shown to play a role in PG, including hormones, medications, and local injury. In fact, a local injury or hormonal factor is identified as a stimulus in more than half of PG patients.¹

The hormone connection. Estrogen promotes production of nerve growth factor, granulocyte-macrophage colony-stimulating factor, basic fibroblast growth factor, vascular endothelial growth factor, and transforming growth factor beta 1. Progesterone enhances inflammatory mediators as well. Although there are no direct receptors for estrogen and progesterone in the oral and nasal mucosa, some of these pro-inflammatory effects create an environment conducive to the development of PG. This is supported by several studies documenting an increased incidence of PGs with oral contraceptive use and regression of PGs after childbirth.^2-4

In more than half of patients with pyogenic granuloma, a local injury or hormonal factor is at work.

Medication may play a role. Drug-induced PG has also been described in several studies.^5,6 Offending medications include systemic and topical retinoids, capecitabine, etoposide, 5-fluorouracil, cyclosporine, docetaxel, and human immunodeficiency virus protease inhibitors.

Local injury may also be a culprit. Nasal PGs are commonly attached to the anterior septum and typically result from nasal packing, habitual picking, or nose boring.⁷ In this particular case, however, we were unable to identify the irritant.

The classic presentation

PG classically presents as a painless mass that spontaneously develops over days to weeks. The mass can be sessile or pedunculated, and is frequently hemorrhagic. Intranasal PG usually presents with epiphora.⁷ While the prevalence of intraoral PG was found to be one in 25,000 individuals³, data for nasal lesions is scarce. Most cases of PG are seen in the second and third decades of life.^1,3 In children, PG is slightly more predominant in males.^1,3 Mucosal lesions, however, have a higher incidence in females.^1,3 Granuloma gravidarum, the term used to describe mucosal PG in pregnant females, was found in 0.2% to 5% of pregnancies.^2,3,8

Differential Dx includes warts, squamous cell carcinoma

The differential diagnosis of PG includes Spitz nevus, glomus tumors, common warts, amelanotic melanoma, squamous cell carcinoma, basal cell carcinoma, Kaposi’s sarcoma, bacillary angiomatosis, infantile hemangioma, and angiolymphoid hyperplasia, among others.^3,5 Foreign bodies, nasal polyps, angiofibroma, meningocele, Wegener’s granulomatosis, and sarcoidosis should also be considered.

Radiologic evaluation may be beneficial—especially with nasal lesions—when looking for findings suggestive of malignancy. Both CT and magnetic resonance imaging with contrast identify PG as a soft tissue mass with lobulated contours,^9,10 but histopathologic analysis is required to confirm the diagnosis. The histopathologic appearance of PG is characterized by a polypoid lesion with circumscribed anastomosing networks of capillaries arranged in one or more lobules at the base in an edematous and fibroblastic stroma.

Alternatives to surgery include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents, but the recurrence rate with these is often higher.

Treatment is determined by the location and size of the lesion

The most suitable treatment is determined by considering the location of the lesion, the characteristics of the lesion (morphology/size), its amenability to surgery, risk of scar formation, and the presence or absence of a causative irritant. Excision is often preferred because it yields a specimen for pathologic analysis. Alternative treatments include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents,^3,6,7 but the recurrence rate is higher (up to 15%) with some of these modalities, when compared with excision (3.6%).³

Our patient underwent excision of the mass and was seen for an annual follow-up appointment. All of her symptoms resolved and no recurrence was noted.

THE TAKEAWAY

Although PG is a common and benign condition, it is rarely seen in the nasal cavity without an obvious history of a possible irritant. PG should be considered as a diagnosis for rapidly growing cutaneous or mucosal hemorrhagic lesions. Appropriate tissue pathology is essential to rule out malignancy and other serious conditions, such as bacillary angiomatosis and Wegener’s granulomatosis.

Treatment is usually required to avoid the frequent complications of ulceration and bleeding. Surgical treatments are preferred. The location of the lesion largely determines whether referral to a specialist is necessary.

THE CASE

A 49-year-old woman visited our family medicine clinic because she’d had 3 episodes of epistaxis during the previous month. She’d already visited the emergency department, and the doctor there had treated her symptomatically and referred her to our clinic.

On physical examination, we noted a whitish mass in the patient’s right nostril that was attached to the nasal septum. The patient’s vital signs were within normal limits. She had a history of hypertension, depression, anxiety, gastroesophageal reflux disease, and post-traumatic stress disorder. Her medications included amlodipine-benazepril, atenolol-chlorthalidone, citalopram, clonazepam, prazosin, and omeprazole. The patient lived alone and denied using tobacco or illicit drugs, but she drank one to 2 glasses of brandy every day. She denied any past medical or family history of similar complaints, autoimmune disorders, or skin rashes.

A complete blood count, international normalized ratio, sedimentation rate, anti-nuclear antibody test, and an anti-neutrophil cytoplasmic antibody panel were normal.

THE DIAGNOSIS

We referred the patient to an ear, nose, and throat doctor for a nasal endoscopy and a biopsy, which showed granulation tissue. A maxillofacial computed tomography (CT) scan revealed a 1.44 cm x 0.8 cm polypoid soft tissue mass in the right nasal cavity adherent to the nasal septum with no posterior extension (FIGURE 1).

Pyogenic granuloma (PG) is a benign vascular tumor of the skin and mucous membranes that is not associated with an infection. Rather, it is a hyperplastic, neovascular, inflammatory response to an angiogenic stimulus. Several enhancers and inhibitors of angiogenesis have been shown to play a role in PG, including hormones, medications, and local injury. In fact, a local injury or hormonal factor is identified as a stimulus in more than half of PG patients.¹

The hormone connection. Estrogen promotes production of nerve growth factor, granulocyte-macrophage colony-stimulating factor, basic fibroblast growth factor, vascular endothelial growth factor, and transforming growth factor beta 1. Progesterone enhances inflammatory mediators as well. Although there are no direct receptors for estrogen and progesterone in the oral and nasal mucosa, some of these pro-inflammatory effects create an environment conducive to the development of PG. This is supported by several studies documenting an increased incidence of PGs with oral contraceptive use and regression of PGs after childbirth.^2-4

In more than half of patients with pyogenic granuloma, a local injury or hormonal factor is at work.

Medication may play a role. Drug-induced PG has also been described in several studies.^5,6 Offending medications include systemic and topical retinoids, capecitabine, etoposide, 5-fluorouracil, cyclosporine, docetaxel, and human immunodeficiency virus protease inhibitors.

Local injury may also be a culprit. Nasal PGs are commonly attached to the anterior septum and typically result from nasal packing, habitual picking, or nose boring.⁷ In this particular case, however, we were unable to identify the irritant.

The classic presentation

PG classically presents as a painless mass that spontaneously develops over days to weeks. The mass can be sessile or pedunculated, and is frequently hemorrhagic. Intranasal PG usually presents with epiphora.⁷ While the prevalence of intraoral PG was found to be one in 25,000 individuals³, data for nasal lesions is scarce. Most cases of PG are seen in the second and third decades of life.^1,3 In children, PG is slightly more predominant in males.^1,3 Mucosal lesions, however, have a higher incidence in females.^1,3 Granuloma gravidarum, the term used to describe mucosal PG in pregnant females, was found in 0.2% to 5% of pregnancies.^2,3,8

Differential Dx includes warts, squamous cell carcinoma

The differential diagnosis of PG includes Spitz nevus, glomus tumors, common warts, amelanotic melanoma, squamous cell carcinoma, basal cell carcinoma, Kaposi’s sarcoma, bacillary angiomatosis, infantile hemangioma, and angiolymphoid hyperplasia, among others.^3,5 Foreign bodies, nasal polyps, angiofibroma, meningocele, Wegener’s granulomatosis, and sarcoidosis should also be considered.

Radiologic evaluation may be beneficial—especially with nasal lesions—when looking for findings suggestive of malignancy. Both CT and magnetic resonance imaging with contrast identify PG as a soft tissue mass with lobulated contours,^9,10 but histopathologic analysis is required to confirm the diagnosis. The histopathologic appearance of PG is characterized by a polypoid lesion with circumscribed anastomosing networks of capillaries arranged in one or more lobules at the base in an edematous and fibroblastic stroma.

Alternatives to surgery include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents, but the recurrence rate with these is often higher.

Treatment is determined by the location and size of the lesion

The most suitable treatment is determined by considering the location of the lesion, the characteristics of the lesion (morphology/size), its amenability to surgery, risk of scar formation, and the presence or absence of a causative irritant. Excision is often preferred because it yields a specimen for pathologic analysis. Alternative treatments include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents,^3,6,7 but the recurrence rate is higher (up to 15%) with some of these modalities, when compared with excision (3.6%).³

Our patient underwent excision of the mass and was seen for an annual follow-up appointment. All of her symptoms resolved and no recurrence was noted.

THE TAKEAWAY

Although PG is a common and benign condition, it is rarely seen in the nasal cavity without an obvious history of a possible irritant. PG should be considered as a diagnosis for rapidly growing cutaneous or mucosal hemorrhagic lesions. Appropriate tissue pathology is essential to rule out malignancy and other serious conditions, such as bacillary angiomatosis and Wegener’s granulomatosis.

Treatment is usually required to avoid the frequent complications of ulceration and bleeding. Surgical treatments are preferred. The location of the lesion largely determines whether referral to a specialist is necessary.

THE CASE

A 49-year-old woman visited our family medicine clinic because she’d had 3 episodes of epistaxis during the previous month. She’d already visited the emergency department, and the doctor there had treated her symptomatically and referred her to our clinic.

On physical examination, we noted a whitish mass in the patient’s right nostril that was attached to the nasal septum. The patient’s vital signs were within normal limits. She had a history of hypertension, depression, anxiety, gastroesophageal reflux disease, and post-traumatic stress disorder. Her medications included amlodipine-benazepril, atenolol-chlorthalidone, citalopram, clonazepam, prazosin, and omeprazole. The patient lived alone and denied using tobacco or illicit drugs, but she drank one to 2 glasses of brandy every day. She denied any past medical or family history of similar complaints, autoimmune disorders, or skin rashes.

A complete blood count, international normalized ratio, sedimentation rate, anti-nuclear antibody test, and an anti-neutrophil cytoplasmic antibody panel were normal.

THE DIAGNOSIS

We referred the patient to an ear, nose, and throat doctor for a nasal endoscopy and a biopsy, which showed granulation tissue. A maxillofacial computed tomography (CT) scan revealed a 1.44 cm x 0.8 cm polypoid soft tissue mass in the right nasal cavity adherent to the nasal septum with no posterior extension (FIGURE 1).

Pyogenic granuloma (PG) is a benign vascular tumor of the skin and mucous membranes that is not associated with an infection. Rather, it is a hyperplastic, neovascular, inflammatory response to an angiogenic stimulus. Several enhancers and inhibitors of angiogenesis have been shown to play a role in PG, including hormones, medications, and local injury. In fact, a local injury or hormonal factor is identified as a stimulus in more than half of PG patients.¹

The hormone connection. Estrogen promotes production of nerve growth factor, granulocyte-macrophage colony-stimulating factor, basic fibroblast growth factor, vascular endothelial growth factor, and transforming growth factor beta 1. Progesterone enhances inflammatory mediators as well. Although there are no direct receptors for estrogen and progesterone in the oral and nasal mucosa, some of these pro-inflammatory effects create an environment conducive to the development of PG. This is supported by several studies documenting an increased incidence of PGs with oral contraceptive use and regression of PGs after childbirth.^2-4

In more than half of patients with pyogenic granuloma, a local injury or hormonal factor is at work.

Medication may play a role. Drug-induced PG has also been described in several studies.^5,6 Offending medications include systemic and topical retinoids, capecitabine, etoposide, 5-fluorouracil, cyclosporine, docetaxel, and human immunodeficiency virus protease inhibitors.

Local injury may also be a culprit. Nasal PGs are commonly attached to the anterior septum and typically result from nasal packing, habitual picking, or nose boring.⁷ In this particular case, however, we were unable to identify the irritant.

The classic presentation

PG classically presents as a painless mass that spontaneously develops over days to weeks. The mass can be sessile or pedunculated, and is frequently hemorrhagic. Intranasal PG usually presents with epiphora.⁷ While the prevalence of intraoral PG was found to be one in 25,000 individuals³, data for nasal lesions is scarce. Most cases of PG are seen in the second and third decades of life.^1,3 In children, PG is slightly more predominant in males.^1,3 Mucosal lesions, however, have a higher incidence in females.^1,3 Granuloma gravidarum, the term used to describe mucosal PG in pregnant females, was found in 0.2% to 5% of pregnancies.^2,3,8

Differential Dx includes warts, squamous cell carcinoma

The differential diagnosis of PG includes Spitz nevus, glomus tumors, common warts, amelanotic melanoma, squamous cell carcinoma, basal cell carcinoma, Kaposi’s sarcoma, bacillary angiomatosis, infantile hemangioma, and angiolymphoid hyperplasia, among others.^3,5 Foreign bodies, nasal polyps, angiofibroma, meningocele, Wegener’s granulomatosis, and sarcoidosis should also be considered.

Radiologic evaluation may be beneficial—especially with nasal lesions—when looking for findings suggestive of malignancy. Both CT and magnetic resonance imaging with contrast identify PG as a soft tissue mass with lobulated contours,^9,10 but histopathologic analysis is required to confirm the diagnosis. The histopathologic appearance of PG is characterized by a polypoid lesion with circumscribed anastomosing networks of capillaries arranged in one or more lobules at the base in an edematous and fibroblastic stroma.

Alternatives to surgery include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents, but the recurrence rate with these is often higher.

Treatment is determined by the location and size of the lesion

The most suitable treatment is determined by considering the location of the lesion, the characteristics of the lesion (morphology/size), its amenability to surgery, risk of scar formation, and the presence or absence of a causative irritant. Excision is often preferred because it yields a specimen for pathologic analysis. Alternative treatments include electrocautery, cryotherapy, laser therapy, and intralesional and topical agents,^3,6,7 but the recurrence rate is higher (up to 15%) with some of these modalities, when compared with excision (3.6%).³

Our patient underwent excision of the mass and was seen for an annual follow-up appointment. All of her symptoms resolved and no recurrence was noted.

THE TAKEAWAY

Although PG is a common and benign condition, it is rarely seen in the nasal cavity without an obvious history of a possible irritant. PG should be considered as a diagnosis for rapidly growing cutaneous or mucosal hemorrhagic lesions. Appropriate tissue pathology is essential to rule out malignancy and other serious conditions, such as bacillary angiomatosis and Wegener’s granulomatosis.

Treatment is usually required to avoid the frequent complications of ulceration and bleeding. Surgical treatments are preferred. The location of the lesion largely determines whether referral to a specialist is necessary.

CASE 1

A 13-month-old boy who was recently adopted from Ethiopia presented to a primary care physician with a 3-week history of bloody diarrhea accompanied by flatulence and bloating. Stool cultures were positive for Campylobacter and Shigella. He was prescribed azithromycin but saw only moderate improvement. He was then referred to the Infectious Diseases Department. Neonatal, pregnancy, and immunization histories were unknown and a review of systems was unremarkable. On exam, the child looked well; he weighed 9.6 kg (15th percentile), was 69.5 cm long (<3rd percentile), and his head circumference was 45 cm (10th percentile). Head and neck, cardiorespiratory, and abdominal examinations were unremarkable.

A complete blood count (CBC) showed an elevated white blood cell (WBC) count of 26 x 10⁹/L (normal: 4-10 x 10⁹/L) with predominant eosinophilia (10.4 x 10⁹/L or 40.1% of WBCs; normal: <0.45 x 10⁹/L or 0%-8%). Hemoglobin and platelets were within normal limits. Stool testing for ova and parasites showed Strongyloides stercoralis larvae. Strongyloides serology was negative and Filaria serology was equivocal.

CASE 2

A 15-year-old boy was assessed for a 3-week history of fever and eosinophilia. He had enlarged cervical lymph nodes, a new rash, and had lost 4 pounds. He denied gastrointestinal symptoms, dyspnea, headaches, or chest pain. His past medical and family histories were unremarkable and he reported no drug use or allergies. He had traveled to Cuba with his family for 15 days 3 months prior to presentation. He recalled diarrhea while traveling, which resolved spontaneously. He and his family had traveled “off the beaten track,” eating foods prepared at local establishments and swimming in local rivers. He received pre-travel immunizations.

On examination, he appeared unwell, though his vital signs were normal. He had diffuse lymphadenopathy and a petechial rash on his chest, back, upper buttocks, legs, and feet. Cardiorespiratory and abdominal examinations were unremarkable. A CBC revealed an elevated WBC count of 76.9 x 10⁹/L with predominant eosinophilia (71.5 x 10⁹/L or 92% of WBCs). Hemoglobin, platelets, electrolytes, and liver function tests were normal. The patient was referred to a tertiary care center and was admitted to the hospital. Stool testing for ova and parasites, as well as serology for parasitic infections, was negative. A bone marrow aspiration and biopsy were performed and revealed the diagnosis of acute lymphoblastic leukemia (ALL).

These 2 cases highlight how the presentation of eosinophilia can vary and how important it is to maintain a broad differential diagnosis (TABLE 1^1-4). Causes of eosinophilia are numerous and can be divided into 3 categories: primary, secondary, and idiopathic.^1,5 Hematologic malignancy, where eosinophilia is clonal, is an example of a primary etiology. Causes of secondary eosinophilia include infectious diseases, drugs (TABLE 2⁵), autoimmune disorders, and allergic conditions. Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage. Dermatologic, pulmonary, gastro­intestinal, and cardiac involvement is most common.²

Eosinophilia associated with parasitic infection

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia, with eosinophilia occurring during tissue migration or penetration.^1,3

Schistosomiasis is a chronic parasitic infection of the human vascular system. It is transmitted by contact with contaminated fresh water, where cercariae penetrate the skin. High prevalence areas include Africa and Southeast Asia. Acute infection can result in Katayama fever—a febrile illness with prominent eosinophilia that occurs 4 to 7 weeks after exposure.⁴ Diagnosis is primarily clinical with appropriate epidemiology, as serology may be negative early in infection. Praziquantel is the treatment of choice, though dosing varies by species, so expert consultation should be considered.

Soil-transmitted helminths, such as Ascaris (Ascaris lumbricoides), whipworm (Trichuris trichiura), and hookworm (Ancyclostoma duodenale and Necator americanus), can also cause eosinophilia during larval tissue migration. Following infection by ingestion or skin penetration, an acute respiratory illness, termed Löffler’s syndrome, can develop with associated eosinophilia.¹ Once the helminths reach the adult stage, eosinophilia subsides. Patients are most commonly treated with albendazole 400 mg orally for 3 days.⁴

Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage.Fascioliasis is common in sheep-rearing areas. Humans are infected through ingestion of aquatic plants (eg, watercress). Parasitic migration through the duodenal wall and liver parenchyma can lead to fever, right upper quadrant pain, and eosinophilia. The incubation period is 6 to 12 weeks. Diagnosis during acute infection is by serology.⁴

Filarial infections, eg lymphatic filariasis, loiasis, and onchocerciasis, can also cause eosinophilia. The rise in eosinophils can be triggered by either the adult worms or circulating microfilariae.⁴ Treatment of fascioliasis and filarial infections varies and expert consultation is recommended.

Eosinophilia associated with primary hematologic malignancy

Eosinophilia is a rare presentation of hematologic malignancy. Acute myeloid leukemia, acute lymphoblastic leukemia (ALL), chronic myeloid leukemia, and myeloproliferative disorders have all been associated with eosinophilia. Hepatosplenomegaly, generalized lymphadenopathy, and cytopenias in other cell lines are often noted. Also, the degree of eosinophilia is often more pronounced (>5 x 10⁹/L). Patients with suspected hematologic malignancy should be urgently referred for expert consultation.⁵

Consider the following approach in the assessment of patients with eosinophilia seen in the ambulatory care setting. Inpatients or patients being seen in developing areas may require a modified approach.

History. All patients with eosinophilia should have a thorough history taken, with particular attention paid to travel history. A travel history should make note of dates, duration and location of travel, and any relevant exposures, such as arthropod bites or swimming in freshwater. Dietary habits, such as ingestion of seafood, game, or undercooked meat can also be helpful in making a diagnosis.^3,4

Causes of secondary eosinophilia include infectious diseases, drugs, autoimmune disorders, and allergic conditions.

Physical exam. In addition to a general physical examination, the following features may be helpful in determining the etiology of eosinophilia. Wheeze is characteristic of parasites in a lung migration phase (eg, strongyloidiasis and ascariasis) or asthma. Hepatomegaly can be seen with liver flukes, visceral larva migrans, or schistosomiasis. Periorbital edema can be observed with Trichinella infection. Loa loa, a type of filarial infection, produces a transient, migratory angioedema, often localized to the wrists and large joints (termed Calabar swelling). Dermatitis of varying intensity may suggest filarial infection, schistosomiasis, or atopy. Perianal dermatitis is observed with strongyloidiasis. Cutaneous larva migrans is characterized by a linear, serpiginous rash.^3,4

Laboratory investigations. Investigation will vary depending on the patient’s history, exposures, exam findings, and degree of eosinophilia. Any patient who is unwell or has significant eosinophilia (≥3 x 10⁹/L) may warrant more urgent referral to infectious disease, travel medicine, or hematology. Basic laboratory investigations should include a CBC with differential, routine serum chemistries, and liver enzymes. In the setting of significant eosinophilia, an electrocardiogram, cardiac enzyme levels, and a chest x-ray should be obtained to screen for end-organ damage related to eosinophilia.^3-5

In patients in whom you suspect hematologic malignancy, bone marrow aspiration and biopsy are often needed to make the diagnosis.⁵

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia.

Parasitic infections are most often diagnosed on stool examination for ova and parasites or by serology. Stool should be collected on 3 separate days to increase diagnostic yield. Certain species of Schistosoma can also be diagnosed on direct microscopy of urine specimens. Serologic assays are available for schistosomiasis, strongyloidiasis, Toxocara, fascioliasis, filariasis, and Trichinella. Further investigations for filiariasis, including blood films, eye exam, and skin snips will vary with filarial species, so expert consultation should be considered.^3,4

Our patients. The first patient with strongyloidiasis was treated with ivermectin 200 µg/kg/day orally for 2 days and experienced symptomatic improvement and resolution of eosinophilia. The second patient with ALL was admitted and referred to hematology and received induction chemotherapy. Treatment was well tolerated and the patient was discharged one week later, with appropriate follow-up.

THE TAKEAWAY

Eosinophilia is commonly encountered in primary care. The approach to eosinophilia and the differential diagnosis can be challenging. The correct diagnosis was reached in both cases by maintaining a broad differential diagnosis. Obtaining a travel and exposure history is fundamental, although noninfectious causes, including allergy, malignancy, and drug reaction, must always be considered.

CASE 1

A 13-month-old boy who was recently adopted from Ethiopia presented to a primary care physician with a 3-week history of bloody diarrhea accompanied by flatulence and bloating. Stool cultures were positive for Campylobacter and Shigella. He was prescribed azithromycin but saw only moderate improvement. He was then referred to the Infectious Diseases Department. Neonatal, pregnancy, and immunization histories were unknown and a review of systems was unremarkable. On exam, the child looked well; he weighed 9.6 kg (15th percentile), was 69.5 cm long (<3rd percentile), and his head circumference was 45 cm (10th percentile). Head and neck, cardiorespiratory, and abdominal examinations were unremarkable.

A complete blood count (CBC) showed an elevated white blood cell (WBC) count of 26 x 10⁹/L (normal: 4-10 x 10⁹/L) with predominant eosinophilia (10.4 x 10⁹/L or 40.1% of WBCs; normal: <0.45 x 10⁹/L or 0%-8%). Hemoglobin and platelets were within normal limits. Stool testing for ova and parasites showed Strongyloides stercoralis larvae. Strongyloides serology was negative and Filaria serology was equivocal.

CASE 2

A 15-year-old boy was assessed for a 3-week history of fever and eosinophilia. He had enlarged cervical lymph nodes, a new rash, and had lost 4 pounds. He denied gastrointestinal symptoms, dyspnea, headaches, or chest pain. His past medical and family histories were unremarkable and he reported no drug use or allergies. He had traveled to Cuba with his family for 15 days 3 months prior to presentation. He recalled diarrhea while traveling, which resolved spontaneously. He and his family had traveled “off the beaten track,” eating foods prepared at local establishments and swimming in local rivers. He received pre-travel immunizations.

On examination, he appeared unwell, though his vital signs were normal. He had diffuse lymphadenopathy and a petechial rash on his chest, back, upper buttocks, legs, and feet. Cardiorespiratory and abdominal examinations were unremarkable. A CBC revealed an elevated WBC count of 76.9 x 10⁹/L with predominant eosinophilia (71.5 x 10⁹/L or 92% of WBCs). Hemoglobin, platelets, electrolytes, and liver function tests were normal. The patient was referred to a tertiary care center and was admitted to the hospital. Stool testing for ova and parasites, as well as serology for parasitic infections, was negative. A bone marrow aspiration and biopsy were performed and revealed the diagnosis of acute lymphoblastic leukemia (ALL).

These 2 cases highlight how the presentation of eosinophilia can vary and how important it is to maintain a broad differential diagnosis (TABLE 1^1-4). Causes of eosinophilia are numerous and can be divided into 3 categories: primary, secondary, and idiopathic.^1,5 Hematologic malignancy, where eosinophilia is clonal, is an example of a primary etiology. Causes of secondary eosinophilia include infectious diseases, drugs (TABLE 2⁵), autoimmune disorders, and allergic conditions. Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage. Dermatologic, pulmonary, gastro­intestinal, and cardiac involvement is most common.²

Eosinophilia associated with parasitic infection

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia, with eosinophilia occurring during tissue migration or penetration.^1,3

Schistosomiasis is a chronic parasitic infection of the human vascular system. It is transmitted by contact with contaminated fresh water, where cercariae penetrate the skin. High prevalence areas include Africa and Southeast Asia. Acute infection can result in Katayama fever—a febrile illness with prominent eosinophilia that occurs 4 to 7 weeks after exposure.⁴ Diagnosis is primarily clinical with appropriate epidemiology, as serology may be negative early in infection. Praziquantel is the treatment of choice, though dosing varies by species, so expert consultation should be considered.

Soil-transmitted helminths, such as Ascaris (Ascaris lumbricoides), whipworm (Trichuris trichiura), and hookworm (Ancyclostoma duodenale and Necator americanus), can also cause eosinophilia during larval tissue migration. Following infection by ingestion or skin penetration, an acute respiratory illness, termed Löffler’s syndrome, can develop with associated eosinophilia.¹ Once the helminths reach the adult stage, eosinophilia subsides. Patients are most commonly treated with albendazole 400 mg orally for 3 days.⁴

Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage.Fascioliasis is common in sheep-rearing areas. Humans are infected through ingestion of aquatic plants (eg, watercress). Parasitic migration through the duodenal wall and liver parenchyma can lead to fever, right upper quadrant pain, and eosinophilia. The incubation period is 6 to 12 weeks. Diagnosis during acute infection is by serology.⁴

Filarial infections, eg lymphatic filariasis, loiasis, and onchocerciasis, can also cause eosinophilia. The rise in eosinophils can be triggered by either the adult worms or circulating microfilariae.⁴ Treatment of fascioliasis and filarial infections varies and expert consultation is recommended.

Eosinophilia associated with primary hematologic malignancy

Eosinophilia is a rare presentation of hematologic malignancy. Acute myeloid leukemia, acute lymphoblastic leukemia (ALL), chronic myeloid leukemia, and myeloproliferative disorders have all been associated with eosinophilia. Hepatosplenomegaly, generalized lymphadenopathy, and cytopenias in other cell lines are often noted. Also, the degree of eosinophilia is often more pronounced (>5 x 10⁹/L). Patients with suspected hematologic malignancy should be urgently referred for expert consultation.⁵

Consider the following approach in the assessment of patients with eosinophilia seen in the ambulatory care setting. Inpatients or patients being seen in developing areas may require a modified approach.

History. All patients with eosinophilia should have a thorough history taken, with particular attention paid to travel history. A travel history should make note of dates, duration and location of travel, and any relevant exposures, such as arthropod bites or swimming in freshwater. Dietary habits, such as ingestion of seafood, game, or undercooked meat can also be helpful in making a diagnosis.^3,4

Causes of secondary eosinophilia include infectious diseases, drugs, autoimmune disorders, and allergic conditions.

Physical exam. In addition to a general physical examination, the following features may be helpful in determining the etiology of eosinophilia. Wheeze is characteristic of parasites in a lung migration phase (eg, strongyloidiasis and ascariasis) or asthma. Hepatomegaly can be seen with liver flukes, visceral larva migrans, or schistosomiasis. Periorbital edema can be observed with Trichinella infection. Loa loa, a type of filarial infection, produces a transient, migratory angioedema, often localized to the wrists and large joints (termed Calabar swelling). Dermatitis of varying intensity may suggest filarial infection, schistosomiasis, or atopy. Perianal dermatitis is observed with strongyloidiasis. Cutaneous larva migrans is characterized by a linear, serpiginous rash.^3,4

Laboratory investigations. Investigation will vary depending on the patient’s history, exposures, exam findings, and degree of eosinophilia. Any patient who is unwell or has significant eosinophilia (≥3 x 10⁹/L) may warrant more urgent referral to infectious disease, travel medicine, or hematology. Basic laboratory investigations should include a CBC with differential, routine serum chemistries, and liver enzymes. In the setting of significant eosinophilia, an electrocardiogram, cardiac enzyme levels, and a chest x-ray should be obtained to screen for end-organ damage related to eosinophilia.^3-5

In patients in whom you suspect hematologic malignancy, bone marrow aspiration and biopsy are often needed to make the diagnosis.⁵

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia.

Parasitic infections are most often diagnosed on stool examination for ova and parasites or by serology. Stool should be collected on 3 separate days to increase diagnostic yield. Certain species of Schistosoma can also be diagnosed on direct microscopy of urine specimens. Serologic assays are available for schistosomiasis, strongyloidiasis, Toxocara, fascioliasis, filariasis, and Trichinella. Further investigations for filiariasis, including blood films, eye exam, and skin snips will vary with filarial species, so expert consultation should be considered.^3,4

Our patients. The first patient with strongyloidiasis was treated with ivermectin 200 µg/kg/day orally for 2 days and experienced symptomatic improvement and resolution of eosinophilia. The second patient with ALL was admitted and referred to hematology and received induction chemotherapy. Treatment was well tolerated and the patient was discharged one week later, with appropriate follow-up.

THE TAKEAWAY

Eosinophilia is commonly encountered in primary care. The approach to eosinophilia and the differential diagnosis can be challenging. The correct diagnosis was reached in both cases by maintaining a broad differential diagnosis. Obtaining a travel and exposure history is fundamental, although noninfectious causes, including allergy, malignancy, and drug reaction, must always be considered.

CASE 1

A 13-month-old boy who was recently adopted from Ethiopia presented to a primary care physician with a 3-week history of bloody diarrhea accompanied by flatulence and bloating. Stool cultures were positive for Campylobacter and Shigella. He was prescribed azithromycin but saw only moderate improvement. He was then referred to the Infectious Diseases Department. Neonatal, pregnancy, and immunization histories were unknown and a review of systems was unremarkable. On exam, the child looked well; he weighed 9.6 kg (15th percentile), was 69.5 cm long (<3rd percentile), and his head circumference was 45 cm (10th percentile). Head and neck, cardiorespiratory, and abdominal examinations were unremarkable.

A complete blood count (CBC) showed an elevated white blood cell (WBC) count of 26 x 10⁹/L (normal: 4-10 x 10⁹/L) with predominant eosinophilia (10.4 x 10⁹/L or 40.1% of WBCs; normal: <0.45 x 10⁹/L or 0%-8%). Hemoglobin and platelets were within normal limits. Stool testing for ova and parasites showed Strongyloides stercoralis larvae. Strongyloides serology was negative and Filaria serology was equivocal.

CASE 2

A 15-year-old boy was assessed for a 3-week history of fever and eosinophilia. He had enlarged cervical lymph nodes, a new rash, and had lost 4 pounds. He denied gastrointestinal symptoms, dyspnea, headaches, or chest pain. His past medical and family histories were unremarkable and he reported no drug use or allergies. He had traveled to Cuba with his family for 15 days 3 months prior to presentation. He recalled diarrhea while traveling, which resolved spontaneously. He and his family had traveled “off the beaten track,” eating foods prepared at local establishments and swimming in local rivers. He received pre-travel immunizations.

On examination, he appeared unwell, though his vital signs were normal. He had diffuse lymphadenopathy and a petechial rash on his chest, back, upper buttocks, legs, and feet. Cardiorespiratory and abdominal examinations were unremarkable. A CBC revealed an elevated WBC count of 76.9 x 10⁹/L with predominant eosinophilia (71.5 x 10⁹/L or 92% of WBCs). Hemoglobin, platelets, electrolytes, and liver function tests were normal. The patient was referred to a tertiary care center and was admitted to the hospital. Stool testing for ova and parasites, as well as serology for parasitic infections, was negative. A bone marrow aspiration and biopsy were performed and revealed the diagnosis of acute lymphoblastic leukemia (ALL).

These 2 cases highlight how the presentation of eosinophilia can vary and how important it is to maintain a broad differential diagnosis (TABLE 1^1-4). Causes of eosinophilia are numerous and can be divided into 3 categories: primary, secondary, and idiopathic.^1,5 Hematologic malignancy, where eosinophilia is clonal, is an example of a primary etiology. Causes of secondary eosinophilia include infectious diseases, drugs (TABLE 2⁵), autoimmune disorders, and allergic conditions. Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage. Dermatologic, pulmonary, gastro­intestinal, and cardiac involvement is most common.²

Eosinophilia associated with parasitic infection

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia, with eosinophilia occurring during tissue migration or penetration.^1,3

Schistosomiasis is a chronic parasitic infection of the human vascular system. It is transmitted by contact with contaminated fresh water, where cercariae penetrate the skin. High prevalence areas include Africa and Southeast Asia. Acute infection can result in Katayama fever—a febrile illness with prominent eosinophilia that occurs 4 to 7 weeks after exposure.⁴ Diagnosis is primarily clinical with appropriate epidemiology, as serology may be negative early in infection. Praziquantel is the treatment of choice, though dosing varies by species, so expert consultation should be considered.

Soil-transmitted helminths, such as Ascaris (Ascaris lumbricoides), whipworm (Trichuris trichiura), and hookworm (Ancyclostoma duodenale and Necator americanus), can also cause eosinophilia during larval tissue migration. Following infection by ingestion or skin penetration, an acute respiratory illness, termed Löffler’s syndrome, can develop with associated eosinophilia.¹ Once the helminths reach the adult stage, eosinophilia subsides. Patients are most commonly treated with albendazole 400 mg orally for 3 days.⁴

Prolonged eosinophilia that is >3 x 10⁹/L is associated with end-organ damage.Fascioliasis is common in sheep-rearing areas. Humans are infected through ingestion of aquatic plants (eg, watercress). Parasitic migration through the duodenal wall and liver parenchyma can lead to fever, right upper quadrant pain, and eosinophilia. The incubation period is 6 to 12 weeks. Diagnosis during acute infection is by serology.⁴

Filarial infections, eg lymphatic filariasis, loiasis, and onchocerciasis, can also cause eosinophilia. The rise in eosinophils can be triggered by either the adult worms or circulating microfilariae.⁴ Treatment of fascioliasis and filarial infections varies and expert consultation is recommended.

Eosinophilia associated with primary hematologic malignancy

Eosinophilia is a rare presentation of hematologic malignancy. Acute myeloid leukemia, acute lymphoblastic leukemia (ALL), chronic myeloid leukemia, and myeloproliferative disorders have all been associated with eosinophilia. Hepatosplenomegaly, generalized lymphadenopathy, and cytopenias in other cell lines are often noted. Also, the degree of eosinophilia is often more pronounced (>5 x 10⁹/L). Patients with suspected hematologic malignancy should be urgently referred for expert consultation.⁵

Consider the following approach in the assessment of patients with eosinophilia seen in the ambulatory care setting. Inpatients or patients being seen in developing areas may require a modified approach.

History. All patients with eosinophilia should have a thorough history taken, with particular attention paid to travel history. A travel history should make note of dates, duration and location of travel, and any relevant exposures, such as arthropod bites or swimming in freshwater. Dietary habits, such as ingestion of seafood, game, or undercooked meat can also be helpful in making a diagnosis.^3,4

Causes of secondary eosinophilia include infectious diseases, drugs, autoimmune disorders, and allergic conditions.

Physical exam. In addition to a general physical examination, the following features may be helpful in determining the etiology of eosinophilia. Wheeze is characteristic of parasites in a lung migration phase (eg, strongyloidiasis and ascariasis) or asthma. Hepatomegaly can be seen with liver flukes, visceral larva migrans, or schistosomiasis. Periorbital edema can be observed with Trichinella infection. Loa loa, a type of filarial infection, produces a transient, migratory angioedema, often localized to the wrists and large joints (termed Calabar swelling). Dermatitis of varying intensity may suggest filarial infection, schistosomiasis, or atopy. Perianal dermatitis is observed with strongyloidiasis. Cutaneous larva migrans is characterized by a linear, serpiginous rash.^3,4

Laboratory investigations. Investigation will vary depending on the patient’s history, exposures, exam findings, and degree of eosinophilia. Any patient who is unwell or has significant eosinophilia (≥3 x 10⁹/L) may warrant more urgent referral to infectious disease, travel medicine, or hematology. Basic laboratory investigations should include a CBC with differential, routine serum chemistries, and liver enzymes. In the setting of significant eosinophilia, an electrocardiogram, cardiac enzyme levels, and a chest x-ray should be obtained to screen for end-organ damage related to eosinophilia.^3-5

In patients in whom you suspect hematologic malignancy, bone marrow aspiration and biopsy are often needed to make the diagnosis.⁵

In returning travelers and international adoptees, multicellular helminthic parasites are the most common causes of eosinophilia.

Parasitic infections are most often diagnosed on stool examination for ova and parasites or by serology. Stool should be collected on 3 separate days to increase diagnostic yield. Certain species of Schistosoma can also be diagnosed on direct microscopy of urine specimens. Serologic assays are available for schistosomiasis, strongyloidiasis, Toxocara, fascioliasis, filariasis, and Trichinella. Further investigations for filiariasis, including blood films, eye exam, and skin snips will vary with filarial species, so expert consultation should be considered.^3,4

Our patients. The first patient with strongyloidiasis was treated with ivermectin 200 µg/kg/day orally for 2 days and experienced symptomatic improvement and resolution of eosinophilia. The second patient with ALL was admitted and referred to hematology and received induction chemotherapy. Treatment was well tolerated and the patient was discharged one week later, with appropriate follow-up.

THE TAKEAWAY

Eosinophilia is commonly encountered in primary care. The approach to eosinophilia and the differential diagnosis can be challenging. The correct diagnosis was reached in both cases by maintaining a broad differential diagnosis. Obtaining a travel and exposure history is fundamental, although noninfectious causes, including allergy, malignancy, and drug reaction, must always be considered.

ILLUSTRATIVE CASE

A 64-year-old woman presents to your office for a follow-up visit for her hypertension. She is currently managed on lisinopril 20 mg/d and hydrochlorothiazide 25 mg/d without any problems. The patient’s blood pressure (BP) in the office today is 148/84 mm Hg, but her home blood pressure (HBP) readings are much lower (see TABLE). Should you increase her lisinopril dose today?

Hypertension has been diagnosed on the basis of office readings of BP for almost a century, but the readings can be so inaccurate that they are not useful.² The US Preventive Services Task Force recommends the use of ambulatory blood pressure monitoring (ABPM) to accurately diagnose hypertension in all patients, while The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommends ABPM for patients suspected of having white-coat hypertension and any patient with resistant hypertension,^3,4 but ABPM is not always acceptable to patients.⁵

Guidelines recommend HBP monitoring for long-term follow-up of hypertension

The European Society of Hypertension practice guideline on HBP monitoring suggests that HBP values <130/80 mm Hg may be considered normal, while a mean HBP ≥135/85 mm Hg is considered elevated.⁹ The guideline recommends HBP monitoring for 3 to 7 days prior to a patient’s follow-up appointment with 2 readings taken one to 2 minutes apart in the morning and evening.⁹ In a busy clinic, averaging all of these home values can be time-consuming.

So how can primary care physicians accurately and efficiently streamline the process? This study sought to answer that question.

STUDY SUMMARY

When 3 of 10 readings are elevated, it’s predictive

This multicenter trial compared HBP monitoring to 24-hour ABPM in 286 patients with uncomplicated essential hypertension to determine the optimal percentage of HBP readings needed to diagnose uncontrolled BP (HBP ≥135/85 mm Hg). Patients were included if they were diagnosed with uncomplicated hypertension, not pregnant, ≥18 years of age, and taking ≤3 antihypertensive medications. Medication compliance was verified by a study nurse at a clinic visit. Patients were excluded if they had a significant abnormal left ventricular mass index (women >59 g/m²; men >64 g/m²), coronary artery or renal disease, secondary hypertension, serum creatinine exceeding 1.6 mg/dL, aortic valve stenosis, upper limb obstructive atherosclerosis, or BP >180/100 mm Hg.

The researchers found that if at least 3 of the last 10 home BP readings were elevated, the patient was likely to have hypertension on 24-hour ambulatory monitoring.

Approximately half of the participants were women (53%), average body mass index was 29.4 kg/m², and the average number of hypertension medications being taken was 2.4. The patients were instructed to take 2 BP readings (one minute apart) at home 3 times daily, in the morning (between 6 am and 10 am), at noon, and in the evening (between 6 pm and 10 pm), and to record only the second reading for 7 days. Only the morning and evening readings were used for analysis in the study. The 24-hour ABP was measured every 30 minutes during the daytime hours and every 60 minutes overnight. The primary outcome was to determine the optimal number of systolic HBP readings above goal (135 mm Hg), from the last 10 recordings, that would best predict elevated 24-hour ABP. Secondary outcomes were various cardiovascular markers of target end-organ damage.

The researchers found that if at least 3 of the last 10 HBP readings were elevated (≥135 mm Hg systolic), the patient was likely to have hypertension on 24-hour ABPM (≥130 mm Hg). When patients had <3 HBP elevations out of 10 readings, their mean (±standard deviation [SD]) 24-hour ambulatory daytime systolic BP was 132.7 (±11.1) mm Hg and their mean systolic HBP value was 120.4 (±9.8) mm Hg. When patients had ≥3 HBP elevations, their mean 24-hour ambulatory daytime systolic BP was 143.4 (±11.2) mm Hg and their mean systolic HBP value was 147.4 (±10.5) mm Hg.

The positive and negative predictive values of ≥3 HBP elevations were 0.85 (95% confidence interval [CI], 0.78-0.91) and 0.56 (95% CI, 0.48-0.64), respectively, for a 24-hour systolic ABP of ≥130 mm Hg. Three elevations or more in HBP, out of the last 10 readings, was also an indicator for target organ disease assessed by aortic stiffness and increased left ventricular mass and decreased function.

The sensitivity and specificity of ≥3 elevations for mean 24-hour ABP systolic readings ≥130 mm Hg were 62% and 80%, respectively, and for 24-hour ABP daytime systolic readings ≥135 mm Hg were 65% and 77%, respectively.

WHAT’S NEW

Monitoring home BP can be simplified

The researchers found that HBP monitoring correlates well with ABPM and that their method provides clinicians with a simple way (3 of the past 10 measurements ≥135 mm Hg systolic) to use HBP readings to make clinical decisions regarding BP management.

CAVEATS

Ideal BP goals are hazy, and a lot of patient education is required

Conflicting information and opinions remain regarding the ideal intensive and standard BP goals in different populations.^10,11 Systolic BP goals in this study (≥130 mm Hg for overall 24-hour ABP and ≥135 mm Hg for 24-hour ABP daytime readings) are recommended by some experts, but are not commonly recognized goals in the United States. This study found good correlation between HBP and ABPM at these goals, and it seems likely that this correlation could be extrapolated for similar BP goals.

Patients using home blood pressure monitors should be counseled on how to determine the appropriate cuff size so that measurements are accurate.

Other limitations are that: 1) The study focused only on systolic BP goals; 2) Patients in the study adhered to precise instructions on BP monitoring. HBP monitoring requires significant patient education on the proper use of the equipment and the monitoring schedule; and 3) While end-organ complication outcomes showed numerical decreases in function, the clinical significance of these reductions for patients is unclear.

CHALLENGES TO IMPLEMENTATION

Cost of device and improper cuff sizes could be barriers

The cost of HBP monitors ($40-$60) has decreased significantly over time, but the devices are not always covered by insurance and may be unobtainable for some people. Additionally, patients should be counseled on how to determine the appropriate cuff size to ensure the accuracy of the measurements.

The British Hypertensive Society maintains a list of validated BP devices on their Web site: http://bhsoc.org/bp-monitors/bp-monitors.¹²

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.