A Quick Quiz in Honor of National Women’s Health Week (May 14-20, 2012)

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If you answered “urinary tract infections” and “Escherichia coli” to the first two questions, you are correct. If you answered “true” to the third question, you’re incorrect—but you’re in good company. Up until very recently, we all believed that ciprofloxacin (Cipro) and Bactrim were the two best antibiotics for eradicating urinary tract infections (UTIs). However, a recent study suggests something very different, and you may want to rethink how you treat UTIs caused by E. coli.

In a study of more than 12 million bacteria, investigators at The George Washington University found that E. coli antimicrobial resistance to Cipro increased more than fivefold from 2000 to 2010. In addition, nearly one in four isolates was resistant to trimethoprim/sulfamethoxazole (TMP-SMX; Bactrim, Septra). Cipro and TMP-SMX are the first and second most commonly prescribed drugs for UTIs. Of note is that the researchers reported minimal resistance to nitrofurantoin (eg, Macrodantin, Macrobid), amoxicillin/clavulanate (eg, Augmentin) and ceftriaxone, a third-generation cephalosporin (eg, Rocephin).

This research was published in the April issue of Antimicrobial Agents and Chemotherapy.[1]

E. coli antimicrobial resistance is a major factor in determining health outcomes in patients with UTIs. It has been associated with lower likelihood of clinical cure and increased risk of infection recurrence. Additionally, antimicrobial resistance significantly increases patient morbidity, costs of treatment, and rates of hospitalization.

Antibiotic resistance has been called one of the world’s most pressing public health problems. Antimicrobial resistance refers to microbes’ natural ability to evolve genetically and “neutralize” the drugs used to kill them off. Some of this is inevitable, but over-prescribing and improper use of antibiotics play a big role. A common misconception is that an individual becomes resistant to specific drugs when in reality, the bacteria themselves become resistant to the drugs.

Almost every type of bacteria has become stronger and less responsive to antibiotic treatment when it is really needed. These antibiotic-resistant bacteria can quickly spread to family members, coworkers, neighbors, and schoolmates—threatening the community with a new strain of infectious disease that is more difficult to cure and more expensive to treat.

As antimicrobial resistance continues to increase, remaining antimicrobial drug options have a higher likelihood of causing unwanted side effects such as gastrointestinal distress, nausea, and vomiting. Due to a lack of drug development, the paucity of new antimicrobial drugs for common infections like UTIs will continue to worsen in the near future.

The Centers for Disease Control and Prevention (CDC) has recommendations for preventing antibiotic resistance in the outpatient setting[2]:

• Prescribe the right antibiotic and be familiar with the resistance trends in your region
• Don’t treat viral syndromes with antibiotics, even if the patient demands it
• Don’t prescribe antibiotics for viral upper respiratory infections
• Refine antibiotic choice once the pathogen causing the infection has been identified
• Don’t prescribe two overlapping antibiotics for the same bacteria; it’s usually not necessary

Clinical Pearl

Ciprofloxacin and TMP-SMX are no longer safe for treating UTIs. Safer antimicrobials for treating outpatient UTIs caused by E. coli are nitrofurantoin (for patients with healthy kidneys), amoxicillin/clavulanate, and third generation cephalosporins.

Jill Shuman, MS, ELS
Published May 15, 2012

References

1. Sanchez GV, Master RN, Karlowsky JA, Bordon JM. In vitro antimicrobial resistance of urinary Escherichia coli isolates among U.S. outpatients from 2000 to 2010. Antimicrob Agents Chemother. 2012;56(4):2181-2183.
2. Get Smart: Know When Antibiotics Work. Centers for Disease Control and Prevention Website. http://www.cdc.gov/getsmart/. Updated May 9, 2012. Accessed May 14, 2012.

Rx: Antibiotic + 1 Cup of Yogurt

Antibiotics are among the most frequently prescribed medications in modern medicine, available to cure minor, as well as life-threatening, infections. However, antibiotics can produce undesirable side effects, some of which are severe enough to compromise patients’ adherence to the full course of treatment. One of the most common is antibiotic-associated diarrhea (AAD), which occurs in up to 30% of patients who take antibiotics.[1]

A recent systematic review published in JAMA[2] suggests that adding probiotics (from pro and biota, meaning “for life”) to a course of antibiotics may lessen or even eliminate the onset of AAD. Probiotics—live bacteria and yeasts—are widely marketed to consumers in the form of capsules, powders, fermented milks, and yogurts. It’s not really clear how they work, but scientists believe that good types of bacteria have long lived in symbiosis with humans and that the positive health effects may have evolved over time.

One likely role for probiotic bacterial cultures is to help bacteria naturally found in the gut to re-establish themselves—particularly during and after a course of antibiotics.[3] An estimated 100 trillion microorganisms representing more than 500 different species inhabit every normal, healthy bowel. Most of these microorganisms are beneficial, keeping pathogens in check, aiding digestion and nutrient absorption, and contributing to immune function. A week-long course of antibiotics will destroy the bacteria causing the acute infection, but can also wipe out these beneficial microorganisms. As this delicate balance in the colon is disrupted, AAD may result.

To try to clarify the role of probiotics in defusing AAD, the JAMA researchers analyzed data from 82 randomized control trials that included children, adults, and the elderly. The most commonly used probiotic (57 studies) was some form of Lactobacillus; 16 studies used an exclusively yeast-based intervention. Among the 11,811 participants, those who took probiotics were 42% less likely to suffer from AAD. While many of the studies were of poor quality, the effect of the probiotics on AAD was sustained—and increased—when the analysis was limited to higher quality trials. Unfortunately, only half of the studies included in the review provided the name of the genus and species of the probiotic and few of the studies included the name of the antibiotic.[2]

Probiotics are available to consumers mainly in the form of dietary supplements (capsules, tablets, and powders) or in foods, such as yogurt, miso, and some juice and soy products, with the bacteria either naturally present or added during the manufacturing process. Most probiotics include bacteria similar to those naturally found in the gut and have names such as Lactobacillus or Bifidobacterium. A few common probiotics are yeasts, such as Saccharomyces boulardii—sometimes taken by patients to treat the diarrhea associated with antibiotic administration.

While foods such as regular yogurt, aged cheeses, and buttermilk naturally contain healthy bacteria, pasteurization can eliminate much of their bacterial presence. The recent boom in probiotic products reflects an effort to re-introduce bacteria to an enthusiastic audience, with companies seeking to attract health-conscious consumers by adding probiotics to products as diverse as yogurt, juices, muffins, and even pizza, as well as in dietary supplements. And Americans are apparently eating it up; spending on probiotic supplements approached $1.26 billion in 2010.[4]

Foods with probiotics are generally considered safe. However, the safety of probiotics has not been thoroughly studied[5] and more information is necessary about their effect on young children, the elderly, and people with compromised immune systems.[6] Side effects, if they occur, tend to be mild and digestive (such as gas or bloating). There is also some concern that by encouraging the growth of bacteria, probiotics could cause infections that need to be treated with antibiotics, especially in people with underlying health conditions.

Companies that sell probiotics claim they offer health benefits ranging from improved digestion and enhancing the immune system to preventing dental caries and colorectal cancer. Some of the claims are based on reputable scientific study. But others are unproven, and advertising claims are often exaggerated because probiotic supplements are regulated as food, not drugs, by the FDA. The quality of probiotic supplements also varies widely and, as a result, patients might have a difficult time choosing among a host of products.[7]

Bottom line? You might want to recommend a course of probiotics for patients who require a long course of antibiotics. If patients ask you about a specific probiotic, suggest they purchase only those that readily identify the bacterial strain, the appropriate serving size, and the expiration date. The further away the date, the more live bacteria the yogurt is likely to contain. Encourage patients to get their daily intake of probiotics from yogurt and other fermented foods instead of from pills or capsules, as the food products contain other needed nutrients such as calcium.

Jill Shuman, MS, ELS
Published May 14, 2012

Reference

1. Barbut B, Meynard JL. Managing antibiotic associated diarrhoea. BMJ. 2002;324(7350):1345-1346.
2. Hempel S, Newberry SJ, Maher A, et al. Probiotics for the prevention and treatment of antibiotic-associated diarrhea: a systematic review and meta-analysis. JAMA. 2012;307(18):1959-1969.
3. D’Souza AL, Rajkumar C, Cooke J, Bulpitt CJ. Probiotics in prevention of antibiotic associated diarrhoea: meta-analysis. BMJ. 2002;324(7350):1361.
4. Gelski J. Staking out probiotic claims: avoid drug implications and use well-researched strains. Food BusinessNews.net Website. http://www.foodbusinessnews.net/News/News%20Home/Features/2010/9/Staking%20out%20probiotic%20claims.aspx. Published September 28, 2010. Accessed May 12, 2012.
5. Hempel S, Newberry S, Ruelaz A, et al. Safety of Probiotics Used to Reduce Risk and Prevent or Treat Disease. Executive Summary, Evidence Report/Technology Assessment No. 200. AHRQ Publication No. 11-E007-1. Rockville, MD: Agency for Healthcare Research and Quality; 2011.
6. Ezendam J, van Loveren H. Probiotics: immunomodulation and evaluation of safety and efficacy. Nutr Rev. 2006;64(1):1-14.
7. Donohue DC. Safety of probiotics. Asia Pac J Clin Nutr. 2006;15(4):563-569.

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Sarcoidosis: An Enigmatic Disease

Patient Case

Cindy is a 39-year-old nurse who works in a 200-bed hospital in a medium size city that is a worldwide tourist destination. She presented to her primary care provider with chief complaints of fatigue, cough, and shortness of breath following an upper respiratory infection that has persisted for more than three weeks. The patient did not receive antibiotic therapy at the onset of symptoms, assuming a viral infection. She was absent from work for three days. She denies weight loss or night sweats. The patient’s mother was diagnosed with sarcoidosis six years ago, at age 65. Cindy’s chest x-ray revealed hilar lymphadenopathy and evidence of calcification of nodes. Her laboratory workup revealed a serum calcium level of 11.3 mEq/dL and urinary calcium of 325 mg/24 hr. On pulmonary function testing, she had a forced vital capacity (FVC) of 80% of predicted. Lung biopsy confirmed granulomatous lesions consistent with the diagnosis of sarcoidosis, but testing of the specimen failed to demonstrate a causative agent, such as bacteria. The patient was started on prednisone, 30 mg/d, and was scheduled to be seen in one month. One month later, she reported improvement in her symptoms, but not resolution. The patient remained on the corticosteroid regimen for an additional two months, at which time her disease appeared to be in remission and treatment was stopped. She is seen twice annually by her pulmonologist.

Introduction

When British Prime Minister Winston Churchill described Russia as “a riddle, wrapped in a mystery, inside an enigma,” he could have been describing sarcoidosis. Defined as a multisystem noncaseating granulomatous disease of uncertain etiology, sarcoidosis has challenged patients and their providers since its initial description in the late 1800s. At present, there is no single diagnostic test, nor any definitive laboratory or imaging study specific for sarcoidosis, nor is there an approved specific therapy. A high index of suspicion, based on knowledge of the wide range of potential signs and symptoms, is an essential tool for the clinician in identifying patients with sarcoidosis. Sarcoidosis remains a diagnosis of exclusion.[1]

Epidemiology and Clinical Presentation

Sarcoidosis occurs throughout the world and can occur at any age. However, the peak incidence appears to be between the ages of 20 to 39 years.[1] In Scandinavian countries, the incidence is bimodal—occurring at one peak at ages 25 to 29, and then again at ages 65 to 69.[2] While sarcoidosis afflicts all races and genders, it is more common in women and among blacks. Among black Americans the prevalence rate is approximately three times the rate seen in white Americans.[3,4] While income and socioeconomic status do not affect risk, they are associated with poorer outcomes. Estimates of its prevalence vary widely. In Northern Europe and the United States, it is estimated that sarcoidosis occurs in 5-40/100,000 persons.[1,5] An interesting report from central Ohio found an increase in the incidence of sarcoidosis; better patient ascertainment and improved diagnostic methods are the suggested reason for the increase.[6]

The signs and symptoms in patients with sarcoidosis also vary both in organ system affected and in severity of disease. It is most commonly seen in the lungs, skin, and eyes, but can also affect the central nervous system, lymph nodes, joints, and/or cardiac system; 90% of patients manifest thoracic involvement.[1,3,5,7] In its cutaneous forms, it has been described as “the great imitator” because it can resemble common disorders and it can mimic rare conditions.[8] Among the more common cutaneous manifestations are erythema nodosum that is often accompanied by unilateral or bilateral hilar and/or right paratracheal lymphadenopathy, anterior uveitis, and/or polyarthritis which is referred to as Lofgren’s syndrome. Other skin lesions associated with sarcoidosis include macular or papular lesions, scaly plaque lesions, and annular lesions.[8]

Cardiac involvement occurs in 20% to 30% of patients with the disease, and yet only 5% of patients with sarcoidosis have clinical manifestations of cardiac disease.[5] Some patients may be asymptomatic at the time of diagnosis, while others have an acute onset of symptoms such as fatigue, chest pain, and dyspnea (Table 1). Many patients require no treatment, other patients require aggressive treatment; as many as 30% of patients develop chronic, progressive disease, and a small percentage (5%) of patients succumb to the disease.[1,3,5,9]

Diagnostic Workup

A careful history will not only explore the onset and nature of the patient’s symptoms, but should also delve into the patient’s family history. Studies have shown that this disease tends to be found among relatives. A genetic predisposition has been suggested by a higher incidence among monozygous twins, as well as by the differences in disease severity between racial groups.[5,10] A Case-Control Etiologic Sarcoidosis Study (ACCESS) found that sarcoidosis patients were five times more likely to report a parent or sibling with sarcoidosis than were healthy control patients.[11]

The diagnostic evaluation of patients suspected of having this disorder should include chest x-ray, positron emission, magnetic resonance imaging, or computer tomography.[4] X-rays have been used to assign stages (1-4) of sarcoidosis, and while some assert this radiographic assessment is helpful in predicting outcome, others feel it does not correlate well with outcome[4,7] (Table 2). Even though pulmonary function testing does not always correlate with radiographic findings, pulmonary function studies are also important to identify obstructive or restrictive disease; 65% of patients with sarcoidosis have impaired pulmonary function.[1] It is important to also evaluate serum calcium because patients with sarcoidosis frequently have hypercalcemia and hypercalciuria. If these conditions go untreated, patients can develop nephrocalcinosis and ultimate progress to renal failure.[12]

The laboratory workup should include a complete blood count and/or complete metabolic panel, guided by the patient’s presenting symptoms. For example, patients with sarcoidosis, like the patient described, frequently have hypercalcemia and hypercalciuria. Thus, evaluation of liver function, renal function, and other organ function is indicated. In addition, serum angiotensin converting enzyme is elevated in a significant percentage of patients with sarcoidosis (50%-80%) and may indicate active disease, particularly in patients with chest involvement. However, because angiotensin-converting enzyme (ACE) can also be elevated in a number of other conditions, such as lymphoma, hepatitis, tuberculosis (TB), and hyperthyroidism, it is not a specific indicator of sarcoidosis, and is controversial.[1,4] Similarly, immunoglobulins, particularly IgM, IgG, and IgA, may be elevated in patients with sarcoidosis, and this finding may help differentiate sarcoidosis from common immunodeficiency disorders which are characterized by low levels.[9] More recently, Hattori and colleagues have suggested that IgE levels may be low in patients with sarcoidosis.[13] Where possible, a biopsy specimen from the affected organ such as the skin, peripheral lymph nodes, lacrimal glands, or conjunctiva should be obtained.[1] Because a significant number of patients have pulmonary involvement, fiberoptic transbronchial biopsies are frequently performed.[1,14]

The granuloma of sarcoidosis typically contains a central follicular area with macrophages, epithelioid cells, and multinucleated giant cells, surrounded by lymphocytes, fibroblasts, and monocytes at the periphery. However, to distinguish these granuloma from those caused by other disorders, cultures, and stains for acid-fast bacilli, fungi, and bacteria are very important.

Immunopathogenesis and Environmental Factors

Over the past two decades, researchers have gained a greater understanding of the pathogenesis of sarcoidosis with respect to potential triggering factors. With that understanding, insights into potential treatment options have emerged targeting specific aspects of the immunopathogenesis. While studies have failed to show a causative role, investigators have posited an important triggering role for environmental factors, such as infection, occupational exposure to fine particulates, and chemicals in genetically susceptible individuals.[1,3,15-17]

As noted by Saidha et al, one enduring theory is that an infectious agent plays an important triggering role in the development of sarcoidosis. Recent studies have shown that pathogens such as Mycobacterium spp, particularly Mycobacterium Tuberculosis (Mtb), occur in patients with sarcoidosis more frequently than in healthy individuals. DNA for the protein Mtb catalase-peroxidase (mKatG) has been found in 38% of biopsy specimens of sarcoidosis patients. Propionibacterium acnes, as well as viruses, have also been implicated in sarcoidosis.[14-16]

Interestingly, initial reports from the site of the World Trade Center disaster indicated that within the first year of exposure to building dust, workers had a higher than expected incidence of sarcoidosis than the general public. However, continuing studies have failed to show typical clinical features of sarcoidosis and a phenotypically distinct form of sarcoidosis is suspected.[15-18]

The ACCESS study data indicated that exposure to environmental factors such as bacteria increased the risk of sarcoidosis in genetically susceptible patients.[19,20] When exposed to an antigen in the environment, antigen-presenting cells interact with CD4+ T cells in a way that stimulates fibroblast proliferation and collagen production. This can lead to progressive pulmonary fibrosis which occurs in 20% to 25% of patients.[21]

Treatment Options

Understanding these complex inflammatory pathways has been important in developing treatment approaches for those patients who do not go into remission. The mainstay of therapy for sarcoidosis has been corticosteroids. As was the case with Cindy, prednisone in a dose of 20 to 40 mg/day is generally initiated at the time of diagnosis and is usually prescribed for one to three months. If the patient responds to this regimen, a tapering dosage schedule may be used.[22.23] Thirty percent of sarcoidosis patients have chronic progressive disease.[24] Thus, if the patient fails to respond, the dose may be increased or another approach may be indicated. Inhaled corticosteroids have been used and studied, but they are less effective than oral steroids. They may have a role in patients whose primary symptom is cough or as maintenance therapy.[25] A number of other agents, based on the mechanism of anti-inflammatory properties, have been suggested. These alternatives, often used initially in combination with corticosteroids, include methotrexate, thalidomide, pentoxifylline, hydroxychloroquine, azathioprine, leflunomide, and infliximab.[24-26] All of these corticosteroid-sparing alternative therapies have been shown to have beneficial effects in some patients, particularly those with chronic, recurrent/relapsing sarcoidosis.[23-24] Since most of these agents require up to nine months to achieve peak effects, steroids should be slowly tapered after the alternative drug is added. However, it should be noted that the effects are modest, are not seen in all patients, and all have significant adverse effects, ranging from nausea and diarrhea to bone marrow suppression, hepatitis, TB, and malignancy[23,25-27] (Table 3). Most suppress immunity. Because of the adverse effects, patients who receive these drugs require monitoring.

As research continues to build upon our current understanding of the pathogenesis of sarcoidosis insights into the role of current medications and development of targeted therapies to improve the lives of patients with sarcoidosis will likely be developed.

Sally Farrand
Published May 8, 2012

References

1. Iannuzzi MC, Rybicki BA, Teirstein AS. Sarcoidosis. N Engl J Med. 2007;357:2153-2165.
2. Milman N, Selroos O. Pulmonary sarcoidosis in the Nordic countries 1950-1982. Epidemiology and clinical picture. Sarcoidosis. 1990;7(1):50-57.
3. Morganthau AS, Iannuzzi MC. Recent advances in sarcoidosis. Chest. 2011;139:174-182.
4. Culver DA. Sarcoidosis. Cleveland Clinic Website. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/pulmonary/sarcoidosis/. Published January 1, 2009. Accessed April 27, 2012.
5. Sekhri V, Sanal S, DeLorenzo LJ, et al. Cardiac sarcoidosis: a comprehensive review. Arch Med Sci. 2011;7(4):546-554.
6. Erdal BS, Clymer BD, Yildiz VO, et al. Unexpectedly high prevalence of sarcoidosis in a representative U.S.Metropolitan population. Respir Med. 2012;106(6):893-899.
7. Belfer MH, Stevens RW. Sarcoidosis: a primary care review. Am Fam Physician. 1998;58(9):2041-2050.
8. Haimovic A, Sanchez M, Judson MA, Prystowsky S. Sarcoidosis: A comprehensive review and update for the dermatologist: Part I. Cutaneous disease. J Am Acad Dermatol. 2012;66(5):699.e1-699.e.18.
9. Arnold DF, Wiggins J, Cunningham-Rundle C, et al. Granulomatous disease: distinguishing primary antibody disease from sarcoidosis. Clin Immunol. 2008;128(1):18-22.
10. Sverrild A, Backer V, Kyvik KO, et al. Heredity in sarcoidosis: a registry-based twin study. Thorax. 2008;63(10):894-896.
11. Rybicki BA , Iannuzzi MC , Frederick MM , et al; ACCESS Research Group. Familial aggregation of sarcoidosis. A case-control etiologic study of sarcoidosis (ACCESS). Am J Respir Crit Care Med. 2001;164(11):2085-2091.
12. Karnchanasorn R, Sarikonda M, Aldasouqi S, Gossain VV. Severe hypercalcemia and acute renal failure: an unusual presentation of sarcoidosis. Case Report Med. 2010;2010:423659.
13. Hattori T, Konno S, Shigemura M, et al. Total serum IgE levels and atopic status in patients with sarcoidosis. Allergy Asthma Proc. 2012;33(1):90-94.
14. Miliauskas S, Zemaitis M, Sakalauskas R. Sarcoidosis?moving to the new standard of diagnosis? Medicina (Kaunas). 2010;46(7):443-446.
15. Saidha S, Sotirchos ES, Eckstein C. Etiology of sarcoidosis: does infection play role? Yale J Biol Med. 2012;85(1):133-141.
16. Kreider ME, Christie JD, Thompson B, et al. Relationship of environmental exposures to the clinical phenotype of sarcoidosis. Chest. 2005;128(1):207-215.
17. Spagnolo P, Richeldi L, duBois RM. Environmental triggers and susceptibility in idiopathic granulomatous diseases. Semin Respir Crit Care Med. 2008;29(6):610-619.
18. Izbicki G, Chavko R, Banauch GI, et al. World Trade Center “sarcoid-like” granulomatous pulmonary disease in New York City Fire Department rescue workers. Chest. 2007;131(5):1414-1423.
19. Newman LS, Rose CS, Bresnitz EA, et al; ACCESS Research Group. A case control etiologic study of sarcoidosis: environmental and occupational risk factors. Am J Respir Crit Care Med. 2004;170(12):1324-1330.
20. Barnard J, Rose C, Newman L, et al; ACCESS Research Group. Job and industry classifications associated with sarcoidosis in A Case-Control Etiologic Study of Sarcoidosis (ACCESS). J Occup Environ Med. 2005;47(3):226-234.
21. Nishino M, Lee KS, Itoh H, Hatabu H. The spectrum of pulmonary sarcoidosis: variations of high-resolution CT findings and clues for specific diagnosis. Eur J Radiol. 2010;73(1):66-73.
22. Hunninghake GW, Costabel U, Ando M, et al. ATS/ERS/WASOG statement on sarcoidosis. American Thoracic Society/European Respiratory Society/World Association of Sarcoidosis and other Granulomatous Disorders. Sarcoidosis Vasc Diffuse Lung Dis. 1999;16(2):149-173.
23. Judson MA. The treatment of pulmonary sarcoidosis [published online ahead of print April 9, 2012]. Respir Med. doi:10.1016/j.rmed.2012.01.013.
24. Chen ES, Moller DR; Medscape. Sarcoidosis–scientific progress and clinical challenges. Nat Rev Rheumatol. 2011;7(8):457-467.
25. Coker RK. Management strategies for pulmonary sarcoidosis. Ther Clin Risk Manag. 2009;5(3):575-584.
26. Baughman RP, Drent M, Kavuru M, et al. Infliximab therapy in patients with chronic sarcoidosis and pulmonary involvement. Am J Respir Crit Care Med. 2006;174(7):795-802.
27. Tong D, Manolios N, Howe G, Spencer D. New onset sarcoid-like granulomatosis developing during anti-TNF therapy: an under-recognised complication. Intern Med J. 2012;42(1):89-94.

The Sun Conundrum: Balancing Known Risk With Possible Benefit

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Overexposure to the sun’s ultraviolet rays is associated with the development of melanoma, a potentially fatal malignancy. However, data continue to suggest that exposure to sunlight increases vitamin D synthesis, which may help prevent heart disease and cancers of the prostate, colon, and breast. How can you help your patients balance the risk of sun exposure with the benefits of obtaining adequate vitamin D? It’s easier than you think!

Skin cancer is the most common of all cancer types, with more than 2 million skin cancers diagnosed each year in the United States. That’s more than cancers of the prostate, breast, lung, colon combined.[1]

Basal cell and squamous cell cancers are the most common cancers of the skin, and 90% of them are associated with exposure to ultraviolet (UV) radiation from the sun.[1] These cancers usually develop on parts of the body typically exposed to the sun, such as the head and neck, and are more likely to occur in people who accumulate a great deal of sun exposure over their lifetime. If left untreated, these cancers can grow quite large and invade nearby tissues, causing scarring, disfigurement, or even loss of function in some parts of the body.

Melanoma, the third type of skin cancer, is the most difficult to treat and most likely to metastasize. Melanomas can occur anywhere on the body, but are more likely to develop in the trunk (men) or the legs (women). This may occur because these sites are not regularly exposed to sun year-round and are more likely to burn on initial exposure to the sun each year.[2] Although melanoma accounts for less than 5% of skin cancers, it is responsible for almost 75% of deaths from skin cancer.[1]

The incidence of melanoma has more than tripled in the white population during the last 20 years, making it the sixth most common cancer in the United States.[1] The American Cancer Society estimates that approximately 76,250 Americans (44,250 men and 32,000 women) developed invasive melanoma in 2009, with an estimated additional 55,120 or more cases of melanoma in situ.[1,3] The incidence may actually be higher due to underreporting to cancer registries, particularly for tumors that are managed in the outpatient setting.[4] Overall, the lifetime risk of developing melanoma is about 1 in 50 for whites, 1 in 200 for Hispanics, and 1 in 1000 for blacks.[1] However, when skin cancer does occur in black patients, they often present with an advanced stage and a worse prognosis than white patients.[5]

Although the median age at diagnosis is 61, melanoma is the most common cancer in women younger than 39 years and is second only to breast cancer.[1] As of 2009, the most rapid increases in melanoma occurrence are among young white women (3% annual increase since 1992 in those between 15 and 39 years of age) and older white men (5.1% annual increase since 1975 in those 65 and older).[1]

Melanoma is one of the most costly cancers to diagnose, follow, and treat, with care for a patient with stage IV melanoma estimated to cost approximately $11,500 per month.[6] There is a significant cost decrement when melanoma is diagnosed at an earlier stage, with a late-stage lesion being approximately 2200% more expensive to diagnose and treat than an early in situ melanoma and 1000% more expensive than a stage I tumor.[7]

Treatments for melanoma range from surgical excision (stage I) to adjuvant treatment with interferon, chemotherapy, radiation therapy, and, at times palliative surgery, at more diffuse stages.[8]  Ipilimumab and vemurafenib are two newer  FDA-approved drugs that may extend survival rates.[1]

Who’s at Risk?

Two major contributing factors place patients at high risk of developing melanoma. The first is prolonged exposure to UV radiation, which is estimated to cause 30% of malignant melanomas.[10] In addition to sun exposure, however, other factors also confer a high risk. These include a fair complexion, excessive childhood sun exposure and blistering childhood sunburns, a family history of melanoma, the presence of a changing mole or evolving lesion on the skin, and, importantly, older age (Box 1).[11,12]

Compared with any other age group, patients older than 65 are more likely to be diagnosed with, and to die from, melanoma. Therefore, elderly patients should be targeted for melanoma prevention, as treatment options in this age group are often limited because of comorbid medical conditions, an inability to tolerate adverse medication effects or toxicity, and the increased likelihood of drug interactions.[13,14]

The Importance of Screening

Melanoma is classified using the American Joint Committee’s TNM system: “T” stands for tumor; “N” for the cancer has spread to the lymph nodes; and “M” for metastasized to distant organs.  The T rating also has numbers (0-4) to describe the tumor’s thickness. The N rating also assigns numbers (0-3) based on if the cells have spread to any lymph nodes or are in the lymphatic channels.[15] This helps the cancer care team determine the patient’s prognosis more accurately.  The good news is that when melanoma is detected and treated in its early stages, the chances for long-term, disease-free survival are excellent. But if left untreated, melanoma is much more likely than basal or squamous cell cancer to metastasize and can be very difficult to treat.

Approximately 40% of medical office visits in the United States are to a family clinician or internist,[16] so primary care practitioners (PCPs) are in a unique position to perform cancer screenings and to provide prevention counseling. Encouragingly, PCPs do find most melanomas at an early stage, although not quite as often or as accurately as dermatologists.[17] Unfortunately, the rate of skin examinations in primary care falls far behind screening for breast, cervical, and colorectal cancer.[16]

In 1985, the acronym ABCD was released as a tool to help both nondermatologists and the public identify the characteristics of early, superficial melanomas.[19] In the years since 1985, the ABCD acronym has changed to ABCDE (Box 2).[19] Since their introduction, some debate has emerged over the chosen criteria; however, they are still strongly supported by the literature.[20] You may find it helpful to go over these criteria with your higher-risk patients as you perform a skin examination and encourage them to look for the “ABCDE” at home between visits. See How to Perform a Skin Self-Exam.

Prevention

The American Cancer Society continues to state that aside from a full-body examination, the best melanoma prevention tools are sun protection and sun avoidance. However, according to data published by St. Louis University, less than one-third of people routinely use sun protection.[20] Emphasize to patients the importance of avoiding unprotected exposure to the sun and other sources of UV light, such as sunlamps and tanning beds. Stress the importance of “Slip! Slop! Slap! Wrap!”—a catch phrase reminding them to “slip on a shirt, slop on sunscreen, slap on a hat, and wrap on sunglasses.” The Skin Cancer Foundation recommends using a sunscreen with an SPF 15 or higher as one important part of a complete sun protection regimen. Sunscreen alone is not enough, however (Box 3).[21] See Facts About Sunscreens.

In addition to ABCDE screening, patient education is key to decreasing the morbidity and mortality associated with melanoma. Data suggest that when PCPs provide patients with photos of suspicious lesions, show them what to look for at home, and offer written guidelines for avoiding excess sun exposure, patients are more likely to examine their skin at home and practice sun-protective behavior.[22] And it’s important to start the message early. By 20 years of age, people have experienced more than half of their lifetime of sun exposure. Try placing posters and handouts [Free Materials Link] in the waiting and examination rooms and distributing these tools as patients leave the office. Run a sun-safety video in the waiting room. Use the outdoor activities of a particular season as an opportunity to reinforce the message (skiing, walking, swimming). Your staff can help you reach a large number of patients in this way, leaving you to focus on the patients who are at particularly high risk.

Higher-risk patients can also be referred to genetic counseling and/or screening. According to guidelines published in 2009, families or individuals with a hereditary pattern of melanoma should see a genetics counselor.[23] Such patients might also wish to be tested for mutations of cyclin-dependent kinase inhibitor 2A (CDKN2A). Up to 40% of patients with hereditary melanoma have CDKN2A mutations, which are also associated with an increased risk for pancreatic cancer. The indicators of a hereditary pattern are 3 or more primary melanomas, or at least 1 case of melanoma and 2 or more other diagnoses of melanoma and/or pancreatic cancer among first- or second-degree relatives on the same side of the family.

The Conundrum

Many of your patients already practice good sun protection when they swim, golf, or sit out on the deck. But how can you reinforce these practices when patients come to you with questions about the link between vitamin D, sunshine, and disease prevention? While it’s too early to draw any definitive conclusions, adequate amounts of vitamin D do appear to be associated with the prevention of certain cancers and heart disease. Unfortunately, data from the National Health and Nutrition Examination Survey (NHANES) showed that at least 40% of men and women in the United States have lower-than-optimal levels of vitamin D for at least part of the year.[24] As vitamin D is partially activated when the sun’s UV rays help convert cholesterol compounds in the skin to active vitamin D, it seems intuitive that the more time patients spend exposed to UV light, the more vitamin D they’ll produce! However, as vitamin D synthesis is dependent on geography, season of the year, and skin color, prolonged sun exposure may never produce sufficient vitamin D. In fact, North Americans who live north of 42 degrees latitude—which would include Boston, Seattle, and Milwaukee—don’t ever absorb enough UVB to produce vitamin D, regardless of how much time they spend outdoors.[25] But if they are high-risk for melanoma, they could absorb enough UVB to add to the melanoma burden.

When it comes to sun exposure and vitamin D, there is a very fine line between enough sun and too much sun. People should be encouraged to get outside and be active as long as they recognize the dangers of overexposure to the sun. The American Academy of Dermatology is emphatic in its advice that everyone avoids unprotected sun exposure and obtains their vitamin D from foods and supplements.[26] The Office of Dietary Supplements at the National Institutes of Health concurs,[27] as does the American Cancer Society.[28] You might emphasize to patients that while prolonged exposure to UV light is one [albeit dangerous] way to obtain vitamin D, there is a better and safer route. Try reminding them that in the United States, there are no seasonal or geographic limitations on natural and fortified food sources of vitamin D, which include salmon, mackerel, and other fish; fish oils; and egg yolks, as well as fortified milk, cereals, and juices.

Patients who insist on sunbathing for aesthetic purposes may be more difficult to sway. While expecting patients to willingly give up all recreational sun exposure is draconian and unrealistic, perhaps you can strike a compromise that balances their need for tanning with a liberal dose of common sense—and sunscreen!

Jill Shuman, MS, ELS
Updated on May 8, 2012
Published on May 10, 2010

References

1. American Cancer Society. Cancer Facts and Figures 2012. Atlanta: American Cancer Society. http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/documents/document/ acspc-031941.pdf. Accessed May 7, 2012.
2. Whiteman DC, Watt P, Purdie DM, et al. Melanocytic nevi, solar keratoses, and divergent pathways to cutaneous melanoma. J Natl Cancer Inst. 2003;95(11):806-812.
3. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2009. CA Cancer J Clin. 2009;59(4):225-249.
4. Cockburn M, Swetter SM, Peng D, et al. Melanoma underreporting: why does it happen, how big is the problem, and how do we fix it? J Am Acad Dermatol. 2008;59(6):1081-1085.
5. Hu S, Sora-Vento RM, Parker DF, Kirsner RS. Comparison of stage at diagnosis of melanoma among Hispanic, Black, and White Patients in Miami-Dade County, Florida. Arch Derm. 2006;142:704-708.
6. Davis KL, Mitra D, Kotapati S, et al. Direct economic burden of high-risk and metastatic melanoma in the elderly: evidence from the SEER-Medicare linked database. Appl Health Econ Health Policy. 2009;7(1):31-41.
7. Alexandrescu DT. Melanoma costs: a dynamic model comparing estimated overall costs of various clinical stages. Dermatol Online J. 2009;15(11):1.
8. Melanoma skin cancer. American Cancer Society Website. http://www.cancer.org/Cancer/SkinCancer-Melanoma/DetailedGuide/melanoma-skin-cancer-treating-by-stage.  Updated January 11, 2012. Accessed May 7, 2012.
9. Triesman J, Garlie N. Systemic therapy for cutaneous melanoma. Clin Plast Surg. 2010;37(1):127-146.
10. Torrens R, Swan BA. Promoting prevention and early recognition of malignant melanoma. Dermatol Nurs. 2009; 21(3):115-122.
11. Cho YR, Chiang MP. Epidemiology, staging (new system), and prognosis of cutaneous melanoma. Clin Plast Surg. 2009;37(1):47-53.
12. Amercian Cancer Society. Why you should know about Melanoma.
    http://www.cancer.org/acs/groups/content/documents/document/acspc-024621.pdf. Updated July 2008. Accessed May 7, 2012.
13. Geller AC, Miller DR, Annas GD, et al. Melanoma incidence and mortality among US whites, 1969-1999. JAMA. 2002;288(14):1719-1720.
14. Swetter SM, Geller AC, Kirkwood JM. Melanoma in the older person. Oncology (Williston Park). 2004;18(9):1187-1196.
15. Detailed Guide: Skin Cancer – Melanoma: How is melanoma staged? American Cancer Society Web site. http://www.cancer.org/Cancer/SkinCancer-Melanoma/DetailedGuide/melanoma-skin-cancer-staging. Updated January 11, 2012. Accessed May 7, 2012.
16. Geller AC, O’Riordan DL, Oliveria SA, et al. Overcoming obstacles to skin cancer examinations and prevention counseling for high-risk patients: results of a national survey of primary care physicians. J Am Board Fam Pract. 2004;17(6):416-423.
17. Chen SC, Pennie ML, Kolm P, et al. Diagnosis and managing cutaneous pigmented lesions: primary care physicians versus dermatologists. J Gen Int Med. 2006;21:678-682.
18. Friedman RJ, Rigel DS, Kopf AW. Early detection of malignant melanoma: the role of physician examination and self-examination of the skin. CA Cancer J Clin. 1985;35(3):130-151.
19. Abbasi NR, Shaw HM, Rigel DS, et al. Early diagnosis of cutaneous melanoma: revisiting the ABCD criteria. JAMA. 2004;292(22):2771-2776.
20. Sun Protection Outreach Teaching by Students. Statistics and facts on skin cancer. St. Louis University School of Medicine Web site. http://dermatology.slu.edu/spots/files/SPOTS%20Manual%203%20Statistics.pdf. Accessed May 7, 2012.
21. Prevention Guidelines. Skin Cancer Foundation Web site. http://www.skincancer.org/prevention-guidelines.html. Accessed May 7, 2012.
22. Hay JL, Oliveria SA, Dusza SW, et al. Psychosocial mediators of a nurse intervention to increase skin self-examination in patients at high risk for melanoma. Cancer Epidemiol Biomarkers Prev. 2006;15(6), 1212-1215.
23. Leachman SA, Carucci J, Kohlmann W, et al. Selection criteria for genetic assessment of patients with familial melanoma. J Am Acad Dermatol. 2009;61(4):677.e1-e14.
24. Looker AC, Dawson-Hughes B, Calvo MS, et al. Serum 25-hydroxyvitamin D status of adolescents and adults in two seasonal subpopulations from J Am Acad Dermatol NHANES III. Bone. 2002;30(5):771-777.
25. Cranney C, Horsely T, O’Donnell S, et al. Effectiveness and safety of vitamin D in Relation to Bone Health. Evidence Report/Technology Assessment No. 158 prepared by the University of Ottawa Evidence-based Practice Center under Contract No. 290-02.0021. AHRQ Publication No. 07-E013. Rockville, MD: Agency for Healthcare Research and Quality, 2007.
26. Position statement on Vitamin D. American Academy of Dermatology and AAD Association. http://www.aad.org/forms/policies/uploads/ps/ps-vitamin%20d.pdf. Updated November 14, 2009. Accessed May 7, 2012.
27. Dietary Supplement Fact Sheet: Vitamin D. Office of Dietary Supplements Website. http://dietary-supplements.info.nih.gov/factsheets/vitamind.asp#en5. Accessed May 7, 2012.
28. Common questions about diet and cancer. American Cancer Society Website. http://www.cancer.org/docroot/PED/content/PED_3_2X_Common_Questions_About_ Diet_and_Cancer.asp. Updated January 11, 2012. Accessed May 7, 2012.

What Is Healthy?

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In a recent article we asked, “Do you routinely take time to ‘take care of you’?” Most said you do “take care of you” (71%), with just over one-fourth saying you did not. One of you asked a very interesting question, “What does that entail?”

What a smart question.  What does ‘taking care of you’ actually mean?   What does it mean to be healthy?

Over half a century ago, the World Health Organization defined health as “a complete state of physical, mental, and social well-being, and not merely the absence of disease or infirmity.”[1] These three areas of health create the health triangle.

Physical Health

Your physical health is determined by sleep, the amount of exercise you get, eating right, and even oral hygiene. Your habits are also considered when it comes to your physical health: Do you exercise regularly? Do you drink or smoke? What are your habits concerning drugs? Do you get regular check-ups with a clinician?

Mental Health

Your mental health helps you handle the stresses of your daily routine, keeping you generally cheerful and optimistic. When you think clearly, you make better judgment calls. Are you controlling your stress and/or anxiety? Do you have hobbies? Do you know how to relax?

Social Health

Finally, your social health. You work longer hours than the average person, but it’s still important that you have a healthy social life. This means you can form positive and supportive relationships with your peers. Do you take time to see your friends and/or family? Do you participate in civic or professional organizations? For many, this also includes their spiritual health.

Health Triangle

Each segment of the health triangle is dependent on the other two. Without a healthy social life, you can get depressed. This can affect your mental health, which can then upset your physical health (eg, lack of sleep, indulging in bad habits). Or you could overindulge in your social life, often out partying and staying out late. This can lead to lack of sleep—and the cycle goes on. When all segments of the health triangle are in sync, you’re taking care of yourself and your health.  However, just one weak link in the triangle compromises the other two.

Published May 3, 2012

Reference

1. World Health Organization. Preamble to the Constitution of the World Health Organization as adopted by the Internal Health Conference, New York, June 19-22, 1946, and entered into force on April 7, 1948.

New Guidelines for Preventing Migraine

Preventive treatment of migraine is the focus of updated guidelines[1,2] co-published by the American Academy of Neurology (AAN) and the American Headache Society. According to data presented at the 64th Annual Meeting of the AAN, few people with migraine use preventive treatment—although many different preventive strategies are available. The AAN last updated its prevention guidelines in 2000. According to the AAN, migraines led to more than 3 million emergency room visits in the United States in 2008 (the last date for which data are available).

Migraine is a common type of headache that typically occurs with symptoms such as nausea, vomiting, or sensitivity to light. The classic migraine episode is characterized by unilateral head pain preceded by various visual, sensory, or motor symptoms, collectively known as an aura. A migraine is caused by abnormal brain activity, which can be triggered by a number of factors; however, the exact chain of events remains unclear. Today, most neurologists believe the attack begins in the brain and involves nerve pathways and chemicals. The changes affect blood flow in the brain and surrounding tissues.

In the current International Headache Society (IHS) categorization, the headache previously described as classic migraine is now known as migraine with aura, and that described as common migraine is now termed migraine without aura.[3] Migraines without aura are the most common, accounting for more than 80% of all migraines. Migraine headaches tend to first appear between the ages of 10 and 45, although they may begin later in life. In addition,

• Migraines occur much more often in women than men
• Some women, but not all, may have fewer migraines when they are pregnant
• The incidence and disability of migraine may decrease once women are postmenopausal
• Family history seems to be a strong risk factor for migraine.  There is a 75% risk of developing migraine if both parents suffer from migraine[4]

Alcohol, stress, anxiety, certain odors or perfumes, loud noises, bright lights, and smoking may trigger a migraine. Migraine attacks may also be triggered by

• Caffeine withdrawal
• Changes in hormone levels during a woman’s menstrual cycle or with the use of birth control pills
• Changes in sleep patterns
• Exercise or other physical stress
• Missed meals
• Smoking or exposure to smoke
• Sensory stimuli, such as bright lights, sun glare, and loud sounds

Migraines can be triggered by certain foods, including

• Processed, fermented, pickled, or marinated foods, as well as foods that contain monosodium glutamate (MSG) and nitrates (bacon, hot dogs, salami, cured meats)
• Baked goods, nuts, peanut butter, and dairy products (chocolate was once thought to be a trigger, but studies are showing it might actually be used as a treatment)[5]
• Foods containing tyramine, which includes red wine, aged cheese, smoked fish, chicken livers, figs, and certain beans
• Produce (avocado, banana, citrus fruit, and onions)

Preventing Migraine

According to data cited in the newly published guidelines,[1,2] migraine is both underrecognized and undertreated. Data also cited that almost 40% of people who suffer from migraine could benefit from preventive treatment, although only 12% actually take a preventive treatment.[6]

Unlike acute treatments, which are used to relieve the pain and associated symptoms of a migraine attack when it occurs, preventive treatments are typically taken every day to prevent attacks from occurring and to lessen their severity and duration when they do occur. Some studies show that migraine attacks can be reduced by more than half with preventive treatments.

The guidelines reviewed all available evidence on migraine prevention. The review did not address the magnitude of any given drug’s efficacy—only the strength of evidence backing their superiority relative to placebo. Among prescription drugs, three seizure drugs (divalproex sodium, sodium valproate, and topiramate) and three beta-blockers (metoprolol, propranolol, and timolol) were effective for migraine prevention and should be offered to people with migraine to reduce the frequency and severity of attacks. Frovatriptan, a serotonin receptor agonist, was found to be effective in the prevention of menstrual migraines. Of note is that the seizure drug lamotrigine was found to be ineffective in preventing migraine.

The guidelines also reviewed over-the-counter treatments and complementary treatments. The top “effective” treatment for preventing migraine was the herbal preparation Petasites (butterbur). Other treatments found to be “probably effective” are the nonsteroidal anti-inflammatory drugs (fenoprofen, ibuprofen, ketoprofen, naproxen, and naproxen sodium), subcutaneous histamine, and complementary treatments: magnesium, MIG-99 (feverfew), and riboflavin.

While no prescription is required for over-the-counter and complementary treatments, patients still should see a healthcare provider regularly for follow-up. Because migraines can get better or worse over time, patients should discuss these changes in the pattern of attacks with their doctors and see whether they need to adjust their dose or even stop their medication or switch to a different medication. In addition, people need to keep in mind that all drugs, including over-the-counter drugs and complementary treatments, can have side effects or interact with other medications, which should be monitored.

Jill Shuman, MS, ELS
Published May 2, 2012

Reference

1. Silberstein SD, Holland S, Freitag F, et al. Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults. Neurology. 2012;78:1337-1345.
2. Holland S, Silberstein SD, Freitag F, et al. Evidence-based guideline update: NSAIDs and other complementary treatments for episodic migraine prevention in adults. Neurology. 2012;78:1346-1353.
3. International Headache Society. The International Classification of Headache Disorders, 2nd edition. Cephalalgia. 2004;24(Suppl 1):1-160.
4. Evans RW. Headaches during childhood and adolescence. In: Evans RW, Mathew NT, eds. Handbook of Headache. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:210.
5. Cady RJ, Durham PL. Cocoa-enriched diets enhance expression of phosphatases and decrease expression of inflammatory molecules in trigeminal ganglion neurons. Brain Res. 2010;1323:18-32.
6. Lipton RB, Bigal ME, Diamond M, et al; American Migraine Prevalence and Prevention Advisory Group. Migraine prevalence, disease burden, and the need for preventive therapy. Neurology. 2007;68(5):343-349.

Measles Cases on the Rise

As the result of high immunization rates with the measles, mumps, and rubella (MMR) vaccine since 1996, measles was officially eliminated in the United States in 2000. However, the disease is less well controlled in the rest of the world. With travel in and out of the United States so easy and common, the number of measles cases reported in the U.S. has slowly started to increase.

According to a new report from the Centers for Disease Control and Prevention (CDC),[1] in 2011 the U.S. saw its highest number of confirmed measles cases in over a decade, with 222 cases and 17 outbreaks. In comparison, from 2001 to 2010, the median was 60 cases and 4 outbreaks annually. Of the 222 cases, 196 occurred in U.S. residents with a median age of 14. Among all of the cases, 90% were imported from other countries, including 26% of people returning to the U.S. from abroad and 10% from foreign visitors. The country that imported the most cases of measles was India (16), followed by France (13), and the Philippines (6). Among a country cluster, Europe was the source of the most cases (33). Seventy of the patients with measles (32%) were hospitalized for diarrhea, dehydration, or pneumonia; no cases of encephalitis or deaths were reported.

Almost 90% of patients were unvaccinated or had an unknown vaccination status, although 85% of them were eligible the MMR vaccine. Among the 66 patients unvaccinated between the ages of 16 months to 19 years, 76% of them had not received the vaccine because of a philosophic, religious, or personal objection.

The increase in measles importations and outbreaks during 2011 serves as a reminder that measles remains endemic in many parts of the world and unvaccinated U.S. residents continue to place themselves and others in their communities at risk for measles and its complications. A drop in MMR vaccination coverage in a community can increase the risk for large sustained measles outbreaks, as experienced recently in Canada and France,[2,3] or reestablishment of endemic transmission, as experienced in the United Kingdom.[4]

The CDC reminds you to

• Suspect measles in patients presenting with febrile rash illness and cough, coryza, or conjunctivitis and who’ve recently traveled internationally or who’ve had close contact with international travelers
• Use isolation measures immediately and report suspected cases to local health departments
• Remind patients who plan to travel internationally of the increased risk for measles and potential exposures during bus, train, air travel, and at large international events or gatherings (eg, Euro 2012 and the 2012 Summer Olympics) and of the importance of vaccination
• Ensure all eligible children and adults are appropriately vaccinated as follows:
• Children: one dose at 12 months; second dose at 4-6 years
• Adults without evidence of measles immunity: one dose
• Unvaccinated healthcare personnel, international travelers, students attending college outside of the United States: two doses
• Anyone older than 6 months who will be traveling outside of the U.S. and is eligible to receive the MMR vaccine should be vaccinated before travel
• Children older than 1 year should receive two doses of MMR separated by at least 28 days prior to travel

Jill Shuman, MS, ELS
Published May 1, 2012

References

1. Centers for Disease Control and Prevention. Measles-United States, 2011. MMWR Morb Mortal Wkly Rep. 2012;61:253-257.
2. European Centre for Disease Prevention and Control. Surveillance report: European monthly measles monitoring, 21 February 2012. Stockholm, Sweden: European Centre for Disease Prevention and Control; 2012. http://ecdc.europa.eu/en/publications/publications/sur_emmo_european-monthly-measles-monitoring-february-2012.pdf . Accessed April 6, 2012.
3. Measles. Ministere de Santé et Services sociaux Quebec Website.  http://www.msss.gouv.qc.ca/en/sujets/prob_sante/measles/measles.php. Published 2012. Accessed April 6, 2012.
4. Measles once again endemic in the United Kingdom. Euro Surveill. 2008;13(27):pii: 18919.

When Patients Lose Their Patience, You Lose, Too!

Dr. Edward Cartwright* has practiced medicine as a solo practitioner in a northern Boston suburb since 1980. The practice generated a comfortable income and after 25 years he was now caring for the children and grandchildren of his original patients. He was active in the community, well-liked among his peers, and still made house calls on occasion. His days were full and he was seeing 15 to 20 patients per day, four days a week. He used an off-site billing service and delegated all management, personnel, and front-of-the-house matters to his long-time office manager, rarely venturing into the front office area for more than a cup of coffee.

In July 2008, Dr. Cartwright noticed that his Fridays were much slower than usual. Chalking it up to summertime in New England, he didn’t really pay much attention. In March 2009, he was notified by the billing service that his insurance receipts for the past 60 days were down by almost 12%. In April, he learned that he had seen 28% fewer patients over the past 90 days compared with the previous year. In November, his billing service reported that they were having trouble collecting payments from self-pay patients who had previously always paid their bills on time. In December, his total number of patient visits was down by 29% compared with the previous year. When reviewing his tax return for the year, he made a mental note that the practice had employed five different medical receptionists during the year.

Situation Critical

Dr. Cartwright spent the weeks before Christmas 2009 desperately trying to work out why his practice was suddenly disintegrating. He couldn’t attribute it to any difference in how he cared for patients or to the office’s physical environment. They had recently installed a new handicapped ramp and updated their waiting room. Patients rarely had to wait more than 15 minutes once they checked in and their prescriptions were electronically submitted in a timely manner.

So what was wrong?

Cartwright’s ‘EUREKA! ’ moment came two days before Christmas. “I bumped into a long-time patient in the supermarket parking lot. I realized that I hadn’t seen her in many months and that she was long overdue for a visit. When I commented that I hadn’t seen her in a very long time, she looked down at the ground and mumbled something. I pleaded with her to tell me what was wrong. She looked me straight in the eye and said, “Your office made me cry.”

That statement was the clue he needed to resuscitate his practice. His first act was to come up with a list of five long-time patients who had not been in for more than nine months. He called each patient himself and asked why he or she had stopped coming for care. Each one alluded to an encounter with the office staff. One woman had been called by the office and told that if she didn’t change her appointment from Tuesday to Friday, “the doctor would never see me again.” While waiting for his appointment, an elderly gentleman was denied access to the restroom because “I’d be late to see the doctor.” Cartwright was appalled and asked patients why they hadn’t said anything, given the 20-plus-year length of their relationships. One by one he was told some version of “I thought you had made new rules and the staff was just doing what you wanted.”

Armed with this information, Dr. Cartwright decided to do some sleuthing. He began making random checks in the reception area, watching as patients were greeted and checked in. He also listened to the tone and content of telephone conversations.

This is what Cartwright witnessed over the course of a week: patients were turned away if they forgot their insurance cards; if they wanted to change an appointment, they were threatened with cancellation fees; the phone often went unanswered; people were yelled at in the waiting room; and numerous HIPAA violations occurred as patient information was shared among the staff in full view and earshot of patients in the reception area.

The Root of the Problem

It didn’t take long to identify several key administrative issues. “Once I actually began to pay attention, it became very clear that the source of the downward spiral was the bizarre behavior of my long-time office manager.”

The core of the problem lay with Joan*, the office manager, who had been with the practice for 16 years. In early 2008, and unbeknownst to Cartwright, Joan had opened her home to her daughter and three granddaughters, who were fleeing an abusive home situation. Many nights, Joan’s abusive son-in-law would try to enter the home, forcing a police confrontation. At other times, the son-in-law would call Cartwright’s office and demand to speak to Joan. Joan was stressed out, afraid, and sleep deprived.

Needing the income, she continued to come to work every day. But her multiple stresses and lack of sleep led to a cascade of abusive behaviors. First, she stopped answering the office telephone and instructed the receptionist to just “let voice mail pick it up. We’ll call them back.” If an employee questioned the wisdom of this or threatened to tell Cartwright, the employee was fired. Joan seemed particularly disdainful of older patients, showing no patience or empathy when they fumbled or required help with an insurance form.

Once Dr. Cartwright was able to identify the problem, he set out to address the issues very quickly. He offered Joan an open-ended leave of absence and put her in touch with a social worker from the hospital who helped her obtain the resources she needed to cope with her family situation. He promoted the medical receptionist—a warm and friendly young woman—to temporary office manager and went to work personally reaching out to patients who had been hurt or dissatisfied by the treatment they had received.

The Warning Signs

A variety of issues cause patients to electively change doctors. According to Bill Bristow, a partner with Doctors Management in Knoxville, Tennessee, the reasons rarely have to do with quality of care. “It’s more about the rude staff and the inability to reach the office or get on the schedule,” Bristow says. “If you start to see a pattern in why patients are leaving your practice, you have to look at it.”

Cartwright learned his lesson the hard way. He’s gradually rebuilding the goodwill of his patients with an outreach program that includes personal calls, letter correspondence, and newspaper advertisements featuring photos of his new warm and caring staff. He estimates it’s taken about two years to regain just about half of the patients who had left. But his real goal is to make sure nothing like this ever happens again. “Instead of staying in my ivory tower treating patients and recording my notes, I make time every day to visit with patients in the reception area, do a sweep of the front office, and make sure that the phone is answered professionally by the third ring.” He’s right to be concerned about the phone calls. In a 2010 survey of 2.7 million patients, patients continue to voice frustrations over the ease of scheduling appointments, the helpfulness of telephone staff and the promptness in return calls.[1]

In some ways, Dr. Cartwright was fortunate. A chance encounter with a long-time patient gave him enough information to fix his practice before it ran itself into the ground. Looking back, he realizes that there were plenty of early signs that something was wrong.

1. Changes to a long-standing schedule. Cartwright’s Friday schedule during the summer was light. This was a departure from practice, and any ongoing change to a long-standing schedule should raise a red flag. To hide the fact that patients were leaving the practice, Joan packed the schedule early in the week, blaming the summer and the approaching weekend for the lighter Fridays.
2. Changes in self-pay billing patterns. When patients don’t pay their bills, it’s sometimes a signal that they were not happy with their care. It’s surprising how often the reason that patients aren’t paying is because they are angry – angry about the way they were treated on the phone or something the receptionist said. For these patients, not paying the bill may be their last chance to express their displeasure.
3. Decreasing patient census. You need to sit up and take note if the number of patients you see continues to decline over more than a 90-day period. In fact, you need to jolt up and ask a resounding, “why?”
4. Excessive employee turnover. Five medical receptionists in one year? In this case, Joan was so intent on covering her tracks that she resorted to employee bullying and drove out five excellent motivated employees. This was corroborated by subsequent phone calls from Dr. Cartwright. “One former employee told me that she loved the patients and really enjoyed her job, but just couldn’t take Joan’s constant harassment and irrational behavior.”

Cartwright notes, “Intellectually, I know that some patients will never be happy, no matter how competent, efficient, and agreeable we are. And I recognize that those patients will probably leave, no matter we do. My goal now is to make sure I know when a patient leaves, and why. I can learn from our mistakes, but only if I’m aware of them.”

* Names have been changed.

Jill Shuman, MS, ELS
Published April 30, 2012

Reference

1. Berry E. Is your telephone hurting your practice? Phone do’s and don’ts. American Medical News Website. http://www.ama-assn.org/amednews/2011/03/07/bisa0307.htm. Posted March 7, 2011. Accessed April 28, 2012.

New Patient-centric Guidelines for Type 2 Diabetes

After several years of planning, discussion, and review, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) have published a new position statement for managing elevated blood glucose levels in people with type 2 diabetes.[1] Neither ADA nor EASD had previously published an official position statement on this topic, instead providing a consensus treatment-based algorithm developed jointly by both groups.

The new guidelines are less rigid than those recommended in the treatment algorithm, and call for a more patient-centered approach that allows for individual patient needs, preferences, and tolerances, and takes into account differences in age and disease progression. The need for a joint task force to review and revise the guidelines was driven by the complex and sometimes controversial nature of the agents used to manage glycemic control in patients with type 2 diabetes, the increasing array of pharmacologic agents now available and mounting concerns about their potential adverse effects, and new uncertainties regarding the benefits of intensive glycemic control on macrovascular complications among certain populations.

The position statement calls for providing all patients with diabetes education in either an individual or group setting that focuses on dietary intervention and the importance of increased physical activity, and when appropriate, weight management. The guidelines also encourage the development of individualized treatment plans built around a patient’s specific symptoms, comorbidities, age, weight, racial/ethnic/gender differences, and lifestyles.

Key points include

• Glycemic targets and glucose-lowering treatments should be tailored to the individual patient
• Diet, physical activity, and education remain the foundation of all diabetes treatment programs
• Metformin should be the first-line medical treatment, unless otherwise contraindicated
• Data are limited regarding treatment beyond metformin, but combination therapy with additional oral or injectable agents is reasonable and expected
• HbA1c goal has been raised to 7%, with some individualization based on age, comorbidities, and patient motivation
• A major treatment goal must be comprehensive cardiovascular risk reduction

In accompanying interviews, Dr. Vivian Fonseca, president for medicine and science of the ADA, says that patient-centered care better reflects the reality of what happens when a patient seeks diabetes treatment. Because there is such a wide range of pharmacologic choices (and conflicting data about some of those choices)—as well as differences in how patients respond to medications—it is difficult to prescribe a single treatment regimen based on an algorithm that is designed to work for everyone. “Diabetes is a complex disease that manifests differently in different people and the best way for one person to manage it may not work for someone else. If we encourage people to work with their healthcare providers to find an individualized personal plan that works well for them and fits their lifestyle and personal needs, it has a higher chance for success in controlling glucose and decreasing the risk of long term complications.”

These guidelines may generate debate among researchers in the field. Some researchers believe that an algorithm-based management plan will provide more consistent treatment guidelines for providers, while others feel that treatment should be based on an individual patient’s pathophysiology. But in an official statement published by ADA and EASD, the editor of Diabetes Care comments, “The most attractive aspect of the new position statement is that more than any other previously reported guidelines to date, it clearly emphasizes that ‘one size clearly does not fit all.’”

Jill Shuman, MS, ELS
Published April 24, 2012

Reference

1. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient-centered approach [published online ahead of print April 19, 2012]. Diabetes Care. doi: 10.2337/dc12-0413. http://care.diabetesjournals.org/content/early/2012/04/17/dc12-0413.short