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Basal cell carcinoma

Basal cell carcinoma (BCC) is the most common skin cancer. It can be destructive and disfiguring. Risk is increased for individuals with a family history of the disease and a high cumulative exposure to UV light via sunlight or, in the past, carcinogenic chemicals especially arsenic. Treatment is with surgery, topical chemotherapy, x-ray, cryosurgery, photodynamic therapy, or topical immune enhancement drugs such as imiquimod. It is rarely life-threatening but if left untreated can be disfiguring, cause bleeding and produce local destruction (eg., eye, ear, nose, lip). more...

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Forms

Various forms are recognised:

  • Nodular: flesh-colored papule with telangiectasis. If it ulcerates, it becomes a "rodent ulcer" (ulcus rodens), an ulcerating nodule with (often) a pearly border.
  • Cystic: rarer and hard to distinguish from the nodular form. It has a central cavity with fluid.
  • Pigmented: a variant of the nodular form that may be confused with melanoma.
  • Sclerosing/cicratising: a scar-like lesion.
  • Superficial: a red scaling patch

About two thirds of the carcinomas occur in sun-exposed areas and onw third occur in non-sun-exposed areas, emphasizing the genetic susceptability of the basal cell cancer patients.

Diagnosis

To diagnose, a biopsy (where tissue is taken for pathological study) is done using local anesthesia. In small lesions, the tumor is generally removed in its entiriety, while larger ones are biopsied first and surgically removed later if it is confirmed that it is malignant.

Histopathology: Basal cell carcinoma is a malignant epithelial tumor arising only in skin, from the basal layer of the epidermis or of the pilosebaceous adnexa. Tumor is represented by compact areas, well delineated and invading the dermis, apparent with no connection with the epidermis. Tumor cells resemble normal basal cells (small, monomorphous) are disposed in palisade at the periphery of the tumor nests, but are spindle-shaped and irregular in the middle. Tumor clusters are separated by a reduced stroma with inflammatory infiltrate. 1

Pathophysiology

Basal cell carcinomas develop in the basal cell layer of the skin. Sunlight exposure leads to DNA crosslinking between thymidine residues. While DNA repair removes most UV-induced damage, not all crosslinks are excised. There is, therefore, cumulative DNA damage leading to mutations. Apart from the mutagenesis, sunlight depresses the local immune system, possibly decreasing immune surveillance for new tumor cells.

Prevention & Early Diagnosis

Basal cell carcinoma is the most common skin cancer. It occurs mainly in fair-skinned patients with a family history of this cancer. Sunlight is a factor in about two thirds of these cancers, but one third occur in non sun-exposed areas. Therefore, dermatologists recommend sun screens and annual skin cancer exams to prevent or provide early detection of this common tumor.

Treatment

Most basal cell carcinomas are removed surgically by dermasurgeons. A common method is "electrodessication and curettage" (ED&C). This is done by scraping the tumor out with a curette and cauterizing the base and margins. The wound is left to heal by itself (secondary intention healing). The cure rate and cosmetic result are excellent, especially in concave areas. It is also the most cost effective treatment. Surgical excision by the dermasurgeon is another option with the margins of excised tissue examined under the microscope. Certain types, like the sclerosing basal cell cancers may need a wider margin, as they develop subtle processes that project outside the visible part of the tumor.

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Diagnosis and treatment of basal cell and squamous cell carcinomas
From American Family Physician, 10/15/04 by Daniel Stulberg

The incidence of basal cell and squamous cell carcinomas, which also are called nonmelanoma skin cancer, has been increasing steadily over the past 30 years. (1,2) The reasons for this increase appear to be largely sociologic and include increasing amounts of sun exposure and use of artificial tanning beds. Primary care physicians can expect to diagnose six to seven cases of basal cell carcinoma and one to two cases of squamous cell carcinoma each year. (3) The major risk factor for the development of skin cancer is exposure to ultraviolet (UV) radiation. In addition, ozone depletion may increase UV radiation exposure and thus increase rates of skin cancer, (4,5) but other factors also increase risks (Table 1).

Natural History

Basal cell and squamous cell carcinomas develop within the epidermis (Figure 1). Basal cell carcinomas are derived from the basal layer of keratinocytes, which is the deepest cell layer of the epidermis. Squamous cell carcinomas arise from the more superficial layers of keratinocytes. Keratinocyte damage is a response to repeated exposure to UV radiation, occurring especially in susceptible persons. One study (6) found that a single tanning session was enough to damage DNA in keratinocytes. The damage results in actinic keratoses, solar lentigo, and dermatoheliosis (i.e., "photoaging"). (7)

[FIGURE 1 OMITTED]

Although not universally accepted at this time, a growing body of evidence suggests that actinic keratoses should be regarded as very early squamous cell carcinomas, based on the pathology of actinic keratoses. (8-11) These lesions can progress to carcinoma in situ and then to invasive cancer. Although metastasis is rare in basal cell carcinoma, local tissue effects can be destructive and disfiguring. Squamous cell carcinomas metastasize about 3 to 4 percent of the time. (12)

A small percentage of squamous cell carcinomas do not follow the above "natural history." Skin cancers may arise in skin wounds, and immunosuppressed persons may have a higher incidence of cancer in general. (13) Genetic syndromes in which there is a defective mechanism for the repair of damaged DNA (e.g., xeroderma pigmentosum) can put patients at increased risk. Such cancers, arising atypically, often have a higher incidence of metastasis.

Prevention

The most important aspect of skin cancer management is prevention. Sun should be avoided during midday hours, when UV intensity is greatest. During exposure, sunscreen and protective clothing should be employed. Sunscreen should be applied generously in quantity and frequency. Many sunscreen users fail to apply sunscreen appropriately or to reapply it after swimming, sweating, or toweling off. (14)

Clothing provides a degree of sun protection, but some harmful rays can penetrate clothing; cloth with a tight weave provides greater protection. Patients with higher risk factors for skin cancer may consider the use of clothing that provides more sun protection. A hat should be worn, preferably one with a 3-inch brim to shield the ears, neck, and nose. The results of a Colorado study (15) show that skiers and winter sports enthusiasts should be aware that the amount of UVB radiation increases by 8 to 10 percent per 1,000 feet of elevation; erythema developed in only six minutes on unprotected skin at 11,000 feet under midday spring sun exposure (Table 2). (16-18)

Skin cancer education and prevention programs have met with only marginal success. Outcome data on skin cancer reduction through use of sunscreen have shown limited success at best. (19,20) In addition, efforts to increase awareness of the danger of sun exposure have had no measurable effect on behavior, even in medical students. (21)

Screening

The key to diagnosing skin cancer is to have a high degree of suspicion. The U.S. Preventive Services Task Force studied whether a thorough screening skin examination affects outcomes and found no evidence to recommend for or against screening. (22) Nevertheless, the Task Force members state that "clinicians should remain alert for skin lesions with malignant features noted in the context of physical examinations performed for other purposes," and recognize that "even without formal screening programs, mortality from basal cell and squamous cell carcinoma is low compared with mortality from melanoma, but early detection and treatment may reduce morbidity and disfigurement from these cancers."

Clinical Evaluation

Patients often present with skin lesions, complaining of increasing size, a raised lesion, bleeding, poor healing, discoloration, or discomfort such as pain or itching. Close scrutiny of the arms, face, and upper chest can uncover many lesions and give the physician clues to the need for a more thorough skin examination.

PHYSICAL FINDINGS--BASAL CELL CARCINOMAS

The hallmark of basal cell carcinoma is a waxy, translucent, or pearly appearance. Commonly, these lesions have central ulceration and a raised pale border (Figure 2). The border may be highlighted by applying traction on the skin around the lesion (Figure 3). Telangiectasias are common (Figure 4) and lead to friability, poor healing, and frequent bleeding. Atrophy is possible (Figure 5), and the borders can be indistinct.

[FIGURE 2-5 OMITTED]

Pigmented basal cell carcinomas are less common and are easily confused with melanoma. They are caused by the presence of melanin within the lesion. (23) These lesions have the same structural features described above but, because of the pigmentation, can be mistaken for melanoma. In melanoma or pigmented basal cell carcinomas, treatment is based on tissue diagnosis.

PHYSICAL FINDINGS--ACTINIC KERATOSES AND SQUAMOUS CELL CARCINOMAS

Actinic keratosis may present as a pinhead-sized area of white scale or as a rough patch several centimeters in diameter (Figure 6). Sometimes it presents as a white scale over a pink macule or papule. Often it can be felt more easily than seen. Patients may mention that they have been picking off the scale, but that it keeps returning.

[FIGURE 6 OMITTED]

Squamous cell carcinomas arising from actinic keratoses are scaly, as are actinic keratoses, but tend to grow thicker, and the pink macular to papular area develops into an erythematous raised base. Sometimes the lesion develops an overlying keratin horn (Figure 7). The lesions may take the form of a patch, plaque, or nodule, sometimes with scaling or an ulcerated center. The borders often are irregular and bleed easily. Unlike basal cell carcinomas, the heaped-up edges of the lesions are fleshy rather than clear in appearance.

[FIGURE 7 OMITTED]

Biopsy

The question of malignancy and cell type of a lesion is often in doubt (Table 3 lists some differential diagnoses). Enlarging or symptomatic lesions that are not clearly benign should be excised (complete removal) or biopsied (partial removal, usually by shave or punch) to determine appropriate treatment. Suspicion of melanoma always warrants full-thickness complete excision unless precluded by the size of the lesion. The extent of local reexcision and consideration of lymph node biopsy are based on the lesion depth on histologic examination. Figure 8 provides a decision tree to guide the type of biopsy chosen.

[FIGURE 8 OMITTED]

Raised lesions (i.e., most basal cell and squamous cell carcinomas) can be sampled easily with a simple superficial shave biopsy. Hemostasis can be obtained with electro-or chemical cautery. If histology confirms malignancy, definitive treatment is pursued as outlined below.

Small lesions with distinct borders can be excised easily in their entirety with a punch biopsy instrument (available in sizes ranging from 2 to 10 mm.) Elliptic excision (excisional biopsy) with a 3- to 4-mm margin may be selected in areas in which tissue loss is acceptable and cosmesis with a linear scar is expected to be good. (24,25) If the excision is complete with clear margins, diagnosis and treatment are done in one procedure.

In the case of large lesions, incisional biopsies, a small punch biopsy (2 to 3 mm), or a shave biopsy is easy to perform. A punch biopsy should not be chosen if the physician is considering electrodesiccation and curettage as the ultimate treatment.

Treatment

Once a lesion has been identified as suspicious, the question becomes how best to treat it. The method of treatment depends somewhat on the diagnosis, lesion size, morphology, and location, as well as patient compliance. If the pathology shows melanoma, reexcision is required, and lymph node sampling might be considered. If the pathology reveals a basal cell carcinoma or squamous cell carcinoma by excisional biopsy and the margins are clear of malignancy, treatment of that lesion is complete, but the physician and patient should be aware of the risk for additional synchronous or future lesions.

Basal cell carcinomas, the most common of all cancers, usually are treated with full-thickness excision, curettage, electrodesiccation and cautery, cryotherapy, or 5-fluorouracil (Efudex), applied topically or intralesionally. (26) Other treatments include photodynamic therapy (PDT), (27) laser therapy, radiotherapy and, more recently (not yet approved for this purpose by the U.S. Food and Drug Administration), imiquimod (Aldara). (28,29) PDT, which uses 5-aminolevulinic acid (Levulan Kerastick) as a tumor sensitizer activated by visible light treatment, can be useful in areas in which loss of tissue would be cosmetically or functionally unacceptable. This process localizes tissue destruction to the cancer without damaging surrounding or deep tissues. Pain and photosensitivity can occur in the first several weeks following treatment. Table 4(8,9,19,27,30-37) provides more detailed information on treatment modalities.

Electrodesiccation and cautery (traditionally, three scraping and burning cycles performed at a single sitting) is most appropriate for intermediate-size lesions. In contrast to full-thickness excision, electrodesiccation and cautery usually maintains the integrity of the underlying dermis, ensuring adequate healing with no overall loss of skin surface area and with minimal scarring.

If punch biopsy was performed previously, electrodesiccation and cautery is more difficult. Curetting inevitably opens up the site of the punch hole, and there will be a defect into the subcutaneous layer. If a shave biopsy was performed, the electrodesiccation and cautery usually will not go through the dermis, and there will be good healing with time.

Cryotherapy has been used to treat basal cell carcinomas, but targeting tissue destruction is less controlled. Two 30-second freeze-thaw cycles should be employed; this regimen results in 95 percent cure rates on facial lesions. (38)

With electrodesiccation and cautery, cryotherapy, 5-fluorouracil, and imiquimod therapy, complete lesion removal cannot be confirmed. 5-fluorouracil and imiquimod are well suited for early, superficial, or diffuse but mild disease, in which the likelihood of deep structure invasion is low, and surgical treatment might yield a cosmetically poor result.

Basosquamous carcinomas, with microscopic features of both basal cell and squamous cell carcinomas (Figure 9), or morphea-like basal cell carcinomas should be excised completely because of their more aggressive nature. This may be done in the primary care office, based on the location of the lesion and the skill of the physician.

[FIGURE 9 OMITTED]

There is scant evidence showing which treatments for squamous cell carcinoma are effective. Squamous cell carcinomas usually are treated with the same modalities as basal cell carcinomas. Because these lesions have metastatic potential, surgical removal or Mohs' micrographic surgery should be considered over destructive techniques. (36) Excision allows the physician to confirm that the surgical margins are free of disease.

Actinic keratoses are considered by many to be an early form of squamous cell carcinoma, although disagreement still exists in the dermatologic community. (39) Cryotherapy is an effective and well-accepted therapy for actinic keratoses. However, actinic keratoses may be diffuse, with clinically unapparent lesions in adjacent skin. Regional therapy with 5-fluorouracil or imiquimod is highly successful in the treatment of early apparent and unapparent lesions. 5-Fluorouracil can be used twice daily for approximately two weeks until marked inflammation develops (Figure 10). Imiquimod is applied three times per week at bedtime for four weeks and washed off each morning. Repeated cycles may be necessary. For the 5 to 20 percent of lesions that do not respond to this treatment, more aggressive therapy (usually cryotherapy) can be used.

[FIGURE 10 OMITTED]

Regardless of the initial treatment choice, all patients should be followed closely; the treated area specifically should be watched for recurrence for up to five years, and other lesions should be looked for in these high-risk patients. If any lesion fails to respond to initial treatment, surgical resection is appropriate.

Referral

Patients with any nonmelanoma skin cancer greater than 2 cm, lesions with indistinct margins, recurrent lesions, and those close to important structures, including the eyes, nose, and mouth, should be considered for referral for complete excision via Mohs' micrographic surgery, with possible plastic repair. The Mohs' surgeon can confirm the complete removal of the lesion by immediately reviewing the pathology during a staged excision which, in these high-risk settings, can require removal of much more tissue than might have been clinically apparent. If a difficult repair is anticipated or a poor cosmetic result is expected, referral is appropriate.

TABLE 1

Risk Factors for Basal Cell and Squamous Cell Carcinomas

Cumulative sun exposure in older patients Gamma radiation exposure (cancer therapy, psoriasis treatment, past acne treatment)

History of actinic keratosis, squamous cell carcinoma, or basal cell carcinoma

HPV infection (in the genitourinary area)

Inorganic arsenic exposure (formerly used in medical treatments)

Old burn scars

Smoking

Ultraviolet radiation exposure (exposure before age 14 is especially significant)

Uncircumcised penis (for squamous cell carcinoma of the penis; occurs mainly in developing countries)

HPV = human papillomavirus.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

The authors thank Lisa Broberg for assistance in the preparation of the manuscript.

Figure 1 is used with permission from Paul Urie, M.D., Ph.D., Department of Pathology, Utah Valley Regional Medical Center. Figures 2 through 7, 9, and 10 are used with permission from Utah Valley Family Medicine Residency Program.

REFERENCES

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(2.) McDonald CJ. Status of screening for skin cancer. Cancer 1993;72(3 suppl):1066-70.

(3.) Strayer SM, Reynolds PL. Diagnosing skin malignancy: assessment of predictive clinical criteria and risk factors. J Fam Pract 2003;52:210-8.

(4.) Kelfkens G, de Gruijl FR, van der Leun JC. Ozone depletion and increase in annual carcinogenic ultraviolet dose. Photochem Photobiol 1990;52:819-23.

(5.) Van der Leun JC, de Gruijl FR. Climate change and skin cancer. Photochem Photobiol Sci 2002;1:324-6.

(6.) Whitmore SE, Morison WL, Potten CS, Chadwick C. Tanning salon exposure and molecular alterations. J Am Acad Dermatol 2001;44:775-80.

(7.) Fitzpatrick TB, Johnson RA, Wolff K, Polano MK, Suurmond D. Color atlas and synopsis of clinical dermatology: common and serious diseases. 3d ed. New York: McGraw-Hill, 1997:226,232-5.

(8.) Ortonne JP. From actinic keratosis to squamous cell carcinoma. Br J Dermatol 2002;146 suppl 61:20-3.

(9.) Czarnecki D, Meehan CJ, Bruce F, Culjak G. The majority of cutaneous squamous cell carcinomas arise in actinic keratoses. J Cutan Med Surg 2002;6:207-9.

(10.) Cockerell CJ. Histopathology of incipient intraepidermal squamous cell carcinoma ("actinic keratosis"). J Am Acad Dermatol 2000;42(1 pt 2):11-7.

(11.) Guenthner ST, Hurwitz RM, Buckel LJ, Gray HR. Cutaneous squamous cell carcinomas consistently show histologic evidence of in situ changes: a clinicopathologic correlation. J Am Acad Dermatol 1999;41(3 pt 1):443-8.

(12.) Lober BA, Lober CW. Actinic keratosis is squamous cell carcinoma. South Med J 2000;93:650-5.

(13.) Euvrard S, Kanitakis J, Pouteil-Noble C, Dureau G, Touraine JL, Faure M, et al. Comparative epidemiologic study of premalignant and malignant epithelial cutaneous lesions developing after kidney and heart transplantation. J Am Acad Dermatol 1995;33(2 pt 1):222-9.

(14.) Neale R, Williams G, Green A. Application patterns among participants randomized to daily sunscreen use in a skin cancer prevention trial. Arch Dermatol 2002;138:1319-25.

(15.) Rigel DS, Rigel EG, Rigel AC. Effects of altitude and latitude on ambient UVB radiation. J Am Acad Dermatol 1999;40:114-6.

(16.) Geller AC, Colditz G, Oliveria S, Emmons K, Jorgensen C, Aweh GN, et al. Use of sunscreen, sunburning rates, and tanning bed use among more than 10 000 US children and adolescents. Pediatrics 2002;109:1009-14.

(17.) Autier P, Dore JF, Negrier S, Lienard D, Panizzon R, Lejeune FJ, et al. Sunscreen use and duration of sun exposure: a double-blind, randomized trial. J Natl Cancer Inst 1999;91:1304-9.

(18.) Autier P, Dore JF, Reis AC, Grivegnee A, Ollivaud L, Truchetet F, et al. Sunscreen use and intentional exposure to ultraviolet A and B radiation: a double blind randomized trial using personal dosimeters. Br J Cancer 2000;83:1243-8.

(19.) Green A, Williams G, Neale R, Hart V, Leslie D, Parsons P, et al. Daily sunscreen application and betacarotene supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial [published correction appears in Lancet 1999;354:1038]. Lancet 1999;354:723-9.

(20.) Weinstock MA. Sunscreen. Curr Opin Oncol 2000; 12:159-62.

(21.) Mawn VB, Fleischer AB Jr. A survey of attitudes, beliefs, and behavior regarding tanning bed use, sunbathing, and sunscreen use. J Am Acad Dermatol 1993;29:959-62.

(22.) US Preventive Services Task Force. Screening for skin cancer: recommendations and rationale. Am J Prev Med 2001;20(3 suppl):44-6.

(23.) Habif TP. Clinical dermatology: a color guide to diagnosis and therapy. 4th ed. New York: Mosby, 2004:729.

(24.) Thomas DJ, King AR, Peat BG. Excision margins for nonmelanotic skin cancer. Plast Reconstr Surg 2003;112:57-63.

(25.) Bisson MA, Dunkin CS, Suvarna SK, Griffiths RW. Do plastic surgeons resect basal cell carcinomas too widely? A prospective study comparing surgical and histological margins. Br J Plast Surg 2002;55:293-7.

(26.) Miller BH, Shavin JS, Cognetta A, Taylor RJ, Salasche S, Korey A, et al. Nonsurgical treatment of basal cell carcinomas with intralesional 5-fluorouracil/epinephrine injectable gel. J Am Acad Dermatol 1997;36:72-7.

(27.) Soler AM, Angell-Petersen E, Warloe T, Tausjo J, Steen HB, Moan J, et al. Photodynamic therapy of superficial basal cell carcinoma with 5-aminolevulinic acid with dimethylsulfoxide and ethylendiaminetetraacetic acid: a comparison of two light sources. Photochem Photobiol 2000;71:724-9.

(28.) Geisse JK, Rich P, Pandya A, Gross K, Andres K, Ginkel A, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study. J Am Acad Dermatol 2002;47:390-8.

(29.) Marks R, Gebauer K, Shumack S, Amies M, Bryden J, Fox TL, et al., for the Australasian Multicentre Trial Group. Imiquimod 5% cream in the treatment of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial. J Am Acad Dermatol 2001;44:807-13.

(30.) Feightner JW. Prevention of skin cancer. In: Canadian Task Force on the Periodic Health Examination. The Canadian guide to clinical preventive health care. Ottawa, Canada: Canada Communication Group--Publishing, 1994;850-9.

(31.) Ferrini RL, Perlman M, Hill L. American College of Preventive Medicine policy statement: screening for skin cancer. Am J Prev Med 1998;14:80-2.

(32.) Committee on Gynecologic Practice, American College of Obstetricians and Gynecologists. Primary and preventive care: periodic assessments. ACOG Committee opinion no. 246. Washington, D.C.: American College of Obstetricians and Gynecologists, 2000.

(33.) National Health and Medical Research Council (Australia). Guidelines for preventive interventions in primary health care: cardiovascular disease and cancer: report of the assessment of preventive activities in the health care system initiative. Canberra, Australia: National Health and Medical Research Council, 1997.

(34.) Bath FJ, Bong J, Perkins W, Williams HC. Interventions for basal cell carcinoma of the skin. Cochrane Database Syst Rev 2004;(3):CD003412.

(35.) Kurwa HA, Yong-Gee SA, Seed PT, Markey AC, Barlow RJ. A randomized paired comparison of photodynamic therapy and topical 5-fluorouracil in the treatment of actinic keratoses. J Am Acad Dermatol 1999;41(3 pt 1):414-8.

(36.) Green A, Marks R. Squamous cell carcinoma of the skin: non-metastatic. Clin Evid 2002;(7):1549-54.

(37.) Motley R, Kersey P, Lawrence C, for the British Association of Dermatologists, British Association of Plastic Surgeons, Royal College of Radiologists, Faculty of Clinical Oncology. Multiprofessional guidelines for the management of the patient with primary cutaneous squamous cell carcinoma. Br J Dermatol 2002;146:18-25.

(38.) Mallon E, Dawber R. Cryosurgery in the treatment of basal cell carcinoma. Assessment of one and two freezethaw cycle schedules. Dermatol Surg 1996;22:854-8.

(39.) Ackerman AB. Opposing views of 2 academies about the nature of solar keratosis. Cutis 2003;71:391-5.

DANIEL L. STULBERG, M.D., is director of the Rose Family Medicine Residency Program in Denver. Dr. Stulberg received his medical degree from the University of Michigan Medical School, Ann Arbor, where he also served a residency in family practice. He was formerly on faculty at the Utah Valley Family Medicine Residency Program in Provo.

BLAIN CRANDELL, M.D., is currently on staff at the Family Health Centers, Okanogan, Wash. Dr. Crandell received his medical degree from the University of Alabama School of Medicine, Birmingham, and completed his residency at the Utah Valley Family Medicine Residency Program.

ROBERT S. FAWCETT, M.D., M.S., is associate director and medical director of the Thomas M. Hart Family Medicine Residency Program at York Hospital in York, Pa. He received his medical degree from the University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, and earned a master of science degree in education at Ball State University, Muncie, Ind.

Address correspondence to Daniel L. Stulberg, M.D., Director, Rose Family Medicine Residency Program, University of Colorado at Denver, 2149 S. Holly St., Denver, CO 80222 (e-mail: dan.stulberg@rfmr.com). Reprints are not available from the authors.

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