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A Guide To Skin Conditions Of The Diabetic Foot

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Issue Number: Volume 17 - Issue 9 - September 2004
Author(s): By Robert G. Smith, DPM, RPh, CPed
One-third of the 17 million patients with diabetes develop manifestations of the disease that affect their
skin.1,2 The cutaneous manifestations and signs of diabetes can heighten the suspicions of the practitioner
regarding the diagnosis of these skin conditions. Patients with diabetes who have peripheral sensory
neuropathy and impaired circulation are at an increased risk of developing complications from skin and
nail conditions like onychomycosis.3 These skin changes of the foot can lead to the formation of a diabetic
foot ulcer and potentially limb-threatening infections. There are four categories of skin manifestations in
diabetes: skin changes associated with diabetes, cutaneous manifestations of diabetes, cutaneous
infections and skin reactions to anti-diabetic treatments. In order to recognize these manifestations and
arrive at an appropriate treatment course, one must have a strong grasp of the various ways that diabetes
can affect the skin and the lower extremities (see Understanding How Diabetes Affects The Skin Of The
Foot below). Understanding How Diabetes Affects The Skin Of The Foot Diabetes affects the skin and
lower extremities in many ways. Glucose comprises between 35 to 65 percent of the blood in the human
epidermis. The transport of glucose into epidermal cells is not dependent on insulin but requires
hexokinase and glucose-C-phosphate. The resulting elevated ratio of glucose in the epidermis of diabetic
patients does not seem to have a pathological effect with the exception of potentating skin infections with
saprophytic organisms like Candida albicans.4 Poor blood glucose control increases the risk for skin and
foot manifestations and cutaneous complications with diabetes, and can compromise a patients vascular
system.5 Researchers have shown that peripheral vascular disease is associated with diabetes.6
Arteriosclerosis of the arteries of the legs results in generalized cutaneous skin changes that may include
a waxy appearance, atrophy, a loss of hair growth, skin temperature cooling at the distal digits, nail
dystrophy, pallor on elevation and mottling on dependence. 7 A reliable sign of large vessel disease is
dependent rubor with a delayed return of color greater or equal to 15 seconds after one has applied
pressure to the skin. 8 Almost all patients with diabetes have capillary basement membrane thickening.
However, this does not lead to occlusive microvascular lesions in and of itself. 9 Thickening of the vessel
walls with perivascular deposition of PAS-positive material and clumping of elastic fibers in the upper
dermis are the most prominent histopathologic markers in diabetic skin. 4 The signs of microangiopathy
may include cutaneous reactive hyperemia and reduced capillary flow. The nail changes associated with
microangiopathy include Beaus lines, pterygium, proximal fold capillary microscopic changes, splinter
hemorrhages and yellow nail discoloration.7,10 Pertinent Pointers On Treating Xerosis Generalized xerosis
or dry skin is one of the most common skin conditions one will see among patients who have type 2
diabetes. It is particularly prevalent among elderly patients. At times, the foot may become very dry,
leading to peeling and cracking. The problem arises with the nerves that control the oil and moisture in the
foot. Sebaceous and sweat glands maintain skin lubrication. The glands become atrophied in the presence
of autonomic neuropathy. Another reason for dryness is the redistribution of blood flow in the soles by
persistent and inappropriate dilatation of arteriovenous shunts. This activity diverts blood away from the
skin surface. When this occurs in combination with alterations in the elasticity of the skin (due to
non-enzymatic glycosylation of structural proteins and glycoproteins), the skin splits and portals for
bacteria are created. Both pruritis and a sensation of burning usually accompany xerosis as principal
symptoms. Structural changes occur among the aligned parallel corneocytes in normal skin as a result of
xerosis. 11 A roughened epidermal surface results from the disruption of these cells. The progression of
xerosis follows a defined pattern. Initially, the skin becomes dry and rough with pronounced skin lines. As
the condition progresses, superficial scaling with fissuring and erythema develops. As a result of xerosis,
the skin loses its flexibility. Therefore, it is less elastic and loses its ability to withstand trauma, which may
result in skin breakdown, leading to a variety of infections. Practitioners can assist these patients by
choosing an agent to maintain skin moisture. One should avoid recommending products that contain
alcohol because they evaporate and their drying action compounds the original problem. Petroleum based
products seal the skin surface and prevent what little lubrication is made from evaporating, but they do not
penetrate the surface of the skin and do not replace skin moisture. Alpha hydroxy acids are frequently
used to treat xerosis. Alpha hydroxy acids include glycolic, citric, lactic, mandelic and tartaric acid.
Through a chemical process, these acids accelerate the softening of the skin, dissolving or peeling the
outer layer of the skin to help maintain the skins capability to hold moisture. Lactic acid in concentrations
of 2.5 percent to 12 percent is the most common alpha hydroxy acid used for moderate to severe xerosis.
When treating patients who have neuropathic disease, one should exercise caution with creams that
contain high concentrations of either urea or acetylsalicylic acid, given the corrosive nature of these
creams. While application of topical emollient creams may not prevent the skins deterioration, the
application process does facilitate regular inspection of the feet among patients with diabetes. A Helpful
Primer On Diabetic Thick Skin, Yellow Skin, Diabetic Dermopathy And Diabetic Anhidrosis The prevalence
of cutaneous disorders does not seem to differ between type 1 and type 2 diabetic patients. However,

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Click1here Achilles Tendonitis
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diabetes develop more autoimmune-type cutaneous lesions. 12-14 Indeed, there are a number of
Amputation
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pathognomonic cutaneous manifestations of diabetes (see Cutaneous Manifestations Associated With
Ankle Arthrodesis
Metatarsal Fractures
Diabetes Mellitus below). Diabetic thick skin. It has been demonstrated by ultrasound and reported by
Ankle Replacement
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Huntley and Walter that patients with diabetes have thicker skin than those patients without diabetes.15
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Tissues
The pathogenesis of diabetic thick skin has not clearly been defined. There are three categories of diabetic
Onychomycosis
Biomechanics
Orthotics
thick skin: scleroderma-like changes of the hand associated with stiff joints and limited mobility;
Bunionectomy
Osteomyelitis
measurable skin thickness that is clinically insignificant and scleredema diabeticorum. There are distinct
Calcaneal Fractures
PAD
Charcot
light and electron microscopic features that can help differentiate between diabetic thick skin and
Peripheral Neuropathy
Coding
Plantar Fasciitis
scleroderma. The collagen fibers of diabetic thick skin are seldom below 60 nm and there is no bimodality
Custom Orthosis
Practice Management
16
Dermatology
of the fibers. Researchers have proposed potential explanations for diabetic thick skin that include the
Pressure Ulcers
Diabetic Foot
Sever's Disease
hydration of collagen secondary to polyol accumulation and nonenzymatic glycosylation of
Diabetic Foot Infection
Split Thickness Skin Grafts
collagen.2,17Yellow skin. Yellow nails and skin are a benign condition of the skin associated with diabetes.
Diabetic Foot Ulcer
Sports Medicine
Diabetic Peripheral
Its cause remains controversial and may be due to nonezymatic glycosylation of dermal collagen or
Staff Management
Neuropathy
Stress Fractures
elevated levels of carotene. This characteristic color of yellow skin may be the result of an accumulation of
EMR/EHR
Tinea Pedis
Fall Prevention
2-(2-furoyl) 4(5)-(2-furanyl)-1H-imidazole, an end product of glycosylation that has a yellow hue.2,18 One
Venous Ulcers
Flatfoot
Wound Care
may see this yellow color on the palms of the hands, soles of the feet and the distal nail plate of the
Hallux Valgus
Wound Debridement
2,18
Hammertoe
hallux. Diabetic dermopathy. This is the most common cutaneous finding in diabetes and is also
Wound Dressings
HBOT
known as shin spots or spotted leg syndrome. Its incidence ranges from 30 to 60 percent among patients
with diabetes.2,4,7,12,19 Shermer, et. al., reported an incidence of 40 percent among diabetic patients in an
Israeli hospital.20 The condition is predominately seen in men over the age of 50. It appears as round to
POLL
oval atrophic, hyperpigmented (brown) raised lesions on the pretibial areas of the lower extremities. They
What is the best course of treatment for
are usually multiple brown atrophic spots resembling large freckles. These lesions present with a
plantar warts?
symmetrical distribution and are usually bilateral. Older lesions may persist or disappear while new lesions
Surgical
appear. Histological studies of the lesions reveal edema of the papillary dermis, thickening of superficial
blood vessels, mild lymphocytic infiltration and extravasations of erythrocytes.2,21,22 These erythrocytes
Non-surgical
leave hemosiderin deposits, which result in brownish hyperpigmentation. Currently, there is no formal
treatment for diabetic dermopathy because these lesions resolve spontaneously although they do leave
Vote
scars.2 No treatment is necessary and these lesions persist indefinitely. Diabetic anhidrosis. This
cutaneous manifestation is related to diabetic autonomic neuropathy. A lesion in the sympathetic nerve
UPCOMING MEETINGS
supply to the skin has been identified as the principal cause. How To Identify Diabetic Bullae Diabetic
bullae. Approximately 0.5 percent of diabetic individuals develop diabetic bullae or bullosis diabeticorum.
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These bullae have only been reported in adults between the ages of 40 and 70.12 The blisters occur
February 25, 2016 to February 27, 2016
spontaneously without trauma and most are non-scarring.2 They are painless bullae on a non-inflammed
Lake Tahoe, NV, United States
base. They occur suddenly and are confined to the patients distal extremities (hands and feet). Bullae
Midwest Podiatry Conference
most commonly appear on the dorsum and sides of the lower legs and feet. The pathogenesis of these
March 31, 2016 to April 3, 2016
lesions has not yet been clearly been elaborated. There are three types of diabetic bullae. The first and
Chicago, IL, United States
most common presenting bullae are sterile and contain fluid. This type of bullae heals without scarring.
Histological findings reveal intraepidermal cleavage without acantholysis.8 The second type of bullae is
Symposium on Advanced Wound Care
hemorrhagic and unfortunately heals with scarring. Histological studies depict cleavage below the
(SAWC) Spring/Wound Healing Society
dermoepidermal junction with destruction of anchoring fibrils.2,7,8,12,23,24 The third type involves multiple,
April 13, 2016 to April 17, 2016
non-scarring bullae on sun-exposed skin.2 These types of bullae lesions reveal cleavages at the lamina
Atlanta, GA, United States
2,23,24
lucida under histological observational studies.
Preventing infection is a primary focus of treating
diabetic bullae. Podiatrists can help prevent infection by ensuring the patient is wearing properly fitting
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shoewear and socks to reduce friction at the bullae sites. The bullae heal spontaneously in two to five
weeks but may recur in the same or new locations. What The Literature Reveals About Necrobiosis
Lipoidica Diabeticorum Necrobiosis lipoidica diabeticorum. This cutaneous manifestation is described
as a degenerative disease of collagen in the dermis and subcutaneous fat with an atrophic epidermis and
granulomatous dermis. 2 The etiology has not clearly been described. Some suggested theories present a
microangiopathic basis with neuropathy resulting in the degradation of collagen.2,4,7,12 Cytokines from
inflammatory cells may cause destruction of the collagenous matrix. 2,4 The majority of the lesions occur on
the pretibial region of the lower legs. Necrobiosis lipoidica diabeticorum lesions occur in 0.3 to 0.7 percent
of the diabetic population and have a greater prevalence among women. A few studies have correlated
necrobiosis lipoidica diabeticorum and the microvascular effects of diabetic induced retinopathy and
nephropathy.2,4,7,12 The initial lesion is described as a well circumscribed erythematous plaque with a
depressed, waxy telangiectatic center. 2,4,7,12 As time passes, granulomatous lesions evolve into a sclerotic
stage of the dermis and subcutaneous fat.2 While there is no standard therapy for this cutaneous
manifestation, some anecdotal reports suggest that nonsteroidal agents or intralesional, systemic or
topical corticosteriods may be helpful.2 What About Perforating Dermatosis And Eruptive Xanthomas?
Perforating dermatosis. One would see this manifestation in a majority of patients who have kidney
failure associated with diabetes. 2,4,12 The associated itching and scratching accompanying perforating
dermatosis is known as Kyrels disease or reactive perforating collagenosis. 2,4,7,12 These lesions are
principally located on the extensor surfaces of the lower extremities and may occur on the face or
trunk.2,4,7,12 These papules are between 2 to 10 mm in diameter and often contain a keratotic plug.
Histological studies reveal that these lesions have a hyperplastic epidermis surrounding a plug of
degenerated material containing leuckocytes, collagen and nuclear debris.2,7,25Eruptive xanthomas. In
diabetes, eruptive xanthomas are accompanied by hyperlipidemic and hyperglycemic states. The lesions
are yellow, waxy papules surrounded by an erythematous rim. They usually occur on the extensor
surfaces and the popliteal regions. Histologic studies of eruptive xanthomas will reveal lipid-laden
histocytes and a mixed lymphoneutrophilic infiltrates in the dermis.2 Key Insights On Tinea Pedis And
Candida Infections Dermatophytic infections are particularly concerning among patients with diabetes
because they may serve as a portal of entry for bacterial infections. Dermatophytic infections are generally
restricted to nonliving, cornified layers of skin, hair or nails. The burning and pruritus symptoms of
dermatophytic infections are due to the accumulation of their metabolic waste products. These symptoms
may either be intense or patients may be asymptomatic. Dermatophytes release keratinases and other
proteolytic enzymes that act upon the proteins present in keratinized structures skin, hair and nails. When
treating patients with diabetes who have severe neurovascular complications, one should always evaluate
these patients for intertriginous or interdigital infections caused by Trichophyton rubrum, Trichophyton
mentagrophytes or Epidermophyton floccosum.4 Tinea pedis caused by Trichophyton mentagrophytes

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macerated and have scaling borders and at times may be vesicular. Trichophyton rubrum produces scaling
and thickening of the soles, often extending just beyond the plantar surface in a moccasin distribution.
Tinea pedis may be complicated by secondary bacterial infection, cellulitis or lymphangitis. If chronic tinea
pedis infections go untreated, they can spread to the toenails and destroy the nail plates. The treatment of
interdigital tinea pedis depends on the severity of the disease. Whether one uses a cream or a gel,
antifungal topical products can help dry interdigital maceration. Researchers have discussed topical
products, classifications and the effectiveness of these agents in both tertiary and primary literature
sources. 26-30Candida infections commonly develop in older patients with diabetes mellitus and may be an
early indicator of undiagnosed diabetes mellitus. Candida paronychia commonly involves the nail fold. Its
symptoms include erythema, swelling, pain and loss of the cuticle. Extensive erythrasma occurs in obese
patients with diabetes and is caused by the infectious agent Corynebacterium minutissimum. Common
bacterial infections of the diabetic skin are caused by Staphylococcus aureus and B-hemolytic
streptococci. The conditions these organisms cause include impetigo, folliculitis, furuncles, carbuncles,
ecthymata, cellulitis and erysipelas.4,7 Lower extremity erysipelas infections are often complicated by
bullous lesions, leading to diabetic gangrene. 4,7,12 Understanding The Possible Consequences Of
Untreated Onychomycosis In Patients With Diabetes Researchers have reported the prevalence of
onychomycosis among diabetic patients to be as high as 35 percent.3,31-33 One commonly sees
onychomychosis in association with tinea pedis. It has an 80 percent prevalence rate among the elderly
because of its strong age dependency. If onychomychosis is neglected in the patient with diabetes, it can
contribute to severe consequences in the diabetic foot. Patients with diabetes who suffer from peripheral
sensory neuropathy and impaired circulation are at a higher risk of developing complications from
onychomycotic nails. 3 Treatment options for onychomycosis are similar for patients with diabetes and
those without the disease. There is a variety of treatment options available to treat onychomycosis. They
include mechanical debridement, topical antifungal medications, oral antifungal agents and surgical
intervention. One should exercise caution when considering surgical intervention in these patients due to
the possible risk of secondary infections. 3 How To Recognize Common Cutaneous Reactions To Diabetes
Medications The incidence of allergic reactions to insulin varies from 5 to 10 percent. 4,7 Both local and
systemic allergic reactions occur within the first month of therapy.12 Historically, allergic reactions have
been attributed to impurities found in both the beef and pork insulin preparations, the insulin molecule, and
preservatives and additives like zinc.12 The highly purified or recombinant insulin have reduced allergy
prevalence to between 0.1 percent and 0.2 percent.12,13 Cutaneous allergic reactions take the form of
erythematous or uticarial pruritic nodules at the injection site. They may appear immediately, within 15
minutes to two hours, or be delayed with an onset of four hours or more after injection. 12 These reactions
spontaneously resolve so treatment may be unnecessary. Podiatrists may be able to intervene at two
points. First, they may observe the patients injection technique to ensure the injection itself is not
intradermal in nature. Also, they may act as patient advocates and suggest to the prescribing physician the
substitution of a more purified insulin as the treatment of choice. Mostly, children and obese women
experience insulin-induced lipatropy or loss of fat at the site of injection. These atrophic plaques appear six
to 24 months after starting injections. Both lipolytic components of insulin preparations or an immune
complex mediated inflammatory process that causes the release of lysosomal enzymes have been
implicated in the pathogenesis of insulin induced lipatrophy.4,7,12 First generation sulfonylureas, such as
chlorpropamide, are agents that have reportedly generated the majority of cutaneous reactions among
patients with diabetes.6,9,14 Of the patients who take a sulfonylurea, 1 to 5 percent develop a self-limiting
maculopapular eruption type of cutaneous reaction with two months of starting therapy. One may also see
morbilliform eruptions, generalized erythema or urticarial lesions.4,7,12,34 Litts Drug Eruption Reference
manual notes that using sulfonylureas can cause other reported cutaneous reactions including generalized
erythema, urticaria, photosensitivity, lichenoid eruptions, erythema multiforme, exfoliative dermatitis and
erythema nodosum.34 The photosensitive reactions caused by sulfonylureas may be either photoallergic or
phototoxic but photopatch tests are often negative.34 The most frequently reported cutaneous reactions
reported by Litts Drug Eruption Reference manual for glyburide included erythema, exanthems,
photosensivity, pruritus and urticaria. The manufacturer states the incidence of rash or dermatitis in
patients receiving metformin alone is similar to that with placebo, while the incidence of dermatological
side effects in patients receiving both metformin and sulfonylurea antidiabetic agents is similar to the
incidence of receiving an oral antidiabetic sulfonylurea alone.34 Stevens-Johnson syndrome has been
reported to occur in less than 1 percent of patients receiving repaglinide. 35 Final Words Early detection of
skin manifestations of diabetes can help prevent potentially devastating complications. Educational
intervention is critical. One should remind patients that bacterial and fungal infections of the skin are often
associated with diabetes. Preventing these infections requires meticulous care of the patients lower
extremities. Dr. Smith has a private practice in Ormond Beach, Fla.

References:
References 1. National Diabetes Fact Sheet: National estimates on diabetes. Available at:
www.cdc.gov/diabetes/pubs/estimates.htm Accessed March 19,2003. 2. Chakrabarty A, Norman RA, and
Phillips TJ. Cutaneous manifestations of diabetes. Wounds 2002; 14(8): 267-274. 3. Pollak RA. How to
treat onychomycosis in diabetic patients. Podiatry Today 2003; 16(3):40-50. 4. Meurer M and Szeimies R.
Diabetes mellitus and skin disease. Curr Probl Dermatol 1991; 20: 11-23. 5. Vowden P. Peripheral arterial
disease. 1: Functional investigations. J Wound Care 1997; 6 (2): 77-78. 6. Vowden KR and Vowden P.
Peripheral arterial disease. An update on epidemiology, pathology and aetilogy of vascular disease. J
Wound Care 1996 5(1): 23-26. 7. Perez MI and Kohn SR. Cutaneous manifestation of diabetes mellitus. J
Am Acad Dermatol 1994;30(4): 519-531. 8. Huntley AC. Cutaneous manifestation of diabetes mellitus.
Dermatol Clin 1989; 7 (3):531-546, 9. LoGerfo FW, Coffman JD. Vascular and microvascular disease of
the foot in diabetes: implications for foot care. N Engl J Med 1984;311 (25):1615-1619. 10. Greene RA,
Scher RK. Nails changes associated with diabetes mellitus. J Am Acad Dermatol 1987; 16(5 pt 1):
1015-1020. 11. Kempers S, Katz HH, Wildnauer R, et al. An evaluation of the effect of an alpha hydroxy

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epidermolytic hyperkerotosis and ichthyosis. Cutis 1998; 61 (6): 347-350. 12. Ferringer T and Miller OF.
Cutaneous manifestations of diabetes mellitus. Dermatol Clin 2002; 20(3): 483-492. 13. Paron NG and
Lambert PW. Cutaneous manifestations of diabetes mellitus. Prim Care 2000; 27 (2): 371-383. 14.
Romano G, Moretti G, Di Benedetto A et al. Skin lesions in diabetes mellitus: prevalence and clinical
correlations. Diabetes Res Clin Pract 1998; 39 (2) 101-106. 15. Huntley AC and Walter RM. Quantitative
determination of skin thickness in diabetes mellitus: relationship to disease parameters. J Med 1990;
21(5): 257-264. 16. Hanna W, Friesen D, Bombardier C et al. Pathologic feactures of diabetic thick skin. J
Am Acad Dermatol 1987; 16 (3): 546-553. 17. Eaton PR. The collagen hydration hypothesis: a new
paradigm for secondary complications of diabetes mellitus. J Chron Dis 1986; 39 (10): 763-766. 18.
Huntley A and Drugge R. Diabetes in skin disease in The Electronic textbook of Dermatology
http:/www.telemedicine.org/stamford.htm Accessed March 2003. 19. Aye M and Masson EA.
Dermatological care of the diabetic foot. Am J Clin Dermatol 2003 3(7): 463-474. 20. Shemer A, Bergman
R, Linn S et al. Diabetic dermopathy and internal complications in diabetes mellitus. Int J Dermatol 1998;
37(2): 113-115. 21. Bauer M, Levan NE. Diabetic dermangiopathy: a spectrum including pretibial
pigmented pathches and necrobiosis diabeticorum. Br J Dermatol 1970; 83 (5): 528-535. 22. Binkley GW,
Giraldo B, Stroughton RB. Diabetic dermopathy: a clinical study. Cutis 1967; 3(9): 955-958. 23. Bernstein
JE, Medenica M, Soltani K, et al Bullous eruption of diabetes mellitus. Arch Dermatol 1979; 115
(3):324-325. 24.Toonstra J. Bullous diabeticorum. J Am Acad Dermatol 1985; 13 (5 pt 1): 799-805. 25.
Zelger B, Hinter H, Aubock J et al. Acquired perforating dermatosis: Transepidermal elimination of DNA
material and possible role of leukocytes in pathogenesis. Arch Dermatol 1991; 127 (5): 695-700. 26.
Burnham TH, Wickersham, RM, Novak KK et al. Anti-infectives topical. In Drug Facts and Comparisons.
St. Louis and Comparsions; 2003 1610-1619 27. Elewski B, Bergstresser PR, Hanifen J, et al. Long-term
outcome of patients with interdigital tinea pedis treated with terbinafine or clotrimazole. J Am Acad
Dermatol 1995; 32 (2 pt 1): 290-292 28. Bergstresser PR, Elewski B, Hanifin J et al. Topical terbinafine
and clotrimazole interdigital tinea pedis: a multicenter comparison of cure and relapse rates with 1 and 4
week treatment regimen. J Am Acad Dermatol. 1993; 28 (4): 648-651 29. Shear NH, Einarson TR, Arikian
SR et al. Pharmacoeconomic analysis of topical treatments for tinea infections. Int J Dermatol. 1998; 37
(1): 64-71. 30. Diehl KB. Topical antifungal agents: an update. Am Fam Physician 1996; 54 (5): 16871692 31. Schlefman BS. Onychomycosis: a compendium of facts and clinical experience. J Foot Ankle
Surg. 1999; 38 (4): 290-302. 32. Gupta AK, Konnikov N, MacDonald P et al. Prevalence and
epidermiology of toenail onychomycosis in diabetic subjects: a multicenter survey. Br J Dermatol. 1998;
139 (4):665-671. 33. Gupta AK, Humke S. The prevalence and management of onychomycosis in diabetic
patients. Eur J Dermatol 2000; 10 (5): 379-384. 34. Litt JZ. Physcians guide to drug eruption. New York:
Parthenon Publishing; 1998. 95. 35. Burnham TH, Wickersham, RM, Novak KK et al. Antidiabetic agents.
In Drug Facts and Comparisons. St. Louis and Comparsions; 2003 305-307.

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