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Anais Brasileiros de Dermatologia

On-line version ISSN 1806-4841

An. Bras. Dermatol. vol.78 no.6 Rio de Janeiro Nov./Dec. 2003

http://dx.doi.org/10.1590/S0365-05962003000600010 

REVIEW ARTICLE

 

Diabetes mellitus and cutaneous affections*

 

 

Lorivaldo MinelliI; Andrei Bungart NoninoII; Jaqueline Cantarelli SalmazoII; Leandro NemeII; Marcelo MarcondesII

IDermatologists, Graduate of the Universidade Estadual de Londrina, Londrina, PR
IIAssociate Professor - Ph.D. in Dermatology, Centro de Ciências da Saúde da Universidade Estadual de Londrina, Londrina, Parana State (PR)

Correspondence

 

 


SUMMARY

Diabetes Mellitus is a metabolic disease that predisposes patients to several other diseases, notably cutaneous ones. The latter have different sources, although infections are the commonest. This article consists of a detailed revision of these disorders, evidencing their clinical aspects as well an adequate therapeutic approach.

Key words: Skin diseases; Diabetes mellitus.


 

 

INTRODUCTION

Due to the complications skin diseases may cause for diabetics, they must be promptly diagnosed and diligently treated, without forgetting the fundamental role of prophylaxis.

 

BIBLIOGRAPHICAL REVIEW

Cutaneous Alterations in Diabetes Mellitus

Carriers of diabetes mellitus (DM) are usually recognized as most vulnerable to a series of complications1 of a metabolic nature and/or of infectious origin, such as bacterial, fungal and viral processes.2-6 This paper discusses the specific implications of the disease. As is already well known, these include vascular and neurological alterations often contributing to aggravation of the effective clinical conditions.4 The cutaneous alterations of DM are therefore subdivided into four groups: lesions strongly-associated with DM, cutaneous infections, reactions to medication and diabetic foot.

 

1. LESIONS STRONGLY ASSOCIATED WITH DIABETES MELLITUS

1.1 Necrobiosis Lipoidica

Necrobiosis lipoidica is a chronic disease whose lesions have a very peculiar morphology and are associated with DM in two out of three cases.7,8,9 It may be caused by vasculitis formed by immunocomplexes. It is very rare in melanodermic and East-Asian patients and virtually always arises among 30 to 40 year olds, and usually in females (3:1).

Its etiology is unknown. Its basic element is microangiopathy formed by immunocomplexes in which IgM and C3 may be observed in the small blood vessel walls (50%) and fibrinogen in the area of necrobiosis. Roughly 80% of cases are related to DM, especially juvenile DM, and may precede, succeed or appear concomitantly with the latter. Some patients, even non-diabetics, show an altered glycemic response curve.5 It is estimated that roughly 15% of patients with necrobiosis lipoidica will go on to develop diabetes several years later in life. Therefore, patients must be followed up over the long term.

Clinically-speaking, the lesions are localized 90% of the time on the lower two-thirds of the legs (pretibial regions). They are generally symmetrical8 but occur rarely on the trunk, face and upper limbs. The lesions are plaques that tend to be confluent and have irregular margins. They are slightly elevated, often brown-red or violet in color, and have a yellow and atrophic center. Their texture may be similar to wax. The lesions associate with telangiectasia and may cause ulceration, at which time they might become painful.

Histology demonstrates thickening of the blood vessel walls, collagen degeneration, and presence of granulomatous infiltrate with an accumulation of lipids in the cytoplasm of histiocytes and in the extracellular environment.9

In terms of treatment, intralesional steroids10 can be beneficial at times. When there is ulceration, excisation and grafts, they may even be useful. Antiplatelet, nicotinamide and pentoxyphylline agents and heparin injections have already been used with variable results. Nonetheless, there was no improvement of the dermatological lesion observed when therapeutic control of diabetes was obtained.4

1.2. Annular Granuloma

Annular granuloma has an unknown cause and is characterized exclusively by cutaneous lesions that are virtually always papulous and whose morphology is annular. Degeneration of the central collagen and peripheral granuloma was revealed during histology.

The disorder has universal incidence, occurring at higher frequency in young adults and children, and especially females. It is possible for DM to be more commonly associated with a generalized form of annular granuloma.2,11,12,13

Its etiology is unknown. Cellular hypersensitivity may occur, as suggested by immunological investigations utilizing direct immunofluorescence, T-cell subtypes, and macrophage inhibition tests. Immunofluorescence inconsistantly reveals IgM and C3 deposits in perivascular disposition, and fibrinogen in the necrobiotic area. Characteristically, the lesion biopsy regresses spontaneously over a span of time that may vary from two to four weeks.

Its most common aspect is that of annular papillary lesions at the onset of which a papule emerges and grows centrifugally to leave a very slight atrophic central area. These papulous rings may end up being a few centimeters in diameter. They have the color of normal or discreetly erythematous or yellowed skin. In some cases there is a single lesion; in others, lesions may be innumerable (disseminated annular granuloma). The lesions often appear on the dorsal aspect of the hands, forearms, elbows, feet and knees, though they may also occur on other areas (face, trunk, scalp and palms). Some are serpiginous and may eventually be nodular.12 A rare morphological variety is represented by papules with small central perforations (perforant annular granuloma).11 In some cases, lesions appear in photoexposed areas in association with pruritus.5

The diagnosis is effected by the clinical aspect and confirmed by histopathology. The latter reveals areas of collagen degeneration on the upper and middle dermis, around which there is a compact infiltrate forming palisades consisting of histiocytes, lymphocytes and fibroblasts.4 The differential diagnosis is annular lichen planus, rheumatoid nodules, erythema elevatum diutinum, necrobiosis lipoidica, tuberculoid leprosy and syphilis.12

It evolves asymptomatically, with spontaneous regression (in one out of two cases) for two years. Generalized cases progress slower (three to four years). A simple biopsy may provoke regression of lesions, though this is not always observed.

Treatment is made preferentially with an intralesional application or corticoid cream under occlusion.12 Cryotherapy has been referred, and chlorochine may be useful for cases of innumerable lesions in sun-exposed areas. Multiple needle punctures may lead to regression of lesions.

1.3. Kyrle Disease

Also known as hyperkeratosis parafollicularis, Kyrle Disease is a characteristic clinical eruption of follicular tamponade, particularly on the legs and forearms.

Its cause is unknown. The condition usual begins at middle-age (30 to 50 years) and at times in association with DM,14 chronic renal insufficiency or hyperlipidemia.

Lesions consist of papules whose diameter varies from a few millimeters to a several centimeters. They are centered by a cornea lid and surrounded by an erythematous zone. The lid stands out from a crater-like depression and may be removed easily. Lesions are most common on the legs and forearms, but may be generalized.5 Occasionally, they merge to form polycyclic plaques. In later lesions, there is depression and penetration of the keratinous lid which may provoke a foreign body reaction on the dermis.4 This is why a few authors place the disorder into a group of acquired perforant dermatoses, such as Flegel's disease, elastosis perforans serpiginosa, perforating folliculitis and reactive perforating collagenosis.

The diagnosis is confirmed by biopsy, and immunohistochemical studies suggest a keratin proliferation disturbance. There is no specific treatment, though topical and/or oral retinoids may be used.14

1.4 Scleredema of Buschke

This disorder consists of hardening of the skin, particularly of the upper back. Its etiology is entirely unknown, but the condition is often preceded by a viral or streptococcal disease. Scleredema of Buschke involves a substitution of the subcutaneous tissue by the conjunctive tissue.15

In the clinical condition, the patient may present with febricula, illness, myalgia and arthralgia, followed by the skin becoming rigid. The cutis has a similar consistency to wood. Lesions occur transversally to the shoulders and on the lateral cervical region. It may spread afterward to the face, arms, thorax and occasionally the buttocks, legs and abdomen. A transient erythema preceding this condition may be observed. At times there are associated cardiac abnormalities.

For most patients the affection heals spontaneously within two years. Nevertheless, there is a chronic variant occurring in association with obesity, DM,15 cardiovascular abnormalities and diabetic retinopathy.

The diagnosis is clinical, but a skin biopsy may be useful. The anti-streptolysin O titer (ASLO) may be high if the prodrome has a streptococcal origin. There is no specific treatment for the disease.

1.5. Bullosis Diabeticorum

Consisting of bullous lesions without an erythematous component, this disease is usually observed on the lower extremities of diabetics.16 It forms over a period of time varying from two to six weeks, and regresses without leaving scarring sequelae. Krane was the first to report this entity in 1930. Cantwell and Martz gave it its current name in 1967.17

This skin disease is twice as frequent in males. Blisters develop intra- and subepidermically without showing signs of acantholysis. Immunofluorescence is negative, though it may be useful for the differential diagnosis with other blisters, such as bullous penphigoid, acquired bullous epidermolysis and late-onset cutaneous porphyria. Electronic microscopy showed a reduction or absence of anchoring fibrils and hemidesmosomes in the recent blisters.17 As these patients are also usually affected by neuropathy, some authors considered the blisters to merely be the result of unperceived mechanical traumas.

1.6 Xanthomas

These diseases are characterized by lipid deposits on the skin and other localizations. They result in hyperlipidemias caused by abnormalities in cholesterol metabolism.

Xanthomas consist of tissue macrophages fagocyting the lipid part of the lipoproteins deposited in certain tissues. The lipids are insoluble and were transported into the plasma as soluble plasmatic lipoproteins. The five lipoprotein fractions may be separated by electrophoresis or by ultracentrifugation according to their respective densities. They are also known as: chylomicrons, very low density lipoproteins (VLDL), low density (LDL) and high density lipoproteins.

The eruptive form of xanthomas is usually associated with DM.

1.6.1. Eruptive Xanthomas

Such xanthomas occur as a myriad of subtlely appearing yellow papules. They are localized in the buttocks, thighs, arms, forearms, back and thorax. They are usually related to excess chylomicrons, and secondarily to decompensated DM, alcohol abuse and exogenic estrogens. They can be extremely inflammatory, often pruriginous and painful on palpation. An erythematous halo appears on the circumference.

In addition to clinical diagnosis, protein electrophoresis and histopathology are also used, the latter of which demonstrates a xanthoma cell infiltrate.4 Treatment is arduous and involves the use of hypolipemiant agents as well as a nutritionist's assistance.

1.7 Generalized Congenital Lipodystrophy (Lawrence-Berardinelli Syndrome)

This syndrome is most likely an autosomal recessive hereditary condition. In the syndrome, generalized lipodystrophy is found to exist, and DM18 is present in all adult patients. The following disorders are usually observed: fatty hepatomegaly, dolichocephalic skull, micrognathia, muscular hypertrophy, acanthosis nigricans, hyperlipidemia, advanced bone aging in childhood, hair thickening, abdominal protrusion and hyperthyroidism.

1.8. Pseudoacanthosis Nigricans

Characterized by velvety thickening of the skin and symmetrical hyperpigmentation of the cutaneous flexures, such as the cervical, axillary and inguinal regions, this disorder may affect the oral mucosa. Histopathology reveals papillomatosis and hyperkeratosis, in addition to hyperpigmentation of the basal layer.

It is frequently associated with DM, obesity and insulin-resistance.19 It may be secondary to the use of some medications, such as nicotinic acid, niacinamid, diethylstilbestrol, oral contraceptives, glucocorticoids and folic acid antagonists. The differential diagnosis must be effected with confluent and reticulate papillomatosis of Gougerot-Carteaud, Haber's syndrome, reticular acropigmentation of Kitamura, Dowling-Degos disease and hystrix ichtyosis.

 

2. CUTANEOUS INFECTIONS

DM is a proven complex entity, progressing continually with significant metabolic alterations. It is responsible for the comparison made of a diabetic patient with a veritable immunodepressive.2 Diabetic neuropathy and peripheral vascular insufficiency are frequent in these cases. They represent factors that certainly favor the installation and development of tegument illnesses.3 Hyperosmolarity of the diabetes serum occasions abnormalities of the leukocyte function with respect to which there is an association with nutrient diffusion reduction and leukocyte migration through the thick blood vessel walls. In other words, the diabetic's skin ends up being an organ open to the most varied forms of affliction, especially by infectious origin. It facilitates complications and/or delays curing of processes that are apparently benign and of short duration.1 Piodermitis, abscess and other equally inflammatory/infectious conditions immediately occur with greater severity in these patients.

The same phenomenon occurs with fungus infections,20 including processes caused by dermatophytes and especially genital candidiasis, which often require more energetic treatment by means of systemic anti-fungus therapy.

The severest infections are observed mainly in the subcutaneous cellular tissue in non-insulin-dependent diabetics. These conditions may be provoked by either aerobic or anaerobic germs. As is often the case, gangrene develops in the affected tissues, which frequently requires debridement and introduction of broad-spectrum antibiotherapy21 via the systemic route.

Such complications occur above all on the lower limbs and in the perineal region, which make for situations of absolute severity. It is common, therefore, when therapeutic measures are not adopted in time or with the required intensity. It may progress into septicemic conditions and even cause the patient's death.

What deserve special attention are nasal and eyelid inflammatory lesions. In these cases, the possibility of rhinocerebral mucormycosis must be immediately examined.22 The latter is an urgent condition. Affliction of the face and affection of the ocular globe are usually observed, with a risk of central nervous system involvement. In the severest cases, onset of a meningitis condition may occur, which may be lethal if not promptly identified.

 

3. REACTIONS TO MEDICATIONS

Such reactions may be associated with the use of insulin or oral hypoglycemics.

 

1. SECONDARY TO THE USE OF INSULIN

1.1. Insulin Edema

In some patients, after severe hyperglycemias have been corrected quickly, the appearance of edema, weight gain and visual perturbation may be observed. These signs and symptoms are most frequently observed during or after a patient's ketoacidosis insulin treatment, or appear in the patient being chronically decompensated. This condition is called insulin edema, but may also be observed in other situations when metabolic control is quickly improved, even if it be through dieting and use of oral hypoglycemics.

The mechanism responsible for this phenomenon is not well understood. Patients' renal function is normal. Part of the process may occur due to the capacity of insulin to retain sodium and water.4

This condition is usually self-limiting and does not require treatment. Yet when the edema is highly accentuated, temporary use of thiazide diuretics for a day or two is recommended.

1.2. Insulin Lipoatrophy or Lipoatrophy Hypodystrophy

This disorder consists of localized areas of hyperesthesia and skin depression due to atrophy of the subcutaneous adipose tissue. It results from fat loss at the site of the insulin injection or in remote sites. It may be concomitant with hypertrophic areas.

Its prevalence is greater among young females, usually developing three to six months after starting insulinotherapy.

The exact mechanism responsible for this phenomenon is not well understood. It seems to arise from the immunologic process associated with some insulin contaminant or occurs with greater frequency in patients treated with less purified bovine insulin, notably in children and women. It is rare in patients using highly purified insulin.5

Patients with this condition also show a high prevalence of atopia. A biopsy of the affected areas indicates the presence of antibodies in the blood vessel walls of the dermis.

Treatment is effected with monocomponent human insulin. It is injected into the edges of the lipoatrophy areas, proceeding toward the center of the lesion after recuperation and filling in of the treated area. Monocomponent pork preparations also provide good results. Addition of corticosteroids (dexamethasone 4µg/U) to insulin may be useful when purified insulin is available, while it has proved to be ineffective in rare lipoatrophy cases with human insulin.

1.3 Hypertrophic lipodystrophy or insulin hypertrophy

These two disorders consist of tumefied areas localized in the regions at which patients repeatedly apply insulin.23 They possibly result from the anabolizing effect of insulin, which is seen in men especially. These areas correspond to hypovascular fibrous masses, which occasion an erratic and incomplete absorption of insulin, and lead to the aggravation of metabolic control. They are often hypoanesthetic, inducing the patient to use the site repeatedly and, therefore, to perpetuate the process.

Hypo-hypertrophy may regress slowly when exchanging insulin for more purified preparations and avoiding those application sites for a few months. By contrast, the local application of purified insulins or corticosteroids does not correct the process.23 Treatment consists in rotating the insulin injection sites.

1.4. Insulin Allergy

Allergic manifestations to insulin may be local or systemic. Reactions vary in intensity, ranging from simple discomfort to lethal manifestations, such as anaphylactic shock.

Recent studies suggest that some patients with local allergic reactions exhibit the identical immunological phenomenon to the one encountered in a systemic manifestation. The severity of the local allergic reaction is variable and ranges from a simple nodule at the injection site to its appearance in areas with intensely pruriginous erythema.

Usually, a passing irritation occurs immediately after insulin injection. Another persistent irritation arises four to eight hours after the injection, characterized by papular erythema. It consists of an IgE-dependent biphasic reaction that may persist as a cutaneous manifestation for several days. The IgE and IgA circulation levels do not prove to be altered. Meanwhile, patients with insulin allergy who respond negatively to the intradermic insulin test show the IgE/IgA relation to be less than in patients whose intradermic test is positive. The blastic transformation of lymphocytes in vitro in allergy patients confronted with different insulins demonstrates response magnitude to be progressively lower in bovine (12%), pork (3.9%) and human insulin (2.4%). In addition to insulin allergy,24 reactions may also occur to protamine, zinc or even to impurities found in the alcohol used for aseptic purposes. The cause of allergy has to be discovered and appropriate therapy must be made with another type of insulin.

The allergic response magnitude to insulin is usually variable, ranging from urticaria to anaphylaxis.4 It results from the interaction between insulin and specific IgE antibodies for insulin found in the mastocytes and basophils of sensitized patients. Formation of IgE insulin complexes stimulates the release of immune response mediators like histamine, which trigger the allergic reaction.

When the clinical condition requires it, anti-histaminics and glucocorticoids are used. Treatment of a systemic allergy to insulin is made with purified insulins. If the condition persists, desensitization occurs. Patients must be hospitalized. If the previous allergic manifestation is very intense, they must be kept in intensive care. Prior to the onset of desensitization a syringe must be prepared with 1:1000 adrenaline. Anti-histaminic and steroid therapy must be suspended prior to desensitization.5

For desensitization, the use of fast-acting human insulin (crystalline) is recommended. When this is not possible, use insulin with a monocomponent or purified pork insulin, and only when using the mixture for lack of being able to obtain others.

 

2. SECONDARIES TO THE USE OF ORAL HYPOGLYCEMICS

2.1. Dermatological Reactions

Chlorpropamide causes cutaneous eruptions in 2 to 3% of patients. While this is usually transient, the drug may bring on severe lesions, such as Stevens-Johnson syndrome, folliative dermatitis, severe photosensitivity and lichenoid cutaneous eruptions. Cutaneous reactions are less frequent than tolbutamide and glyburide.

2.2. Antabuse Effect

Another undesirable action of sulphonilureas is the antabuse-like effect. It is observed in roughly 30% of diabetics making use of chlorpropamide when they consume alcohol. It is characterized by facial flushing, a sensation of dizziness, tachycardia and cephalia, beginning 20 minutes after alcohol intake.

The mechanism involved has not been elucidated. It is assumed that chlorpropamide inhibits aldehyde dehydrogenasis, one of the main enzymes simultaneously involved in the metabolism of alcohol and serotonin. There was an increase of serotonin and acetaldehyde levels, a metabolite of ethyl alcohol, which also requires aldehyde dehydrogenasis for its metabolization.5 The increase in serotonin and/or acetaldehyde could provoke precipitation of the antabuse syndrome.

 

3. DIABETIC FOOT

The feet are convergence points of virtually all chronic complications to which diabetes is subject. The topic deserves a separate discussion as a function of its high potential to produce incapacitating events. A large number of lower limb amputations in diabetic persons occurs annually. It is estimated that more than half of them could have been avoided through appropriate care given to the feet.

Six risk factors of "diabetic foot":

- Over 40 years of age
- SmokerBeing diabetic for over 10 years
- Reduction of arterial or hypesthesia pulses
- Anatomical deformities (arthropathy, callosity)
- Presence of previous ulcerations or amputations

There are numerous clinical variants in accordance with the predominance of each of these pathogenic components.

3.1. Plantar Neurotrophic Ulcer

This ulcer represents the final complication of pathological alterations provoked by neuropathy due to the formation of fissuring and ulcerating plantar callosities.25 The most common localization is in the projection of the first, second or fifth metatarsal bone, but it may have other localizations, such as the heel, and outer edge of the foot or fingers. They are painless lesions insofar as surface and depth sensitivity are eliminated. This is the reason for which the lesions do not prevent walking and do not cause discomfort for patients. In such circumstances, patients do not subject themselves to rest, and continually traumatize the ulcerated location with progressive deterioration of local conditions. The underlying tissues, consisting of muscles, tendons and joints experience a slow process of fibrosis with movement being limited at the ulcer level.

Despite how extensive and severe the ulcers may be, the clinical condition is maintained stable in the absence of deep tissue layer infections, showing only small quantities of fetid secretions without any clinical importance.

Most of the time, the neurotrophic ulcers are not accompanied by truncal artery obstructions or, when these are present, they do not lead to foot ischemia. However, the lasting presence of neurotrophic lesions is not compatible with ischemia.4

Participation of microangiopathy in these cases of long-term progression is not likely with respect to clinical importance. Therefore, in the particular case of plantar neurotrophic ulcers, the clinical balance may only be broken by onset of deep tissue layer infections. Owing to this, the aim of therapy is to prevent infection in addition to helping in the healing process.

Even in a balanced state, without any deep tissue layer infections, there are important manifestations of the skin and its annexes, such as mycotic infection of the nails,26 ungual margins and interdigital spaces.20 Dry and scaly skin is inhabited by altered bacterial flora.3 Local hygiene is important, though frequently neglected by a patient for reasons including the very limitations resulting from DM, such as visual deficiency and obesity. Absolute rest and keeping weight off the foot, i.e. "off-loading" the foot, is effective in preventing complications and allowing the lesion to heal in some cases, albeit slowly and over several months.27 However, rest under these conditions interferes exceedingly in patients' habits and is therefore not tolerated by most of them.

There is a need to modify harmful plantar support and the methods employed undergo constant change. Inelastic dressings and plaster casts are barely effective initial attempts, which may be employed for lack of being able to adopt other techniques. The use of orthopedic inner soles, in accordance with various "off-loading" foot techniques using various material features, has led to excellent results. Applying such podiatric assistance is necessary either as the sole treatment or in association with local surgical interventions.

The infection of the deep layers, leading to phlegmon being propagated in the tendon sheath with great tissue destruction, is the severest complication of neurotrophic plantar ulcer and may appear at an advanced stage due to local insensitivity. In these cases, surgical drainage with resection of the necrosed tissue, at times including underlying bones, is a necessity. It must be effected repeatedly by the formation of new suppurations, followed by second intention healing, which is always slow and subject to failure even under effective medical vigilance.25 In addition to the extension of the affected tissue, the presence of ischemia by truncal obstruction may condition the non-viability of limb conservation. Amputation then becomes necessary. Even in cases in which local surgery is successful, it is necessary to adopt preventive measures to prevent new ulcerations.4

Prophylactic surgery of neurotrophic ulcers (for example, resection of the involved metatarsal head or the whole finger) is not common practice, but may be carried out in selected cases. It should always be complemented by redistributive measures of plantar "off-loading".27

There exist radioisotopic techniques that are still not demonstrable to simple radiology, which allow the implementation of early prophylactic measures.

3.2 Microangiopathic Ulcer

Microangiopathic ulcers have a preferential localization in the calcaneus, in the malleolar regions, dorsal aspect of the foot and lateral and posterior faces of the leg. Necrosis plaques preceding the ulcers arise after traumatisms, cutaneous infections or spontaneously.25 The delimitation of the necrosis is completed by a groove formation between the lesioned area and the skin itself, which occurs between two to four weeks with pain being reduced. The cutaneous necrosis plaque slowly separates from the deep tissues and is eliminated, leaving the ulcer of more or less nitidus limits with a slightly granulous background and covered over with necrotic-fibrosic material. These are painful lesions that may heal with treatment over a period varying from three to six months.5

This treatment requires prolonged rest, hygiene and rigorous local protection. The pain is countered with the usual measures and vasodilators. In the chronic phase it may require surgical lumbar sympathectomy and at times arterial restoration.

3.3. Superficial And Deep Infections

The conditions of the leg skin and dorsal aspect of the foot are averse to bacterial colonization. The latter does not occur in the interdigital spaces, where humidity is greater and pathogenic microorganisms exist that are not found at a close level.

The presence of the latter and occurrence of cutaneous lesions in diabetic persons represent the substratum for the occurrence of severe infections.2,3

Ungual infections resulting from fungi26 and bacteria are frequent, leading to significant nail alterations that may favor the appearance of secondary infections, such as paronychias.

Deep tissue layer invasion or quick progression on the superficial planes has variable significance, depending on the state of local blood circulation. Truncal artery obstruction and microangiopathy favor the onset of infection, and lead to conditions of septic necrosis for a large variety of pathogenic germs. Crepitation often results from the production of gas. However, this does not always form the clostridiosis infection.

3.4. Ischemic Lesions by Truncal Arteriopathy

The obliterating arteriosclerosis of DM patients over a long duration presents more severe clinical and anatomopathological characterics. The most extensive arterosclerotic disease exhibiting the most accelerated clinical progression propitiates ever more conditions for the development of trophic lesions. It also offers fewer opportunities for applying surgical therapeutic measures, as seen in the use of truncular arterial circulation. Leg artery lesions especially limit the possibility of surgery. But in cases having anatomically appropriate conditions for derivative operations, the latter have been accompanied by similar success rates to those for non-diabetic patients.5

From the clinical point of view, diabetic patients with peripheral ischemia show severe cases requiring arterial restorations, but with precarious or inexistent anatomic conditions. When there are neurotrophic lesions or lesions in association with infections, even successful restorations may not be able to prevent a limb amputation.

In monitoring severe ischemia, often aggravated by quickly progressing infections with significant systemic repercusions,21 a leg amputation is necessary in order to save the patient's life. This situation is managed according to the same technical principles of amputation for the ischemic limbs of non-diabetic patients.4

Rehabilitation after a lower limb amputation is limited in diabetic patients by visual deficiency, obesity, and by lesions occurring on the remaining limb. But it is not impossible and may be effected in cases having favorable clinical conditions.27

 

CONCLUSION

Diabetic persons show peculiarities that become susceptible to skin diseases uncommon in non-diabetics. Many of their diseases require quick diagnosis and immediate treatment for occasionally severe complications or even fatal ones to be averted.

 

REFERENCES

1. Koivukangas V et al. Delayed restoration of epidermal barrier function after suction blister injury in patients with diabetes mellitus. Diabet Med 1999; 16(7): 563-7.        [ Links ]

2. Sibbald RG. The skin and diabetes mellitus. Int J Dematol 1984; 23: 567.        [ Links ]

3. Huntley AC. The cutaneous manifestations of diabetes mellitus. JAAD 1986; 14: 612.        [ Links ]

4. Romano G et al. Skin lesions in diabetes mellitus: prevalence and clinical correlations. Diabetes Res Clin Pract 1998; 39(2): 101-6.        [ Links ]

5. Jelinek JE. Cutaneous manifestations of diabetes mellitus. Int J Dermatol 1994; 33(9): 605-17.        [ Links ]

6. Shemer A et al. Diabetic dermopathy and internal complications in diabetes mellitus. Int J Dermatol 1998; 37(2): 113-5.        [ Links ]

7. Ho KK, O'loughlin S, Powell FC. Familial non-diabetic necrobiosis lipoidica. Austral J Dermatol 1992; 33(1): 31-4.        [ Links ]

8. Llajam MA. Koebner's phenomenon and necrobiosis lipoidica diabeticorum. Br J Clin Pract 1990; 44(12): 765.        [ Links ]

9. Yigit S, Estrada E. Recurrent necrobiosis lipoidica diabeticorum associated with venous insufficiency in an adolescent with poorly controlled type 2 diabetes mellitus. J Pediatr 2002; 141(2): 280-2.        [ Links ]

10. Bouhanick B et al. Necrobiosis lipoidica: treatment by hyperbaric oxygen and local corticosteroids. Diabetes Metab 1998; 24(2): 156-9.        [ Links ]

11. Jelinek JE. Perforating granuloma annulare and diabetes mellitus. Int J Dermatol 1990; 29(6): 458.        [ Links ]

12. Mahlbauer Je. Granuloma annulare. JAAD 1980; 3: 217.        [ Links ]

13. Wong GA, Verbov JL. Subcutaneous granuloma annulare of the scalp in a diabetic child. Pediatr Dermatol 2002; 19(3): 276-7.        [ Links ]

14. Cunningham SR et al: Kyrle's disease. JAAD 1987; 16: 117.        [ Links ]

15. Venencie PY et al. Scleredema. Review of 33 cases. JAAD 1984; 11: 128.        [ Links ]

16. James WD et al. Bullous eruption of diabetes mellitus. Arch Dermatol 1980; 116: 1191.        [ Links ]

17. Toonstra J. Bullosis diabeticorum. Report of a case with a review of the literature. J Am Acad Dermatol 1985; Nov; 13(5 Pt 1): 799-805.        [ Links ]

18. Oseid S, Beck-Nielsen H, Pedersen O, Sovik O. Decreased binding of insulin to its receptor in patients with congenital generalized lipodystrophy. N Engl J Med 1977; Feb; 296(5): 245-8.        [ Links ]

19. Hermanns-Le T, Hermanns JF, Pierard GE. Juvenile acanthosis nigricans and insulin resistance. Pediatr Dermatol 2002; 19(1): 12-4.        [ Links ]

20. Torres JE, Lugo SA, Sanchez JL. Response to treatment and recurrence of dermatomycosis in patients with diabetes. PR Health Sci J 1993; 12(3): 189-90.        [ Links ]

21. Shea KW. Antimicrobial therapy for diabetic foot infections. A practical approach. Postgrad Med 1999; 106(1): 85-6, 89-94.        [ Links ]

22. Garcia-Bustinduy M et al. Primary cutaneous mucormycosis: a diagnosis to consider. J Eur Acad Dermatol Venereol 1999; 12(3): 258-62.        [ Links ]

23. Samadaei A et al. Insulin lipodystrophy, lipohypertrophic type. JAAD 1987; 17: 506.        [ Links ]

24. Stromberg LG, Ludvigsson GJ, Bjorksten B. Atopic allergy and delayed hypersensitivity in children with diabetes. J Allergy Clin Immunol 1996; 96(2): 188-92.        [ Links ]

25. Saye DE. The foot: corns, calluses, ingrown nails and diabetic ulcers. Ostomy Wound Manage 1994; 40(1): 16-9, 22-7.        [ Links ]

26. Albreski DA, Gupta AK, Gross EG. Onychomycosis in diabetes. Management considerations. Postgrad Med 1999; 26-30.        [ Links ]

27. Chantelau E. Therapeutic footwear in patients with diabetes. JAMA 2002; 288(10): 1231-2.        [ Links ]

 

 

Correspondence to
Lorivaldo Minelli
Rua Espírito Santo, 1443 - 12° andar - apto 1201
Londrina PR 86020-350
Tel.: (43) 3322-1297

Received in November, 07th of 2000
Approved by the Consultive Council and accepted for publication in March, 10th of 2003

 

 

* Work done in the "Hospital Universitario Regional do Norte do Paraná - Universidade Estadual de Londrina"