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PubMed2004

Collagenolytic (necrobiotic) granulomas: part 1--the "blue" granulomas.

A collagenolytic or necrobiotic non-infectious granuloma is one in which a granulomatous infiltrate develops around a central area of altered collagen and elastic fibers. The altered fibers lose their distinct boundaries and exhibit new staining patterns, becoming either more basophilic or eosinophilic. Within the area of altered collagen, there may be deposition of acellular substances such as mucin (blue) or fibrin (red), or there may be neutrophils with nuclear dust (blue), eosinophils (red), or flame figures (red). These color distinctions can be used as a simple algorithm for the diagnosis of collagenolytic granulomas, i.e. "blue" granulomas vs. "red" granulomas. Eight diagnoses are included within these two groupings, which are discussed in this two-part article. In this first part, the clinical presentation, pathogenesis, and histologic features of the "blue" collagenolytic granulomas are discussed. These are the lesions of granuloma annulare, Wegener's granulomatosis, and rheumatoid vasculitis. In the subsequent half of this two-part series, the "red" collagenolytic granulomas will be discussed; these are the lesions of necrobiosis lipoidica, necrobiotic xanthogranuloma, rheumatoid nodules, Churg-Strauss syndrome, and eosinophilic cellulitis (Well's syndrome).

Arthritis, Rheumatoid↗

PubMed2004

Collagenolytic (necrobiotic) granulomas: part II--the 'red' granulomas.

A collagenolytic or necrobiotic non-infectious granuloma is one in which a granulomatous infiltrate develops around a central area of altered collagen and elastic fibers. The altered fibers lose their distinct boundaries and exhibit new staining patterns, becoming either more basophilic or eosinophilic. Within the area of altered collagen, there may be deposition of acellular substances such as mucin (blue) or fibrin (red), or there may be neutrophils with nuclear dust (blue), eosinophils (red), or flame figures (red). These color distinctions can be used as a simple algorithm for the diagnosis of collagenolytic granulomas, i.e. 'blue' granulomas vs. 'red' granulomas. Eight diagnoses are included within these two groupings, which are discussed in this two-part article. In the previously published first part, the clinical presentation, pathogenesis and histologic features of the 'blue' collagenolytic granulomas were discussed. These are the lesions of granuloma annulare, Wegener's granulomatosis, and rheumatoid vasculitis. In this second half of the series, the 'red' collagenolytic granulomas are discussed; these are the lesions of necrobiosis lipoidica, necrobiotic xanthogranuloma, rheumatoid nodules, Churg-Strauss syndrome, and eosinophilic cellulitis (Well's Syndrome).

Churg-Strauss Syndrome↗

PubMed2005

Rapid improvement of recalcitrant disseminated granuloma annulare upon treatment with the tumour necrosis factor-alpha inhibitor, infliximab.

Granuloma annulare (GA) is a chronic inflammatory disorder of unknown aetiology, which is characterized clinically by erythematous plaques preferentially localized to the distal extremities, although disseminated variants exist. In light of the chronic relapsing nature of GA and lack of satisfactory treatment options, we initiated treatment with infliximab in a patient with chronic disseminated GA that was recalcitrant to standard treatment. The 59-year-old female patient with insulin-dependent diabetes had experienced GA lesions for more than 4 years despite various systemic and topical treatments. Systemic glucocorticoids were not a therapeutic option because of the preexisting unstable insulin-dependent diabetes. Infliximab was administered intravenously at 5 mg kg(-1) day(-1) at weeks 0, 2 and 6 and thereafter at a monthly interval for an additional 4 months. Most of the GA plaques resolved within 4-6 weeks, leaving postinflammatory brownish macules. Newly arising plaques disappeared within 2 weeks and new GA lesions were not observed during the entire observation period of more than 16 months. Infliximab may be an additional option in the treatment of recalcitrant forms of GA as well as in other chronic granulomatous skin disorders, such as sarcoidosis and necrobiosis lipoidica.

Antibodies, Monoclonal↗

PubMed2006

Necrobiotic xanthogranuloma with paraproteinaemia.

Necrobiotic xanthogranuloma is a rare cutaneous condition that can be mistaken for atypical necrobiosis lipoidica. It has a strong association with a paraproteinaemia, which may progress to frank haematological malignancy. We describe four patients with variable cutaneous features, and their treatment response.

Aged↗

PubMed1993

Generalised granuloma annulare successfully treated with pentoxifylline.

Generalised granuloma annulare (GA) is a chronic disease of unknown aetiology and is recalcitrant to many treatment regimes. Some investigators have suggested that an immune medicated vasculitis may be involved in the pathogenesis of GA. We describe a patient with a ten year history of generalised GA, who showed dramatic clearing of the majority of papules after four weeks of treatment with pentoxifylline. This drug has shown promising results in the treatment of many dermatologic disorders including necrobiosis lipoidica diabeticorum, leukocytoclastic vasculitis and Raynaud's phenomenon. Pentoxifylline is thought to reduce blood viscosity via effects on all major blood components, and its clinical effectiveness in generalised GA lends support to a model of immune-medicated vasculitis in the pathogenesis of this disorder. Thus, pentoxifylline offers a well-tolerated and effective alternative to the treatment options available for patients with granuloma annulare.

Blood Viscosity↗

PubMed1988

Actinic granuloma (O'Brien).

Twelve cases of actinic granuloma (O'Brien) are reported. It is concluded that actinic granuloma is a specific disease characterized by clinical lesions indistinguishable from granuloma annulare, but occurring on solar damaged skin. Histologically, elastic tissue is destroyed by the granulomatous process in actinic granuloma, but not in granuloma annulare. It would appear that actinic granuloma, granuloma multiforme, necrobiosis lipoidica of the face and scalp (Wilson-Jones) and Miescher's granuloma of the face (Mehregan and Altman) are the same disease.

Adult↗

PubMed1988

Necrobiotic xanthogranuloma: a case without paraproteinemia but with transepithelial elimination.

We report a female patient, now aged 60, followed for 20 years for lesions originally diagnosed as necrobiosis lipoidica diabeticorum. In fact, the anatomical and clinical features of her disorder correspond to the new entity described as necrobiotic xanthogranuloma. Two elements distinguish this from earlier cases: 1) two examinations failed to reveal paraproteinemia; 2) there was transepithelial elimination of cholesterol crystals and degenerated xanthomatous cell debris via hair follicles. This demonstrates the characteristic histology of the disorder and indicates that the diagnosis of necrobiotic xanthogranuloma should be considered even in the absence of paraproteinemia.

Cholesterol↗

PubMed1987

Rheumatoid nodule in the oral mucosa. A case report with immunohistochemical study.

A case of rheumatoid nodule in the buccal mucosa is reported. Histologically, 3 of zones characteristic rheumatoid nodules were recognized: a central necrotic area, an intermediate zone with palisading mesenchymal cells and an outer layer composed of chronic inflammatory cells. By immunohistochemical studies, ferritin was found in some of the cells in the intermediate zone, suggesting that these cells may be of histiocytic origin. Granuloma annulare and necrobiosis lipoidica may be differential diagnoses.

Aged↗

PubMed2005

Phototherapy and photochemotherapy of sclerosing skin diseases.

The treatment of sclerosing skin diseases [systemic sclerosis, localized scleroderma, lichen sclerosus et atrophicus, sclerodermoid graft-vs.-host disease, scleredema adultorum (Buschke), scleromyxedema and necrobiosis lipoidica] is difficult and remains a great challenge. Numerous treatments, some with potentially hazardous side effects, are currently used with only limited success. The introduction of phototherapy and photochemotherapy for sclerosing skin diseases has considerably enriched the therapeutic panel and proven useful in a number of sclerosing skin diseases especially in localized scleroderma. Two phototherapeutic modalitites are used for the treatment of sclerosing skin diseases, long-wave ultraviolet A and psoralen plus ultraviolet A (PUVA). This article reviews current knowledge about the application of phototherapy and photochemotherapy to various sclerosing skin disorders.

Humans↗

PubMed1983

Diabetic scleredema.

Many skin lesions are specific for diabetes mellitus. Necrobiosis lipoidica, lipoatrophy and idiopathic bullae (bullosis diabeticorum) are usually associated with diabetes. However, diabetic scleredema has not been noticed by internists, although dermatologists have paid attention to such a cutaneous manifestation. We reported a clinical case of a female diabetic patient aged 15 who had been afflicted with diabetic scleredema. She had been treated with insulin since 5 years of age. She noticed stiffness of the skin in April 1980. Skin biopsy showed thickness of the dermis and accumulation of acid mucopolysaccharide. After control of blood glucose with continuous subcutaneous insulin infusion (CSII) and administration of tocopherol acetate and hyaluronidase, the skin lesion improved. Etiology of diabetic scleredema is unknown. Such skin lesion which is observed frequently in insulin dependent obese patients is different from a category of scleredema of Buschke.

Adolescent↗

PubMed2002

Dermatological care of the diabetic foot.

Approximately 30% of patients with diabetes mellitus will have disease-related dermatological problems. Dry skin can be associated with autonomic neuropathy and may be fragile, promoting bacterial invasion. Any potentially infected 'diabetic foot' must be taken seriously, and non-painful deep sepsis suspected if there is evidence of sensory loss. Consideration should be given to eliminating nasal carriage of staphylococci if recurrent superficial sepsis occurs in the presence of poor diabetic control. Fungal infections, both of skin and nails, are common but usually not serious in the absence of immunosuppression. Treatment with topical antifungals may need to be combined with systemic therapy for successful eradication. Systemic antifungal therapy should be carefully considered as treatment needs to be prolonged and is potentially toxic, particularly in individuals with diabetes mellitus who often have co-morbidities. Varicose eczema should be treated by physical therapies intended to improve venous return and prevent peripheral edema and tissue injury. Allergic dermatitis is commonly associated with topical treatments and other sensitizers. Many reactions are not apparent from history, and patch testing for sensitivity is recommended. There are several diabetes mellitus-specific conditions that dermatologists must be aware of, including, necrobiosis lipoidica diabeticorum, granuloma annulare, diabetic dermopathy (spotted leg syndrome or shin spots), diabetic bullae (bullosis diabeticorum), and limited joint mobility and waxy skin syndrome. Ulceration, due to varying combinations of peripheral vascular disease and sensory neuropathy, is the province of the specialist team dealing with the diabetic foot and should ideally be referred to an appropriate multidisciplinary team.

Diabetes Complications↗

PubMed2003

Cutaneous manifestations of endocrine disorders: a guide for dermatologists.

Dermatologists may commonly see skin lesions that reflect an underlying endocrine disorder. Identifying the endocrinopathy is very important, so that patients can receive corrective rather than symptomatic treatment. Skin diseases with underlying endocrine pathology include: thyrotoxicosis; hypothyroidism; Cushing syndrome; Addison disease; acromegaly; hyperandrogenism; hypopituitarism; primary hyperparathyroidism; hypoparathyroidism; pseudohypoparathyroidism and manifestations of diabetes mellitus. Thyrotoxicosis may lead to multiple cutaneous manifestations, including hair loss, pretibial myxedema, onycholysis and acropachy. In patients with hypothyroidism, there is hair loss, the skin is cold and pale, with myxedematous changes, mainly in the hands and in the periorbital region. The striking features of Cushing syndrome are centripetal obesity, moon facies, buffalo hump, supraclavicular fat pads, and abdominal striae. In Addison disease, the skin is hyperpigmented, mostly on the face, neck and back of the hands. Virtually all patients with acromegaly have acral and soft tissue overgrowth, with characteristic findings, like macrognathia and enlarged hands and feet. The skin is thickened, and facial features are coarser. Conditions leading to hyperandrogenism in females present as acne, hirsutism and signs of virilization (temporal balding, clitoromegaly).A prominent feature of hypopituitarism is a pallor of the skin with a yellowish tinge. The skin is also thinner, resulting in fine wrinkling around the eyes and mouth, making the patient look older. Primary hyperparathyroidism is rarely associated with pruritus and chronic urticaria. In hypoparathyroidism, the skin is dry, scaly and puffy. Nails become brittle and hair is coarse and sparse. Pseudohypoparathyroidism may have a special somatic phenotype known as Albright osteodystrophy. This consists of short stature, short neck, brachydactyly and subcutaneous calcifications. Some of the cutaneous manifestations of diabetes mellitus include necrobiosis lipoidica diabeticorum, diabetic dermopathy, scleredema adultorum and acanthosis nigricans.

Acromegaly↗

PubMed2005

Manifestations of cutaneous diabetic microangiopathy.

The etiologies of a variety of skin conditions associated with diabetes have not been fully explained. One possible etiological factor is diabetic microangiopathy, which is known to affect the eyes and kidneys in patients with diabetes. There are many mechanisms by which diabetes may cause microangiopathy. These include excess sorbitol formation, increased glycation end products, oxidative damage, and protein kinase C overactivity. All of these processes occur in the skin, and the existence of a cutaneous diabetic microangiopathy has been well demonstrated. These microangiopathic changes are associated with abnormalities of skin perfusion. Because the skin plays a thermoregulatory role, there is significant capillary redundancy in normal skin. In diabetic patients, loss of capillaries is associated with a decrease in perfusion reserve. This lost reserve is demonstrable under stressed conditions, such as thermal stimulation. The associated failure of microvascular perfusion to meet the requirements of skin metabolism may result in diverse skin lesions in patients with diabetes. Many skin conditions peculiar to diabetes are fairly rare. Necrobiosis lipoidica diabeticorum (NLD) and diabetic bullae occur very infrequently as compared with diabetic retinopathy and nephropathy. Conversely, there is a correlation between diabetic microvascular disease and NLD. This correlation also exists with more common skin conditions, such as diabetic dermopathy. This relationship suggests that diabetic microangiopathy may contribute to these conditions even if it is not primarily causal. Clinically, the major significance of diabetic cutaneous microangiopathy is seen in skin ulceration which is very common and has a major impact on diabetic patients. Many factors contribute to the development of diabetic foot ulcers. Neuropathy, decreased large vessel perfusion, increased susceptibility to infection, and altered biomechanics all play a role, but there is no doubt that inadequate small blood vessel perfusion is a major cause of the inability to heal small wounds that eventually results in ulcer formation. The accessibility of skin capillaries makes cutaneous diabetic microangiopathy an attractive model for research on the evolution of microvascular disease in diabetic patients.

Aldehyde Reductase↗

PubMed2000

Finger 'pebbles'. A dermatologic sign of diabetes mellitus.

A 35-year-old obese man presented with a chief complaint of hand dryness of 5 years' duration. He was a store manager and denied exposure to chemicals, repetitive trauma, chronic irritation, and hard manual labor. However, he did admit to frequent hand washing. He had no itching or swelling in his hands, but on occasion he had tenderness in the dry areas. He had no personal or family history of diabetes, heart disease, or renal disease, and he stated that at his annual physical examination 6 months earlier, routine blood work was normal. He reported polyuria (every 2 hours), nocturia (five times per night), and polydipsia but no weakness, weight loss, visual changes, or neurosensory changes. Examination revealed xerosis of his hands and "pebbles" on the dorsal aspect of his fingers. The papules were most dense over the knuckles and interphalangeal joints (figures 1 through 3). He also had dozens of acrochordons (i.e., cutaneous papillomas, or skin tags) 1 to 4 mm in diameter on his neck, axilla, and groin. No other cutaneous lesions were noted. Specifically, there was no scleredema adultorum, necrobiosis lipoidica diabeticorum, acanthosis nigricans, bullae, or patchy pretibial pigmentation, although he did have several brown macules 1 to 5 mm in diameter on the sides of his lower legs. The macules had been present for years. Levels of hemoglobin A1c and glycated hemoglobin were 7.5% and 9.5%, respectively (normal, 4.4% to 5.9% and 5.0% to 7.3%). The patient was referred to his family physician, and his diabetes has been well controlled with insulin.

Adult↗

PubMed1992

Successful treatment of chronic skin diseases with clobetasol propionate and a hydrocolloid occlusive dressing.

The lesions of 141 patients with chronic skin diseases unresponsive to therapy were treated once a week with clobetasol propionate lotion left under the completely occlusive patch Duoderm. In 131 patients the lesions resolved completely, while partial remission was observed in the remaining 10. The mean interval to complete remission was: for chronic plaque psoriasis, 12 days; psoriasis on palms and soles, 2.5 weeks; palmoplantar pustulosis, 2.2 weeks; skin lesions of Reiter's syndrome, 3 weeks; chronic lichenified eczema, 2.0 weeks; neurodermatitis, 3.1 weeks; breast eczema, 9 days; discoid lupus erythematosus, 3.7 weeks; lichen planus, 2.8 weeks; sarcoidosis, 4 weeks; and lichen sclerosus et atrophicus, 2 weeks. Other conditions benefitting from the treatment were pompholyx, necrobiosis lipoidica, granuloma annulare and pretibial myxedema. The amount of topical corticosteroids needed was reduced to at most 1/20 and to as little as 1/100, compared with common topical steroid preparations.

Adult↗

PubMed1998

Cutaneous manifestations of diabetes mellitus.

Of 100 cases of diabetes mellitus examined for cutaneous findings 82% showed cutaneous lesions. Infection (49%) was the most common finding followed by involvement of foot (30%). High incidence of vitiligo (10%) and localized anogenital pruritus (19%) was an unusual feature. Some of the cutaneous markers of diabetes mellitus like necrobiosis lipoidica diabeticorum, diabetic bullae, acquired perforating dermatoses and scleredema were not seen in this study.

Adolescent↗

PubMed2000

Considerations for the global assessment and treatment of patients with recalcitrant wounds.

Many factors, both intrinsic and extrinsic, may contribute to wound recalcitrance. For example, arterial circulation may be impaired by atherosclerosis, vasospastic disorders, microemboli, thromboangiitis obliterans, vasculitis, sickle cell anemia, and antiphospholipid syndrome, all of which may impair healing. Inflammatory disorders that may lead to recalcitrance include pyoderma gangrenosum and necrobiosis lipoidica. Chronic venous insufficiency, infection, diabetes mellitus, systemic malignancy, malnutrition, and exposure to pressure and shear prolong the healing process. Wounds secondary to primary skin carcinoma will not heal. Calciphylaxis, a life-threatening metabolic disorder, leads to multiple ulcerations that are especially difficult to heal. Knowledge of common factors that lead to wound recalcitrance is essential to the wound care clinician, as accurate diagnosis results in appropriate treatment. To arrive at the diagnosis, the wound care clinician must perform a thorough history and physical examination and order relevant investigative studies. Treatment is based on correction of the identified underlying condition. By utilizing a systematic approach in the management of each patient with a chronic wound, the wound care clinician increases the probability of achieving wound closure.

Bandages↗

PubMed1992

[Effective treatment of chronic inflammatory skin diseases. Once a week occlusion therapy with clobetasol propionate and Duoderm].

The lesions of 161 patients with chronic skin diseases that were unresponsive to therapy were treated once a week with clobetasol propionate lotion left under the completely occlusive patch Duoderm. The lesions completely resolved after a period of nine days to four weeks in 148 patients, while partial remission was observed in the remaining 13. The following diseases responded favourably: chronic plaque psoriasis, psoriasis on palms and soles, palmoplantar pustulosis, skin lesions related to Reiter's syndrome, chronic lichenified eczema, neurodermatitis, breast eczema, discoid lupus erythematosus, lichen planus, sarcoidosis, lichen sclerosus et atrophicus and lymphocytic infiltrate of Jessner. Relapses were infrequent when complete histological remission had been achieved. Other diseases which improved with this treatment were pompholyx, necrobiosis lipoidica, granuloma annulare and pretibial myxoedema.

Administration, Cutaneous↗