DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
BY:
Dr. Gamal Soltan
Erythema represents a change in the color of the skin that is due to the dilation of blood vessels in the papillary and reticular dermis. As arteries or veins may be involved, the color can vary from pink to dark red to violaceous
DR.GAMAL SOLTAN
(1) diffuse (e.g. scarlet fever)(2) regional, i.e. limited to one anatomic region
(e.g. palmar erythema) or localized area(s) of the skin (e.g. erysipelas)
(3) reticulated (e.g. cutaneous polyarteritisnodosa
(4) annular( figurate).
Although most erythemas last days to months, some last for only minutes (e.g. flushing).
DR.GAMAL SOLTAN
Result of formation of a localized highly viscous focus of ground substance by proliferating fibroblasts in response to cytokines secreted by granulocytes. Antigens or Immune complexes diffuse in the less viscous perimeter of the growing focus.
DR.GAMAL SOLTAN
Erythema Annulare Centrifugum √
Erythema Chronicum Migrans √
Erythema Marginatum Rheumaticum√
Erythema Gyratum Repens √
Necrolytic Migratory Erythema
Annular Erythema of Infancy
Chronic Granulomatous Disease
DR.GAMAL SOLTAN
The term ‘erythema annularecentrifugum’ (EAC) has been applied to a broad spectrum of clinical findings.
As a result, it has come to encompass more than just annular erythematousplaques with scale.
DR.GAMAL SOLTAN
A hypersensitivity reaction to:– Infections
Bacterial (E. coli, Strept. TB)Viral (EBV, poxvirus)Fungual (Dermatophytid)Parasitic (Ascaris, Filaria)
– DrugsAntimalarials, thiazides, estrogen, cimetidine …
– Systemic DiseasesSLE, Sjögren, liver disease, thyroid (Graves) …
– Internal MalignancyLymphomas, leukaemias, nasopharyngeal carc., Sqcc, …
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
They begin as firm pink papules that expand centrifugally and then develop central clearing.
An individual lesion can enlarge to greater than 6 cm in diameter over a period of 1 to 2 weeks.
DR.GAMAL SOLTAN
If expansion of the annular plaque is not uniform, incomplete arcs appear, as do polycyclic lesions, or simply festooned bands.
These lesions are minimally elevated, and there is desquamation at the inner margin, i.e. trailing scale
DR.GAMAL SOLTAN
The scale may not be present in all the lesions in a particular patient
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
– Other annular erythemas
– Other annular lesionstinea corporis
annular psoriasis
annular urticaria
allergic urticarial eruption
autoimmune disorders including linear IgA bullous dermatosis, Sjgren’ssyndrome and lupus erythematosus
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
non-specific, with mild spongiosis and microvesiculation with focal parakeratosis with mild superficial perivascularlymphohistiocyticinfiltrate.
Characteristically, the inflammatory cells form a fairly tight aggregate around
vessels, the so-called ‘coat sleeve’ anomaly.
Treating underlying disorder
Topical corticosteroids applied to the advancing border of the lesions
Topical antipruritics and antihistamines
Antibiotics or antifungal agents.
Although systemic corticosteroids can induce a clinical remission, recurrences are common when medication is discontinued.
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
Synonyms:
Erythema marginatum rheumaticum
Erythema annulare rheumaticum
Key features■ Cutaneous manifestation of acute rheumatic fever
■ Associated findings include carditis, migratory polyarthritis, chorea and subcutaneous nodules
■ common in children than in adultsDR.GAMAL SOLTAN
An abnormal immunologic response to infection with group A β-hemolytic streptococci and by the triad of fever, arthritis and carditis.
Cutaneous manifestations include erythema marginatum and subcutaneous nodules are seen in a minority of patients
DR.GAMAL SOLTAN
the criteria for the diagnosis of rheumatic fever:
major criteria : carditis,migratorypolyarthritis, chorea, erythema marginatumand subcutaneous nodules.
Minor criteria : fever, arthralgias and abnormal laboratory findings (elevated ESR, elevated C-reactive protein, or prolonged PR interval on an ECG).
To establish the diagnosis of acute rheumatic fever, two major or one major and two minor criteria
DR.GAMAL SOLTAN
The mechanisms that underling are unknown.
Presumably, there is an abnormal humoraland cellular immune response to one or more antigens associated with group A β-hemolytic streptococci.
Antigenic mimic cross-reacting with group A streptococcal antigens have been identified in human myosin, actin, tropomyosin, keratin, laminin, N-acety-lglucosamine, and vimentin.
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
Erythematousmacules spread peripherally and become patches or plaques
absence of associated scale.
Erythema marginatumcan also have a polycyclic arrangement
DR.GAMAL SOLTAN
The lesions are usually asymptomatic, and, over a period of 12 hours migrate by 2–12 mm; in areas of previous involvement, the skin appear pale or lightly pigmented. The most common locations are the trunk, axillae and proximal extremities
New lesions usually last from a few hours to a few days a. Recurrent crops can occur over a number of weeks.
Erythema marginatum is associated primarily with the active phase of rheumatic fever, and, it is seen in conjunction with the carditis and precedes joint manifestations.
DR.GAMAL SOLTAN
An interstitial and perivascular infiltrate composed predominantly of neutrophils without vasculitis is observed.
There extravasation of erythrocytes in later stages.
Direct immunofluorescence microscopy for
immunoglobulins and complement is negative.
Although these histologic findings are not unique to erythema marginatum, they are helpful in excluding other entities in the differential diagnosis
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
annular erythema of infancyo Recurrent annular erythematous
plaques, usually lasting a few days; typically affects infants 3–11 months of age
primarily annular urticaria
hereditary periodic fever syndromes
annular erythema
hereditary angioedema
no specific therapy.
Usually, its clinical course is unaltered by treatment of the underlying acute rheumatic fever;
however, symptoms are usually mild and lesions resolve spontaneously.
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
Synonyms:
Erythema chronicum migrans
Lyme borreliosis
Lyme disease
Afzelius’ disease
DR.GAMAL SOLTAN
Lyme disease is an infection due to Borrelia burgdorferispirochetes that are transmitted by bites from several species of Ixodes ticks (e.g. I. scapularis, I. pacificus, I. ricinus).
Erythema migrans represents initial cutaneous manifestation.
DR.GAMAL SOLTAN
After Borrelia organisms have entered the body, spirochetal lipoproteins may trigger the innate immune system, with cytokines production by macrophages.
In addition, (Th1) response is triggered as part of the adaptive immune system.
Both adaptive T-cell and B-cell responses facilitate the synthesis of auto-antibodies to different antigens of Borrelia
DR.GAMAL SOLTAN
Lyme borreliosis is divided into three clinical stages:
(1) early localized disease;
(2) early disseminated disease
(3) chronic disease
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
Erythema migrans is
an important clinical feature of early disease.
Typically, 7–15 days after tick bite, an erythematous annular plaque appears that may have a lighter-colored central area
DR.GAMAL SOLTAN
The diameter is usually at least 5 cm. Lesions of primary erythemamigrans favor the trunk, axilla, groin and popliteal fossa. the advancing edge may be crusted or even vesicular.
DR.GAMAL SOLTAN
Early:Fever, malaise, arthralgia
Urticaria, malarerythema, ECM
Late:Skin: Acrodermatitischronica atrophicans
Chronic arthritis (knee)
Cardiac: Heart block
Neurologic: meningitis, neuropathies
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
not specificmay contain eosinophilsand plasma cells in the infiltrate. In addition, multiple apoptotic cells may be observed in the epidermis.
A silver stain such as the Warthin–Starry stain that is used to detect Treponemapallidum can also demonstrate Borreliaspirochetes in the skin.
Early localized diseaseDoxycycline 100 mg bd 14-21 d. √Amoxycilline 500 mg tid 14-21 d.Penicillin G 20 mil. u. / d 14-21 d.
Early disseminated and chronic diseaseCeftriaxone 2 g (75–100 mg/kg) iv once
daily 14-28 days Cefotaxime 2 g (50–70 mg/kg) iv q8h
14028 days
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
Synonym:
Gammel’s disease
A paraneoplastic figurate erythema.
The cutaneous lesions arise as a result of an immune reaction against tumor-associated antigens with the subsequent recognition of similar antigens in the skin.
DR.GAMAL SOLTAN
An immune reaction in which there is a cross-reaction between tumor antigens and cutaneous antigens.
the tumor produces a modification in its basement membrane and this subsequently induces an immune response.
Recognition of similar antigens in the BMZ of the skin then leads to the cutaneous eruption.
The responsible antigen(s) is not known
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN
multiple Annular erythematouslesions develop scale at their edges and advance at a rapid rate (up to 1 cm per day). spread is significantly faster than that of EAC. Lesions have a wood-grain or zebra-like pattern, due to the development of ‘rings within rings
DR.GAMAL SOLTAN
85 % of erythema gyratumrepens is associated with an underlying neoplasm,
Most commonly lung, breast, stomach or esophagus.
The cutaneous lesions develop
from 1 year prior to 1 year after the diagnosis of the neoplasm.
EpidermisParakeratosis,
Focal Spongiosis
Exocytosis, neutrophils and eosinophils
DermisSuperficial perivascular lymphohistiocytic Infiltrate
Eosinophils and melanophages
DR.GAMAL SOLTAN
In addition to excluding the other types of figurate erythema, erythema gyratumrepens-like lesions may be seen in patients with:
bullous pemphigoid
epidermolysis bullosa acquisita
figurate forms of psoriasis
linear IgA bullous dermatosis
resolving pityriasis rubra pilaris
DR.GAMAL SOLTAN
Erythema gyratum repens resolves when the associated neoplasm is successfully treated.
There may be a return of cutaneous lesions in association with the development of metastases or local recurrences of the malignancy.
DR.GAMAL SOLTAN
DR.GAMAL SOLTAN