Annular erythema

by: Dr. Gamal Soltan

1. DR.GAMAL SOLTAN

2. BY:
Dr. GamalSoltan

3. Erythemarepresents 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 pinkto
dark redto violaceous
DR.GAMAL SOLTAN

4. (1) diffuse (e.g. scarlet fever)
(2) regional, i.e. limited to one anatomic region
(e.g. palmarerythema) or localized area(s) of
the skin (e.g. erysipelas)
(3) reticulated (e.g. cutaneous polyarteritis
nodosa
(4) annular( figurate).
Although most erythemaslast days to months,
some last for only minutes (e.g. flushing).
DR.GAMAL SOLTAN

5. 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

6. ErythemaAnnulareCentrifugum√
ErythemaChronicumMigrans√
ErythemaMarginatumRheumaticum√
ErythemaGyratumRepens√
NecrolyticMigratory Erythema
Annular Erythemaof Infancy
Chronic GranulomatousDisease
DR.GAMAL SOLTAN

7. The term ‘erythemaannulare
centrifugum’ (EAC) has been applied to
a broad spectrum of clinical findings.
As a result, it has come to encompass
more than just annular erythematous
plaques with scale.
DR.GAMAL SOLTAN

8. A hypersensitivity reaction to:
–Infections
Bacterial (E. coli, Strept. TB)
Viral (EBV, poxvirus)
Fungual(Dermatophytid)
Parasitic (Ascaris, Filaria)
–Drugs
Antimalarials, thiazides, estrogen, cimetidine…
–Systemic Diseases
SLE, Sjögren, liver disease, thyroid (Graves) …
–Internal Malignancy
Lymphomas, leukaemias, nasopharyngeal carc., Sqcc, …
DR.GAMAL SOLTAN

9. 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.

10. DR.GAMAL SOLTAN
If expansion of the
annular plaque is not
uniform, incomplete
arcs appear, as do
polycycliclesions, or
simply festooned
bands.
These lesions are
minimally elevated,
and there is
desquamation at the
inner margin, i.e.
trailing scale

11. DR.GAMAL SOLTAN
The scalemay
not be present
in all the lesions
in a particular
patient

12. DR.GAMAL SOLTAN

13. DR.GAMAL SOLTAN

14. –Other annular erythemas
–Other annular lesions
tineacorporis
annular psoriasis
annular urticaria
allergic urticarialeruption
autoimmune disorders including linear
IgAbullousdermatosis, Sjgren’s
syndrome and lupus erythematosus
DR.GAMAL SOLTAN

15. DR.GAMAL SOLTAN
non-specific, with mild
spongiosisand
microvesiculationwith focal
parakeratosiswith mild
superficial perivascular
lymphohistiocytic
infiltrate.
Characteristically, the
inflammatory cells form a
fairly tight aggregate around
vessels, the so-called ‘coat
sleeve’ anomaly.

16. Treating underlying disorder
Topical corticosteroids applied to the
advancing border of the lesions
Topical antipruriticsand antihistamines
Antibioticsor antifungalagents.
Although systemic corticosteroids can
induce a clinical remission, recurrences are
common when medication is discontinued.
DR.GAMAL SOLTAN

17. DR.GAMAL SOLTAN

18. Synonyms:
Erythemamarginatumrheumaticum
Erythemaannularerheumaticum
Key features
■Cutaneous manifestation of acute rheumatic fever
■Associated findings include carditis, migratory
polyarthritis, chorea and subcutaneous nodules
■common in children than in adults
DR.GAMAL SOLTAN

19. An abnormal immunologic response to
infection with group A β-hemolytic
streptococci and by the triad of fever,
arthritis and carditis.
Cutaneous manifestations include
erythemamarginatumand
subcutaneous nodules are seen in a
minority of patients
DR.GAMAL SOLTAN

20. the criteria for the diagnosis of rheumatic
fever:
major criteria : carditis,migratory
polyarthritis, chorea, erythemamarginatum
and subcutaneous nodules.
Minor criteria : fever, arthralgiasand
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

21. The mechanisms that underling are unknown.
Presumably, there is an abnormal humoral
and cellular immune responseto 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

22. DR.GAMAL SOLTAN
Erythematous
maculesspread
peripherally and
become patches or
plaques
absence of associated
scale.
Erythemamarginatum
can also have a
polycyclic
arrangement

23. 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, axillaeand
proximal extremities

24. New lesions usually last from a few
hours to a few daysa. Recurrent crops
can occur over a number of weeks.
Erythemamarginatumis associated
primarily with the active phase of
rheumatic fever, and, it is seen in
conjunction with the carditisand
precedes joint manifestations.
DR.GAMAL SOLTAN

25. An interstitial and perivascularinfiltrate
composed predominantly of neutrophilswithout
vasculitisis observed.
There extravasationof erythrocytes in later
stages.
Direct immunofluorescencemicroscopy for
immunoglobulinsand complement is negative.
Although these histologicfindings are not unique to
erythemamarginatum, they are helpful in excluding
other entities in the differential diagnosis
DR.GAMAL SOLTAN

26. DR.GAMAL SOLTAN
annular erythemaof infancy
oRecurrent 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

27. 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

28. DR.GAMAL SOLTAN

29. Synonyms:
Erythemachronicummigrans
Lymeborreliosis
Lyme disease
Afzelius’ disease
DR.GAMAL SOLTAN

30. Lyme disease is an infection
due to Borreliaburgdorferi
spirochetes that are transmitted
by bites from several species of
Ixodesticks (e.g. I. scapularis, I.
pacificus, I. ricinus).
Erythemamigransrepresents
initial cutaneous manifestation.
DR.GAMAL SOLTAN

31. After Borreliaorganisms have entered the body,
spirochetallipoproteins 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-antibodiesto
different antigens of Borrelia
DR.GAMAL SOLTAN

32. Lyme borreliosisis divided into
three clinical stages:
(1) early localized disease;
(2) early disseminated disease
(3) chronic disease
DR.GAMAL SOLTAN

33. DR.GAMAL SOLTAN
Erythemamigransis
an important clinical
feature of early disease.
Typically, 7–15days
after tick bite, an
erythematousannular
plaque appears that
may have a lighter-
colored central area

34. DR.GAMAL SOLTAN
The diameter is usually
at least 5 cm. Lesions of
primary erythema
migransfavor the
trunk, axilla, groin and
poplitealfossa. the
advancing edge may be
crusted or even
vesicular.

35. DR.GAMAL SOLTAN
Early:
Fever, malaise, arthralgia
Urticaria, malar
erythema, ECM
Late:
Skin: Acrodermatitis
chronicaatrophicans
Chronic arthritis (knee)
Cardiac: Heart block
Neurologic: meningitis,
neuropathies

36. DR.GAMAL SOLTAN

37. DR.GAMAL SOLTAN

38. DR.GAMAL SOLTAN
not specific
may contain eosinophils
and 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 Treponema
pallidumcan also
demonstrate Borrelia
spirochetes in the skin.

39. Early localized disease
Doxycycline100 mg bd14-21 d. √
Amoxycilline500 mg tid14-21 d.
Penicillin G 20 mil. u. / d 14-21 d.
Early disseminated and chronic disease
Ceftriaxone2 g (75–100 mg/kg) iv once
daily 14-28 days
Cefotaxime2 g (50–70 mg/kg) iv q8h
14028 days
DR.GAMAL SOLTAN

40. DR.GAMAL SOLTAN

41. Synonym:
Gammel’sdisease
A paraneoplasticfigurate 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

42. 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

43. DR.GAMAL SOLTAN
multiple
Annular erythematous
lesions
develop scale at their
edges and advance at a
rapid rate (up to 1 cm per
day). spreadis
significantly faster than
that of EAC. Lesions have a
wood-grain or zebra-like
pattern, due to the
development of ‘rings
within rings

44. DR.GAMAL SOLTAN
85 % of erythemagyratum
repensis 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.

45. Epidermis
Parakeratosis,
Focal Spongiosis
Exocytosis, neutrophilsand eosinophils
Dermis
Superficial perivascularlymphohistiocyticInfiltrate
Eosinophilsand melanophages
DR.GAMAL SOLTAN

46. In addition to excluding the other types of
figurate erythema, erythemagyratum
repens-like lesionsmay be seen in patients
with:
bullouspemphigoid
epidermolysisbullosaacquisita
figurate forms of psoriasis
linear IgAbullousdermatosis
resolving pityriasisrubrapilaris
DR.GAMAL SOLTAN

47. Erythemagyratumrepensresolves
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

48. DR.GAMAL SOLTAN