Middennal elastolysis 
Case report 
MIDDERMAL ELASTOLYSIS 
K. Peris, G.P. Mazzochetti, S. Dietrich and S. Chimenti 
ABSTRACT 
Middermal elastolysis (MDE) is an acquired idiopathic non-inflammatory dermatosis, clinically characterized by areas of 
fine wrinkling of the skin, and histopathologically exhibiting a rniddermal los s of elastic fibers. We report two cases of idiopathic 
rniddermal elastolysis recently observed in our department. After considering the main differential diagnoses, we discuss the 
etiopathogenetic hypothesis underlying the most appropriate therapies. 
KEYWORDS 
middermal elastolysis, idiopathic 
INTRODUCTION 
Middermal elastolysis (MDE) is characterized by well 
circumscribed areas of fine wrinkling of the skin which 
histopathologically exhibit rniddermal loss of elastic fibers. 
The first reported case was preceded by a recurrent urticarial 
eruption, which led Shelley and Wood (1977) to postulate 
that dermal inflammation may have resulted in specific zonal 
destruction of elastic tissue (1). The histological exarnination 
showed a striking absence of elastic tissue in a band-like 
region, strictly lirnited to the rniddle derrnis of the involved 
area. Subsequently, Brenner et al. described a similar 
idiopathic loss of middermal elastic tissue leading to 
wrinkling of the skin and perifollicular protrusion in a 33-
year-old, otherwise healthy white woman. However, no 
clinical or histologic evidence of inflammation was found, 
leading them to propose the term non-inflammatory dermal 
elastolysis for this entity (2). 
More recently, Brodet al. have pointed out an inflamma-
tory pathogenesis of MDE (3), and Kirn and Su have 
acta dermatovene rologica A .P.A. Vol 5, 96, No 1 
speculated that sun exposure may be one of the main 
causative factors (4). It has been proposed that the presence 
or absence of inflammation may mainly depend on the stage 
of the skin lesions at the tirne of presentation. 
The authors describe two cases of MDE : the first case a 
39-year-old woman who presented with wrinkling of the 
abdorninal skin; the other one a 29-year-old woman with 
numerous yellowish papules on the chest, back and arms. 
CASEREPORT 
Case l. A 39-year-old woman with widespread areas of 
fine skin wrinkling occurring mainly on the arms and 
abdomen was exarnined . There was no previous history of 
skin diseases . Results of laboratory exarninations, che~t x-
ray and ECG were normal. 
Thyroid function tests revealed no abnormalities. Anti-
nuclear antibodies were within the normal range. Biopsy 
27 
Middermal elastolysis 
specimens of two lesions stained with hematoxylin and eosin 
showed no epidermal abnormalities, but disclosed the 
complete absence of elastic tissue in foci lirnited to the 
rniddermal region. The reticular derrnis appeared normal and 
no inflarnmatory cell infiltrate was present. Collagen fibers 
showed no alteration. Histochernical stain specific for elastic 
fibers confirmed that the absence of elastic fibers was lirnited 
to the rnid-derrnis (Fig. 1). 
Fig. 1. Histological stain far elastica shows the absence of 
elastic fibers to the middle dermis (1 Ox) 
Case 2. In a 29 year-old woman, numerous, asymptomatic, 
discrete, yellowish papules, 0.5-0.8 cm in diarneter appeared 
Fig. 2. Clinical aspects of middermal elastolysis 
28 
progressively on the upper chest, back, and arms (Fig. 2) . 
There was no previous history of skin disease. Results of 
laboratory exarninations, chest x-ray and ECG were un-
remarkable. Thyroid function tests disclosed no abnor-
malities. Antinuclear antibodies were within the normal 
range. A skin biopsy specimen was obtained from the left 
arrn. Hematoxylin eosin staining demonstrated a normal 
epiderrnis and a band-like rniddermal region with complete 
loss of elastic fibers. The loss of elastic tissue did not involve 
perifollicular areas, and the hair follicles were surrounded 
by well-preserved elastic fibers. A sparse superficial and deep 
infiltrate of lymphohistiocytic cells was also observed. 
Collagen fibers displayed no alteration. Histochernical stain 
with Verhoeff-van Gieson confirmed that the absence of 
elastic fibers was lirnited to the rnid-derrnis. 
Patient number 1 was treated according to the literature, 
using daily application of topical retinoid acid cream of 
increasing concentration. Patient number 2 was treated with 
topical retinoic acid cream once daily in conjunction with 
70% glycolic acid once weekly. Although a discrete 
improvement of clinical rnanifestations was observedin both 
cases after 6 months of therapy, patient number 2 improved 
visibly sooner, beginning with the third month of treatment. 
This earlier improvement presumably resulted from the 
epidermolytic action of glycolic acid, and suggests enhancing 
the efficacy of other specific topical therapies (12). 
DISCUSSION 
MDE is a rare acquired idiopathic dermatosis that 
predorninantly affects rniddle-aged women. Lesions 
frequently involve the arrns, trunk and shoulders, while the 
face is generally spared. Usually, there is no farnily history 
or systernic involvement. There are no signs of atrophy or 
herniation. According to Trueb, the lesions can be classified 
as localized or generalized, congenital or acquired (5,6). Two 
morphologic patterns ofMDE have been described: type 1 
lesions, as in our case 1, appear as tiny wrinkles arranged 
parallel to the skin cleavage lines. Histology reveals that the 
elastic tissue is preserved in the superficial derrnis but absent 
in the rniddle derrnis. Generally no inflarnmatory infiltrate 
is present. 
Type 2 lesions, as in our case 2, appear as small soft papules 
that consist of perifollicular protrusions. The diffuse los s of 
elastic tissue in the rniddle derrnis is interrupted by hair 
follicles surrounded by well-preserved elastic fibers (6). 
An inflarnmatory infiltrate may also be observed. Histo-
logic sirnilarities between anetodermia and type 2 MDE 
suggest the possibility of a related pathogenesis, so that some 
authors consider type 2 MDE to be a clinical form of 
anetoderrnia (3). MDE should be differentiated from other 
disorders of acquired elastolysis. In fact, solar elastosis differs 
acta dermatovenerologica A.PA. Vol 5, 96, No 1 
Middermal elastolysis 
from MDE by its onset in older patients and involvement of 
sun-exposed areas, by hyperplasia, abnormalities of elastic 
fibers, and by basophilic degeneration of the collagen in the 
papillary dermis (4). 
Anetodermia is characterized by the absence of widespread 
wrinkling, and by the presence of herniation as well as 
elastolytic features involving the entire dermis (7). Cutis laxa 
differs from MDE by the presence of lax pendulous skin, 
and the frequent involvement of internal organs (8). 
Postinflammatory elastolysis and cutis laxa differ fromMDE 
by their occurrence in African women, by the occurrence of 
preceding urticaria and/or papuloplaques, and by the 
presence of atrophy and severe disfigurement (9). 
The etiology of MDE is poorly understood. Immune 
reactions, defects in synthesis of elastic tissue, and the release 
of elastase by inflammatory cells have all been postulated 
as possible mechanisms (4). Some authors have also 
hypothesized that sun exposure could be a contributing factor 
in the genesis of this disorder. However, the extensive 
involvement of sun-protected areas and the absence of 
histological evidence of solar elastosis are not consistent with 
the latter view that the damage to elastin in MDE results 
from sun-exposure (3,4). Recently, Fimiani et al. have shown 
that ultra-violet A (UV-A) stimulation of fibroblasts from 
two patients with MDE does not change the quantity of 
elastolytic enzymes, butincreases the level ofthese enzymes 
in fibroblasts from healthy subjects (10). Lacking a well-
understood pathophysiologic genesis for MD E, therapeutic 
measures are of an empiric nature. At this moment, the most 
promising treatment consists of topical retinoic acid cream 
in conjunction with the use of sunscreens (11). 
REFERENCES 
l. Shelley WB, Wood MG. Wrinkles due to idiopathic loss 
of middermal elastic tissue. Br J Dermatol 1977; 97: 441-
445 
2. Brenner W, Gschnait F, Konrad K, Holubar K, Tappeiner 
J. Non-inflammatory dermal elastolysis. Br J Dermatol 1978; 
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3. Brod BA, Rabkin M, RhodesAR, Jegasoty BV. Middermal 
elastolysis with inflarnmation. J Am Acad Dermatol 1992; 
26: 882-884 
4. Kirn JM, Su WPD. Middermal elastolysis with wrinkling: 
report of two cases and review of the literature. J Am Acad 
Dermatol 1992; 26: 169-173 
5. Trueb RM, Burg G. ldiopathic middermal elastolysis. 
Dermatol 1993; 187:62-66 
6. Maghraoui S, Grossin M, Crickx B, Blanchet P, Belaich 
S. Middermal elastolysis: report of case with a predominant 
perifollicular pattern. J Am Acad Dermatol 1992; 26: 490-
492 
7. Cerroni L, Orlando GC, Peris K, Lunghi F, Chimenti S. 
Anetodermia di Schweninger-Buzzi Giorn lot Derm Ped 
1990; 1: 23-29 
8. Harris RB, Heaphy MR, Perry HO. Generalized elastolysis 
(cutis laxa). AmJ Med 1978; 65: 815-822 
9. Lewis PG, HoodAF, Barnett NK et al. Postinflammatory 
elastolysis and cutis laxa. J Arn Acad Derrnatol 1990; 22: 
40-48 
10. Fimiani M, Mazzatenta C, Rubegna P, Lungarella G. 
Midderrnal elastolysis: Aspetti ultrastrutturali e ruolo delle 
proteasi elastolitiche. In Riassunti 69' Congresso SIDEV 
Sorrento, 1994 
11. Rae V, Falanga V. Wrinkling due to middermal elastolysis. 
Arch Derrnatol 1989; 125: 950-951 
12. Van Scott EJ, Yu RJ. Alpha hydroxyacids: therapeutic 
potential. Canadian J Dermatol 1989; 1: 108-112 
AUTHORS' ADDRESSES 
Ketty Peris MD, Departrnent of Dermatology, University of L' Aquila, Via Vetoio-Coppito 2, 67100 L' Aquila, ltaly . 
Claudia Cotellessa MD, same address 
Giampero Mazzocchetti MD, same address 
Sergio Chimenti MD, Professor and Chairrnan of the Departrnent of Dermatology, University of L' Aquila, same address 
acta dermatovenerologica A.P.A. Vol 5, 96, No 1 29