Case presentation

Ahmad Dhyiaa M.
Under supervision of
Dr.Ahmad AlHajamy
Athraa Shiaa , 22 y old , live in sayed dukhail , married before 9
years and having 4 Childs
Have PMHx significant for 2 successive abortion --- no cardiac or
CNS or eye dosrder
Presneted with gradually enlarging single plaque ( or fold of
redundant skin ) at lower lateral half of neck which had irregular
border and slightly hypertrophied then become multiple with single
one behind the ear.
It was itchy and easily irritated by perfumes .
Patient now under rx with clobetasol and scalin
So from hx and examination
DDX
1. Hypertrophic scar
2. Cutis laxa ,
3. Mid dermal elastolysis
4. Perforating calcific elastosis
5. Linear focal elastosis
6. pseduxanthoma elasticum ,
7. PXE like papillary dermal elastolysis
 Cutis Laxa ( generalized elastolysis )
Cutis laxa, also known as dermatomegaly, dermatolysis, chalazoderma,
and pachydermatocele, is characterized by inelastic loose, redundant
skin. Around the eyelids, cheeks, and neck, the drooping skin
produces a bloodhound-like facies.
Usually, the entire integument is involved. The abdomen is
frequently the site of large, pendulous folds.
There are two welldescribed genetic forms of cutis laxa, the autosomal
dominant and autosomal recessive types.
The dominant form is primarily a cutaneous, cosmetic form, with a
good prognosis.
The recessive form is more common and associated with significant
internal involvement, including hernias, diverticula, pulmonary
emphysema, cor pulmonale, aortic aneurysm, dental caries, large
fontanelles, and osteoporosis. Pulmonary emphysema, cor pulmonale,
Frameshift and splicing mutations in the elastin gene have
been reported in autosomal dominant disease.
Both homozygous and heterozygous missense mutations in the
gene for fibulin 5 have been reported in some patients with the
disease, especially in families with the recessive form. Gene
mutations for fibulin 4 may cause autosomal recessive cutis
laxa associated with emphysema, vascular tortuosity,
ascending aortic aneurysm, inguinal and diaphragmatic hernia,
joint laxity, and pectus excavatum.
X-linked recessive cutis laxa is now known as the occipital
horn syndrome . It is caused by a mutation in the copper-
binding ion-transporting ATPase, ATP7A, and is allelic to
another X-linked disorder, Menkes disease. Nonfamilial cases
have been associated with urticaria, lupus erythematosus,
glomerulonephritis, plasma cell dyscrasias, and systemic
amyloidosis
These acquired cases may have a preceding inflammatory
phase with large numbers of interstitial neutrophils,
eosinophils, or macrophages engulfing elastic f ibers. Isolated
acral disease has been associated with myeloma and
rheumatoid arthritis.
• The Costello syndrome is characterized by increased prenatal
growth, postnatal growth retardation, coarse facies, loose skin
that resembles cutis laxa, cardiomyopathy, and gregarious
personality. Patients are predisposed to abdominal and pelvic
rhabdomyosarcoma in childhood. The disorder appearsto be inherited
as an autosomal dominant trait.
• The de Barsy syndrome is associated with severe cutis laxa, mental
and growth retardation, joint laxity, ocular abnormalities, and
skeletal disease.
Middermal elastolysis
is an acquired, noninherited condition that usually affects
young women. Wide areas of skin demonstrate atrophic
wrinkling. Histologically, elastic tissue is absent from the
middle dermis. Many cases appear to be induced or
aggravated by ultraviolet light exposure.
Clinical features
• In mid-dermal elastolysis, patients can have well-circumscribed to large diffuse
areas of fine wrinkling , usually in a symmetric distribution (type I). The
wrinkles themselves tend to follow cleavage lines.
• Discrete perifollicular papules are seen in some patients (type II), with the site of
the central hair follicle being indented.
• Occasionally, erythematous patches, telangiectasias, and reticulated erythema
may be present (type III).
• Although in the majority of patients there is no history of a prior inflammatory
dermatosis, some patients do report previous mild to moderate erythema and,
rarely, the elastolysis is pre-ceded by urticarial lesions or granuloma annulare.
• Sites of predilection are the trunk, lateral neck, and upper extremities.
• Once the patches of wrinkling have appeared, they usually remain stationary.
They are asymptomatic and give the skin a prematurely aged appearance.
• The affected areas usually have normal pigmentation and no associated scaling,
induration, or herniation.
• There is neither associated systemic involvement nor a family history of similar
lesions.
• While diagnosis is usually confirmed via histologic examination of involved skin,
non-invasive imaging techniques such as optical coherence microscopy or high-
frequency ultrasound may also prove helpful.
 Perforating calcific elastosis
• PERFORATING CALCIFIC ELASTOSIS Also known as periumbilical
perforating PXE and localized acquired cutaneous PXE,
perforating calcific elastosis is an acquired, localized
cutaneous disorder most frequently found in obese,
multiparous, middle-age women.
• Lax, wellcircumscribed, reticulated, or cobblestoned
plaques occur in the periumbilical region with keratotic
surface papules.
• It is a distinct disorder that shares some features of
PXE.
• As in PXE, patients may have calcific elastosis in the
middermis; however, hereditary PXE rarely causes
perforating channels.
None of the systemic features of PXE occurs in perforating calcific elastosis.
It is suggested that repeated trauma of pregnancy, obesity, and abdominal surgery
promote elastic fiber degeneration, resulting in localized disease. PXE can cause
periumbilical lesions, and in the absence of documented perforation, evaluations to
exclude PXE should be performed. There is no effective therapy for perforating
calcific elastosis.
Linear focal elastosis
This elastosis variant presents with asymptomatic, palpable, or
atrophic, yellow lines of the middle and lower back, thighs, arms,
and breasts
Linear focal elastosis is more common in males. Histologically,
increased elastic fibers are seen, characterized by thin, wavy, and
elongated as well as fragmented bundles. Electron microscopy reveals
thin, elongated, irregularly shaped, swollen elastic fibers with
degenerative changes.
 PXE like papillary dermal elastolysis
PXE-like papillary dermal elastolysis
Usually 6th–9th decades; primarily women presented with Multiple 2–3 mm yellow or
skin-colored papules coalescing to form plaques with a cobblestone appearance;
common at neck, flexor forearms, axillae, lower abdomen, inframammary folds
Hitology Decreased elastic tissue in a band-like distribution in the papillary dermis,
with fragmentation and clumping of elastic fibers
 PSEUDOXANTHOMA ELASTICUMP
pseudoxanthoma elasticum (PXE) is an inherited disorder involving the
connective tissue of the skin, eye, and cardiovas-cular system. Many
cases appear to be sporadic. In familial cases, both a recessive and a
dominant inheritance pattern have been reported, with the recessive
form apparently more common. The skin changes generally present as
small, circumscribed, yellow to cream-colored papules on the sides of
the neck and flexures, giving the skin a “plucked chicken skin”
appearance .
Lax, redundant folds of skin may be present . Nuchal comedones
and milia en plaque may also be seen. Characteristic exaggerated
nasolabial folds and mental creases are common. Mental creases
appearing in patients under age 30 are highly suggestive of PXE. In
addition, the inguinal, periumbilical, and periauricular skin, as well as the
mucosa of the soft palate, inner lip, stomach, rectum, and vagina, may be
involved. The characteristic retinal change is the angioid streak, which is
the result of breaks in Bruch’s elastic membrane.
PXE can be demonstrated in more than half of patients with angioid streaks, and 85% of
PXE patients will have retinal findings. PXE, Paget’s disease of the bone, and sickle
cell disease account for the vast majority of patients with angioid streaks. On
funduscopic examination, a reddish brown band is evident around the optic disk, from
which glistening streaks extend. On fluorescent photography, early fluorescence of the
angioid streaks and macular lesions is noted. In addition, there may be hemorrhages and
exudates. Progressive loss of vision often starts after minor trauma to the eye.
Drusenlike spots are often present and show increased autofluorescence, unlike age-
related drusen. Vascular involvement frequently leads to hemorrhage. These
vascular events are caused by the degeneration of the elastic fibers in the vascular
media. Gastric hemorrhage occurs in 10% of patients, and on gastroscopy, diffuse
rather than focal bleeding is common. Epistaxis occurs frequently, but hematuria
is rare. PXE affects the elastic tissue of the cardiac valves, myocardium, and
pericardium. In one study, mitral valve prolapse was found in 71% of 14 patients
examined. Hypertension occurs in many patients older than age 30. Any patient
with hypertension at a young age should be examined for stigmata of PXE. Leg
cramps and intermittent claudication occur prematurely, and peripheral pulses are
diminished or absent. Calcification of peripheral arteries is seen in many patients
over age 30 and may be detected by radiography. Accelerated coronary artery
disease (CAD) can occur, especially in association with hypertension.
Extensive cutaneous calcification and renal and testicular stones may occur. Mutations
in the adenosine triphosphate (ATP)–binding cassette transporter protein subfamily C
member 6 gene (ABCC6) on the short arm of chromosome 16 have been implicated in
the pathogenesis of PXE in a majority of patients, who also have a higher incidence of
CAD. Although the most prominent manifestations of the disease are in the skin, eye,
gut, and heart, mineralization of elastic fibers can be found in many organs.
Histologically, elastic fibers are fragmented and mineralized with calcium. The fibers
stain gray-blue with hematoxylin and eosin (H&E) and are twisted, curled, and broken,
suggesting “raveled wool.” Blind biopsies of scars or axillary skin in patients with a
family history of PXE or with angioid streaks may show early changes of PXE.
Calcium stains are helpful in identifying early disease.
Thank
you
Pathology
• Histologic findings are similar to those of scars and depend upon the stage of
evolution of the striae at the time the biopsy is performed.
• The epidermis can be normal during the early stages, but eventually becomes
atrophic with blunted rete ridges.
• The dermal thickness is decreased, as is the collagen in the upper dermis.
• The collagen bundles lie parallel to the epidermis. Alterations in elastic fibers
are variable, but they can be fragmented, and specific elastin staining can
demonstrate a marked reduction compared with adjacent normal dermis.
There is an absence of both hair follicles and other adnexal structures..
DDX
The diagnosis of striae distensae is usually straightforward, but the differential
diagnosis does include linear focal elastosis (elastotic striae), an entity first described
by Burket et al.28 in 1989. Linear focal elastosis is characterized by rows of yellow,
palpable, striae-like bands on the lower back. Unlike striae, the lesions are raised
and yellow rather than depressed and white. Elderly men are most commonly
affected. Histologically, there is a focal increase in the number of elongated or
fragmented elastic fibers as well as a thickened dermis. It is postulated that linear
focal elastosis may represent an excessive regenerative process of elastic fibers and
could be viewed as a keloidal repair of striae distensae .

An entity referred to as linear lumbar localized elastolysis is said to occur most often
in young men; the linear, raised bands are skincolored and histologically there is
elastolysis within the mid dermis.
Treatment
• Striae distensae have no medical consequences, but they are frequently distressing
to those afflicted.
• As striae tend to improve spontaneously over time, the value of anecdotal
therapies without case controls difficult to assess.
• Treatment of early-stage striae with tretinoin 0.1% cream can improve their
appearance, and its application has been shown to decrease the length and
width of striae.
• Other topical treatments, including 0.05% tretinoin/20% glycolic acid and 10%
L-ascorbic acid/20% glycolic acid, may also improve the appearance of stretch
marks .
• Several lasers have been used to treat striae: the 585 nm pulsed dye laser may
improve the appearance of striae rubrae, but it has no effect
• on striae albae;
• secondary pigmentary alterations in darker skin are a potential complication.
Improvement in the leukoderma of striae albae was noted with the 308 nm
excimer laser, but maintenance treatment was required to sustain the cosmetic
benefit.
• Use of radiofrequency and pulsed magnetic fields may also lead to improvement.
However, currently, there is no specific therapy that results in a complete
response.
 Mid Dermal elastolysis
Introduction
• Mid-dermal elastolysis is a rare acquired disorder of elastic
tissue.
• Clinically, it is usually characterized by diffuse fine wrinkling,
most often located on the trunk, neck, and arms.
• Histologically, a clear band of elastolysis is present in the mid
dermis.
Pathogenesis
• The cause of the acquired elastic tissue degeneration in mid-dermal elastolysis is
still unclear.
• Exposure to UV light is thought to be a major contributing factor in the
degeneration of elastic fibers4 (as in annular elastolytic giant cell granuloma).
• There are reports of mid-dermal elas-tolysis developing after significant UV
exposure, including natural sun-light, UVA (tanning salon), and narrowband UVB
phototherapy5.
• Other possible mechanisms include defects in the synthesis of elastic fibers,
autoimmunity against elastic fibers, and damage to elastic fibers via the
release of elastase by inflammatory cells or fibroblasts.
• An imbalance between matrix metalloprotein-ases (MMPs) and
tissue inhibitors of metalloproteinases (TIMPs) may also be playing
a role, in addition to CD34+ dendritic fibroblasts.
• Recently, a decrease in lysyl oxidase-like 2 (LOXL2) expression,
potentially affecting elastin renewal, was observed in this
condition7.
Clinical features
• In mid-dermal elastolysis, patients can have well-circumscribed to large diffuse
areas of fine wrinkling , usually in a symmetric distribution (type I). The
wrinkles themselves tend to follow cleavage lines.
• Discrete perifollicular papules are seen in some patients (type II), with the site of
the central hair follicle being indented.
• Occasionally, erythematous patches, telangiectasias, and reticulated erythema
may be present (type III).
• Although in the majority of patients there is no history of a prior inflammatory
dermatosis, some patients do report previous mild to moderate erythema and,
rarely, the elastolysis is pre-ceded by urticarial lesions or granuloma annulare.
• Sites of predilection are the trunk, lateral neck, and upper extremities.
• Once the patches of wrinkling have appeared, they usually remain stationary.
They are asymptomatic and give the skin a prematurely aged appearance.
• The affected areas usually have normal pigmentation and no associated scaling,
induration, or herniation.
• There is neither associated systemic involvement nor a family history of similar
lesions.
• While diagnosis is usually confirmed via histologic examination of involved skin,
non-invasive imaging techniques such as optical coherence microscopy or high-
frequency ultrasound may also prove helpful.
Pathology
• The epidermis is normal in appearance and, occasionally, a mild
peri-vascular infiltrate is noted in the dermis.

• Elastic tissue stains, such as Verhoeff–van Gieson or Weigert’s stain,

reveal a selective loss of elastic fibers in the mid dermis
• There is preservation of normal elastic tissue in the superficial
papillary dermis above, in the reticular dermis below, and along
adjacent hair follicles.
• The preservation of elastic tissue around the hair follicles explains the
perifollicular papules observed in some patients.
• By electron microscopy, phagocytosis of normal as well as degener-
ated elastic fiber tissue by macrophages has been described7.
• Elasto-phagocytosis by macrophages is also occasionally observed by
routine histology.
Differential diagnosis
Mid-dermal elastolysis must be differentiated from the other disorders of elastic tissue
such as anetoderma, pseudoxanthoma elasticum (PXE), PXE-like papillary dermal
elastolysis, elastoderma and cutis laxa, espe-cially the acquired form .

• Clinically, anetoderma is characterized by soft macules and papules that herniate

upon palpation, as opposed to diffuse wrinkling. Histo-logically, elastolysis can
occur in the papillary and/or mid-reticular dermis in anetoderma .
• Patients with generalized cutis laxa have loose, redundant skin, hanging in folds,
and histologic examination shows elastolysis that frequently involves the entire
dermis.
• Acquired cutis laxa, both generalized and acral, can be a manifestation of an
underlying paraproteinemia, with binding of immunoglobulins to elastic fibers
• .
• In addition, there is a form of post-inflammatory elastolysis and cutis laxa that was
originally described in young girls of African descent; an inflammatory phase
consisting of indurated plaques or urticaria, malaise and fever precedes the
develop-ment of diffuse wrinkling, atrophy, and severe disfigurement.
• Insect bites may be the trigger for the initial inflammatory lesions9.
• Less often, mid-dermal elastolysis is confused with solar elastosis or
the perifollicular elastolysis that is usually seen on the trunk in
association with acne vulgaris.

• Solar elastosis differs clinically by its onset in an older age group,

restriction to only sun-exposed areas, yellow color, and coarser
wrinkling and differs histologically by hyperplasia of abnor-mal
elastic fibers and basophilic degeneration of the collagen in the
papillary dermis.

• Perifollicular elastolysis leads to a selective and almost complete

loss of the elastic fibers that surround hair follicles, compared
with preservation of elastic fibers around follicles in mid-dermal
elastolysis.
Treatment
Currently, there is no effective treatment for mid-dermal
elastolysis. Sunscreens, colchicine, chloroquine, vitamin E,
and topical agents (reti-noic acid, corticosteroids) have been
tried without success2.
 ANETODERMA
Introduction
•The term “anetoderma” is derived from anetos, the Greek word for slack, and derma
for skin.
•Anetoderma is an elastolytic disorder characterized by localized areas of flaccid skin,
which may be depressed, macular or papular; the latter can reflect herniation of
the subcutaneous tissue.
•Anetoderma may be idiopathic or associated with an inflamma-tory disorder of the
skin
Pathogenesis
The pathogenesis of anetoderma is not known. These lesions could be considered
unusual scars, since scars also have decreased elastic tissue.
The loss of dermal elastin may reflect an impaired turnover of elastin, caused by
either increased destruction or decreased synthesis of elastic fibers.
There are a number of proposed explanations for the focal elastin destruction, e.g. the
release of elastase from inflammatory cells, the release of cytokines such as interleukin-
6, an increased production of progelatinases A and B12, and the phagocytosis of elastic
fibers by mac-rophages. In addition, immunologic mechanisms may play a role in
anetoderma and may explain the reported associated findings of antiphospholipid
antibodies, antinuclear antibodies, false-positive sero-logic testing for syphilis or
• In primary anetoderma, there is no underlying associated disorder and lesions
arise within clinically normal skin. It can be classified into two major forms: those
with preceding inflammatory lesions (the Jadassohn–Pellizzari type) and those
without preceding inflammatory lesions (the Schweninger–Buzzi type) .
• This clinical clas-sification is primarily of historical interest, since the two types
of lesions can coexist in the same patient and their histopathology is often the
same (i.e. inflammation has been observed in both types of lesions);

• the presence or absence of clinical inflammation at the onset of the disease is not
related to prognosis .

• Secondary anetoderma can arise in the setting of a primary inflam-matory

dermatosis, skin infection or cutaneous tumor, as well as in patients with
systemic disorders (e.g. autoimmune). Over the past decade, an association with
antiphospholipid antibody syndrome has been highlighted.

• Although the vast majority of cases are sporadic, familial anetoderma has been
described and is usually not associated with pre-existing lesions.
Clinical features
• The characteristic lesions are flaccid, circumscribed areas of slack
skin that are a reflection of a marked reduction or absence of
dermal elastic fibers; they can appear as depressions, wrinkling, or
sac-like protrusions .
• These atrophic lesions vary in number from a few to hun-dreds, and
they typically measure 1–2 cm in diameter and are skin-colored to
blue–white in color.
• The skin surface can be normal in appearance or wrinkled, and a
central depression may be seen.
• Coalescence of smaller lesions can give rise to larger herniations.
• The examining finger sinks into a distinct pit with sharp borders as if
into a hernia ring.
• The bulge reappears when the pressure from the finger is released.
This clinical finding is referred to as the “buttonhole” sign and is
similar to that observed in neurofibroma .
Predilection sites for these asymptomatic lesions are the chest, back, neck, and upper
extremities.
Primary anetoderma usually develops in young adults, and new lesions often
continue to form for many years as the older lesions fail to resolve.
Secondary anetoderma implies that the characteristic atrophic lesion has appeared in
the same site as a previous specific skin lesion. Some authors also consider lesions
associated with an underlying disease (e.g. HIV infection, antiphospholipid antibody
syndrome, autoimmune thyroiditis) as secondary anetoderma; however, in this instance,
the atrophic areas do not necessarily develop within areas of known inflammation.
Evaluation for the presence of antiphospholipid antibodies should be performed
before patients with idiopathic anetoderma are labeled as having primary
anetoderma.

The range of heterogeneous conditions associated with secondary anetoderma are

outlined in Table 99.3. With the exception of distribution (and perhaps size), the
clinical features are the same as those of primary anetoderma.
Anetoderma has increasingly been reported in premature infants.
In most neonates, it appears to be related to the use of cutaneous monitoring leads or
adhesives , as well as extreme prematurity .
In patients with anetoderma, a variety of systemic abnormalities have been reported,
including ocular, endocrinologic, skeletal, cardiac, pulmonary, and gastrointestinal
Because there has been no consistency with regard to these associated abnormalities,
they are probably coincidental, although the possibility exists that they may reflect a
more generalized elastolytic disorder that has yet to be defined.

Pathology
In routinely stained sections, the collagen within the dermis of affected skin appears
normal. Perivascular lymphocytes are often present but do not correlate with clinical
findings of inflammation. The majority of lymphocytes are T helper cells. The
predominant abnormality (as revealed by elastic tissue stains) is a focal, more or less
complete loss of elastic tissue in the papillary and/ or reticular dermis. There are
usually some residual abnormal, irregular, and fragmented elastic fibers .

Plasma cells and histiocytes with occasional granuloma formation can be seen.
Direct immunofluorescence sometimes shows linear or granular deposits of
immunoglobulins and complement along the dermalepidermal junction or around
the dermal blood vessels in affected skin. However, these findings are not helpful
diagnostically. By electron microscopy, the elastic fibers are fragmented and irregular in
shape and occasionally they are engulfed by macrophages.

Differential diagnosis
Anetoderma must be differentiated from other disorders of elastic tissue such as mid-
However, the major differential diagnosis consists of post-traumatic scars and
papular elastorrhexis. The latter is an acquired disorder characterized by firm, white,
non-follicular papules that measure 2–5 mm in diameter and are evenly scattered
on the trunk
The lesions usually appear during adolescence or early adulthood. Histology
demonstrates focal degeneration of elastic fibers and normal collagen. There are no
associated extracutaneous abnormalities. This disorder is believed by some authors
to be a variant of connective tissue nevi1 or an abortive form of the Buschke–Ollendorff
syndrome, while others think that these lesions represent papular acne scars.

In contrast to anetoderma, lesions of papular elastorrhexis are firm and non

compressible .
Less often, anetoderma is confused with perifollicular elastolysis (see above), nevus
lipomatosus, or focal dermal hypoplasia (Goltz syndrome). Nevus lipomatosus
superficialis of Hoffman and Zurhelle presents as a clustered group of soft, skin-
colored to yellow nodules, usually located on the lower trunk and present since
birth
Histology shows ectopic mature lipocytes located within the dermis. The lesions of
Goltz syndrome (including telangiectasias, vermiculate dermal atrophy,
hypopigmentation, hyperpigmentation, and fatty herniations/ hamartomas) are in a
linear array along the lines of Blaschko .

Histologically, a decrease in dermal content is seen as well as extension or deposition of

subcutaneous fat into the dermis.

Treatment

• Various therapeutic modalities have been tried, but have not resulted in improvement
of existing atrophic lesions; these include intralesional injections of triamcinolone
and systemic administration of aspirin, dapsone, phenytoin, penicillin G, vitamin E,
and inositol niacinate.
• Some authors have reported improvement with hydroxychloroquine. Surgical
excision of limited lesions may be helpful, with informed consent from the patient
regarding the risk of scar formation.
• The utility of soft tissue fillers is inconclusive.
 Striae
Introduction
• Striae are a very common condition in most age groups. They are linear atrophic
depressions of the skin that form in areas of dermal damage produced by
stretching of the skin. They are associated with various physiologic states,
including puberty, pregnancy, rapid growth, weight gain or loss, obesity, and
disorders that lead to hypercortisolism.
• Striae also develop at sites of potent topical corticosteroid application, in
particular occluded intertriginous zones.

Pathogenesis
Factors leading to the development of striae have not been fully elucidated. Striae
distensae are a reflection of “breaks” in the connective tissue that lead to dermal
atrophy. A number of factors, including hormones (particularly corticosteroids),
mechanical stress and genetic predisposition, appear to play a role.

Clinical features
• Striae are usually multiple, symmetric, well-defined, linear atrophic lesions that
often follow the lines of cleavage. They are usually more of a cosmetic concern, but
Over time, the color gradually fades, and the lesions become atrophic, exhibiting a fine
wrinkled appearance. These striae albae are usually permanent, but they may fade
somewhat over time.
The striae can measure several centimeters in length and a few millimeters to a few
centimeters in width.
During puberty, striae appear in areas where there is a rapid increase in size. In
girls, the most common sites are the thighs, hips, buttocks and breasts, whereas in
boys, they are seen on the shoulders, thighs, buttocks, and lumbosacral region .

Other less common sites include the abdomen, upper arms, neck, and axillae. Striae
distensae are a common finding on the abdomen, and less so on the breasts and
thighs, of pregnant women, especially during the last trimester. They are more common
in younger primigravidas than in older pregnant women, in those who gained more
weight during pregnancy, and/or those who had babies with a higher birth weight.
The development of striae gravidarum has been associated with an increased risk of
laceration during vaginal delivery as well as subsequent pelvic relaxation and
clinical prolapse.
The striae associated with systemic corticosteroid therapy and Cushing syndrome can
be larger and more widely distributed .
Flexural and intertriginous areas are particularly at risk for developing striae from
the use of potent topical corticosteroids. Atrophic striae may become elevated and
Pathology
• Histologic findings are similar to those of scars and depend upon the stage of
evolution of the striae at the time the biopsy is performed.
• The epidermis can be normal during the early stages, but eventually becomes
atrophic with blunted rete ridges.
• The dermal thickness is decreased, as is the collagen in the upper dermis.
• The collagen bundles lie parallel to the epidermis. Alterations in elastic fibers
are variable, but they can be fragmented, and specific elastin staining can
demonstrate a marked reduction compared with adjacent normal dermis.
There is an absence of both hair follicles and other adnexal structures..
DDX
The diagnosis of striae distensae is usually straightforward, but the differential
diagnosis does include linear focal elastosis (elastotic striae), an entity first described
by Burket et al.28 in 1989. Linear focal elastosis is characterized by rows of yellow,
palpable, striae-like bands on the lower back. Unlike striae, the lesions are raised
and yellow rather than depressed and white. Elderly men are most commonly
affected. Histologically, there is a focal increase in the number of elongated or
fragmented elastic fibers as well as a thickened dermis. It is postulated that linear
focal elastosis may represent an excessive regenerative process of elastic fibers and
could be viewed as a keloidal repair of striae distensae .

An entity referred to as linear lumbar localized elastolysis is said to occur most often
in young men; the linear, raised bands are skincolored and histologically there is
elastolysis within the mid dermis.
Treatment
• Striae distensae have no medical consequences, but they are frequently distressing
to those afflicted.
• As striae tend to improve spontaneously over time, the value of anecdotal
therapies without case controls difficult to assess.
• Treatment of early-stage striae with tretinoin 0.1% cream can improve their
appearance, and its application has been shown to decrease the length and
width of striae.
• Other topical treatments, including 0.05% tretinoin/20% glycolic acid and 10%
L-ascorbic acid/20% glycolic acid, may also improve the appearance of stretch
marks .
• Several lasers have been used to treat striae: the 585 nm pulsed dye laser may
improve the appearance of striae rubrae, but it has no effect
• on striae albae;
• secondary pigmentary alterations in darker skin are a potential complication.
Improvement in the leukoderma of striae albae was noted with the 308 nm
excimer laser, but maintenance treatment was required to sustain the cosmetic
benefit.
• Use of radiofrequency and pulsed magnetic fields may also lead to improvement.
However, currently, there is no specific therapy that results in a complete
response.