Smith-Lemli-Opitz Syndrome

Smith-Lemli-Opitz Syndrome (SLOS)
By: Suraj Gathani

Description and Occurrence
* Autosomal recessive disorder
o Cholesterol metabolism effected.
* Common characteristics:
o Multiple malformations at birth.
o Mental retardation later.
* Occurrence:
o 1 in 20,000 people of central European decedents.
o Rare in Africans and Asians.

Clinical Features
* Clinical anomalies:
o Mental retardation (100% affected)
o Small brain at birth (microcephaly) >90%
o Second and third toe fusion (synadactyly) ~98%
o Genital abnormalities in males >50%
o Muscle weakness (hypotonia) ~50%
o Polydactyly
o Abnormalities of heart, lung, kidneys, and liver.

Smith-Lemli-Opitz Syndrome
* Distinctive facial features:
o High, broad forehead
o Narrow temples
o Upward pointing nostrils
o Drooping eyelids and a broad nasal bridge
* Behavioral characteristics:
o Repeated self injury
o Prolonged temper tantrums & violent outbursts
o Hyperactivity

Molecular Defects
* Caused from mutation in the DHCR7 gene
o Located at 11q12-13
o Encodes for sterol-Δ7-reductase
* Defects in sterol-Δ7-reductase
o Build up of 7-dehydrocholesterol
o Deficiency of cholesterol
* Importance of cholesterol
o Important component in cell membrane and myelin sheaths
o Precursor for steroid hormones such as progesterone
o Precursor for bile salts

Cholesterol Metabolism
Diagnosis and Treatment
* Diagnosis:
o Detection of an elevated level of 7-dehydrocholesterol in plasma
* Treatment:
o Individuals with SLOS need support and care
o Congenital abnormalities can be corrected with surgery.
o Dietary cholesterol supplementation is beneficial.

Reference

Smith-Lemli-Opitz Syndrome.ppt

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Management Considerations for Patients on Anticoagulants

Management Considerations for Patients on Anticoagulants

Dental Management of Patients on Anticoagulant and Antiplatelet Drugs
By:Donald A. Falace, DMD
Professor and Division Chief
Oral Diagnosis and Oral Medicine
University of Kentucky College of Dentistry


Normal Hemostasis

Following injury to a blood vessel:
* Vascular retraction (vasoconstriction) to slow blood loss

2. Adherence of platelets to the vessel wall (endothelium) and then to each other to form a platelet plug

3. Initiation of the coagulation cascade resulting in the formation and deposition of fibrin to form a clot

Coagulation Cascade
* Extrinsic pathway: Factor VII is activated by tissue factor (phospholipid) that is released by injured perivascular or vascular tissues; very rapid reaction
* Intrinsic pathway: Factor XII is activated by exposure to collagen from vessel wall (endothelium) or blood cell membrane; slower reaction

* Anticoagulants:
o Inhibit the production of clotting factors
* Antiplatelet Agents:
o Interfere with the functioning of platelets, thus inhibiting platelet aggregation

Anticoagulants
Coumarin Derivitives (dicoumarol, warfarin: Coumadin, Panwarfin)
Coumadin antagonizes the production of vitamin K
Vitamin K is necessary for the synthesis of four of the coagulation factors (VII, IX, X and prothrombin)

Pharmacologic Properties (warfarin: Coumadin)
* Taken orally
* Metabolized in the liver
* Half-life: 1.5-2.5 days
* Duration of action: 2-5 days (it takes several days for dosage changes to take effect)
* Increased anticoagulant effect when combined with:
o Antibiotics
o Aspirin
o NSAIDs
o Antifungals
o Tramadol
o Tricyclic antidepressants
o Certain herbals (gingko, ginsing, ginger, garlic)

Co-morbid Conditions That Can Contribute to Increased Bleeding
* Liver disease
* Kidney disease
* Tumor
* Bone marrow failure
* Chemotherapy
* Autoimmune diseases

Conditions for which Coumadin is prescribed to prevent unwanted blood clotting
* Prophylaxis/Treatment of:
o Venous thrombosis (DVT)
o Pulmonary embolism
o Atrial fibrillation
o Myocardial infarction
o Mechanical prosthetic heart valves
o Recurrent systemic embolism

Laboratory Tests to Monitor the Activity of Coumadin
* Prothrombin Time (PT): time for fibrin formation via the extrinsic pathway-factor VII
o Test performed by taking a sample of the Pt’s blood and adding a reagent (thromboplastin) and calculating the time required to form a clot; expressed in seconds
* PT Ratio: Pt’s PT/Normal PT
* Normal PT ration = 1
* Problem: There is variation among thromboplastin reagents, therefore the results from lab to lab are not comparable

Same patient- Same blood
5 different laboratories - 5 different PT Ratios!
Solution: International Normalized Ratio (INR)
o A mathematical “correction” that corrects for the differences in the sensitivity of thromboplastin reagents
o Each thromboplastin is assigned an ISI number which is a sensitivity index
o This correction makes INR values comparable from lab to lab
o Normal INR = 1 (an INR of 2 means that their INR is 2 times higher than normal)

Same Patient-Same Blood
Reported by INR

Recommended Therapeutic Range for Oral Anticoagulant Therapy
(American College of Chest Physicians: Chest 1998; 114(suppl): 439-769s)

INR: 2.0-3.0
Prophylaxis or treatment of venous thrombosis
Treatment of pulmonary embolus
Prevention of systemic embolism
Tissue heart valves
Acute MI
Atrial fibrillation

Recommended Therapeutic Range for Oral Anticoagulant Therapy
(American College of Chest Physicians: Chest 1998; 114(suppl): 439-769s)
* INR: 2.5-3.5
o Mechanical prosthetic valves (high risk)
o Acute MI (to prevent recurrent MI)
o Certain patients with thrombosis and the antiphospholipid antibody syndrome (antibodies that interfere with the assembly of phospholipid complexes and thus inhibit coagulation)


Dental Management Guidelines
* There are no uniformly accepted guidelines for managing anticoagulated patients during dental treatment
* Previous AMA/ADA recommendation was that it was safe to perform surgery on a patient if the PT was 1.5-2.5x normal. This, however, is equivalent to an INR of 2.6-5.0 depending on the sensitivity of the various thromboplastins; an average PT of 1.6 = INR of 3!

* This clinical problem is not amenable to a “cookbook” approach
* Each patient must be considered individually and you must take into consideration the risk-benefit of stopping vs continuing anticoagulation (they are on anticoagulants because they are at risk for thromboembolism)
* Your decision depends upon:
o Medical condition/stability
o Degree of anticoagulation
o Magnitude of planned surgery
o Scientific evidence
* If questionable, decision should be a shared with physician

What does the scientific literature tell us?

* Updated a previous study (Wahl,MJ: Dental surgery in anticoagulated patients. Arch Int Med. 1998;158:1610-1616) and added more cases (26 studies)
* A review of more than 2400 cases of dentoalveolar surgery on more than 950 patients undergoing multiple extractions, full mouth exts, alveoloplasties whose anticoagulant was continued (many with INR > than therapeutic levels)
o 12 cases (0.5%) experienced bleeding that was uncontrollable by local measures alone
o Of these 12, 7 had an INR> than therapeutic levels & 3 were on antibiotics
o 3 required vitamin K administration to stop the bleeding

* Reviewed case reports of 493 patients whose anticoagulant had been discontinued prior to dental extractions and other dental procedures
* 5 pts (1%) suffered significant adverse outcomes
o 4 patients had fatal embolisms
o 1 patient had a non-fatal embolism

Devani,P: Dental extractions in patients on warfarin: Is alteration of anticoagulant regime necessary?
Brit JOMFS 1998;36;107-111

* Compared 2 groups of extraction patients undergoing an average of 2 extractions (range of 1-9 teeth)
o 32 pts with anticoagulant discontinued prior to surg with INR 1.5-2.1, and
o 33 pts with anticoagulant continued with INR of 2.3-3.4. Local measures only for hemostasis (atraumatic technique, sutures, gauze, etc)
* None in either group had significant post-op bleeding; 1 pt in each group required additional local measures to control delayed oozing
* Compared blood loss of 3 groups of dentoalveolar surgery pts
o 12 pts who continued anticoagulant with INR 1.2-2.9
o 13 pts who discontinued anticoagulant 3-4 days with INR 1.1-3.0
o 10 pts who were never on anticoagulant (INR not tested)
* No significant difference in blood loss among groups and no serious postoperative bleeding requiring intervention

* Conducted a systematic review and synthesis of the English language literature from 1966-2001 examining the perioperative management and outcomes of patients receiving long term oral anticoagulant therapy; included a comprehensive review of 26 case reports and studies examining bleeding and thromboembolism after dental procedures (minor ext, fmx, alveolectomies)
* Conclusion: Most patients undergoing dental procedures can undergo the procedure without alteration of the OAC regimen. The current literature suggests that the perioperative stroke rate for patients who have OAC withheld may be substantially greater than would be normally predicted

Conclusions
* It would thus appear that most patients who are on anticoagulant therapy (Coumadin) can undergo minor dentoalveolar surgery without discontinuance of anticoagulant using local/topical measures if:
o INR is within the therapeutic range (<3.5)
o No assoc aggravating conditions (e.g. antibiotics, liver or kidney disease)
o Planned surgery is “minor” (extractions, alveoloplasty, biopsy)
* If anticoagulant needs to be adjusted (INR>3.5), this is the responsibility of the physician

Antiplatelet Agents Normal Platelet Function

Platelets adhere to the area of injured endothelium (mediated by von Willebrand factor)
Platelets adhere to each other and form a scaffolding for fibrin deposition (von Willebrand
factor is a carrier protein for factor VIII)

Uses for Antiplatelet Drugs
* Prevention of heart disease
* During heart attack
* Unstable angina
* Following heart attack
* During or following angioplasty and stenting
* Prevention of stroke or TIA
* Atrial fibrillation (low risk patient)
* Peripheral vascular disease

Antiplatelet Drugs
* Aspirin (irreversible effect for life of the platelet ~ 7-10 days)
* NSAIDs (reversible effect; limited to duration of drug)
o Cox-1 (renal blood flow, fluid/electrolyte transport, stomach mucosal integrity, vasomotor tone, platelet aggregation)
o Cox-2 (inflammation)
* Clopidogrel (Plavix)
* Ticlopidine (Ticlid)
* Dipyridamole (Persantine)

Action of Antiplatelet Drugs
*The life of a platelet is about 7-10 days
Laboratory Tests to Monitor the Effects of Antiplatelet Drugs
* Ivy Bleeding time: measures the length of time a patient bleeds after a standardized incision.
o low reproducibility
o questionable sensitivity
o poor correlation to clinical bleeding tendency
o normal: 1-6 or 7 minutes
o conventionally, a bleeding time >20 minutes has been considered likely to result in clinically significant bleeding
* Platelet Function Analyzer (PFA-100)
o currently the most widely used autoanalyzer
o not yet available in all laboratories
o measures the time it takes to form a platelet plug across the aperature of a capillary tube
o normals: 60-120 seconds
o guidelines not currently available for application of PFA-100 results to clinical bleeding probability
Antiplatelet Drugs and Postoperative Bleeding?

* Very limited literature on this topic
* Most of the studies deal with aspirin
* Little information available on the other antiplatelet drugs
* Most of the recommendations are based upon clinical experience, case reports and expert opinion

Aspirin and Bleeding
* In all studies, aspirin was continued
* All three studies found no significant difference in perioperative or postoperative blood loss between patients taking aspirin and controls
* Medline review and analysis of all articles from 1966-2002 on surgery and bleeding complications due to aspirin
* No clinically relevant bleeding complications were reported for cardiovascular, vascular, or orthopedic surgery, or epidural anesthesia; there was an increase in clinically non-relevant bleeding induced by aspirin
* Conclusion: There is no scientific evidence to support the withdrawal of aspirin in patients prior to surgery
Current Practice in Great Britain
* The general consensus of opinion from this survey suggests that most vascular surgeons do not stop antiplatelet drugs preoperatively
Expert Opinion Canada
* Conclusion: Aspirin should not be withdrawn in most cases
o If pt is on aspirin, clopidogrel or ticlopidine and intraoperative bleeding is feared, a short-acting NSAID can be temporarily substituted

Summary: Antiplatelet Agents
* Clinical experience, expert opinion, anecdotal reports and available studies suggest that for most patients undergoing dentoalveolar surgery, it is not necessary to discontinue the use of aspirin or other antiplatelet agents if used alone. The use of these agents is not usually associated with significant (serious) operative or postoperative bleeding.
* If two agents are used together (e.g. aspirin and clopidogrel), the risk for bleeding is likely increased, and depending upon the extent of the surgery, should be discussed with the physician

Local Measures to Control Postoperative Bleeding
* Careful, atraumatic surgical technique
* Use of absobable hemostatic agent in socket (e.g. Gelfoam,Avitene,Surgicel)
* Careful suturing; primary closure over sockets not essential
* Post-operative pressure pack (damp gauze for 30-60 minutes); especially important for flap compression
* May use antifibrinolytic agents: tranexamic acid [Cyklokapron Oral] or epsilon amino caproic acid [Amicar] as a mouthwash or to soak pressure gauzes

Antifibrinolytic Mouthrinses
* Epsilon amino caproic acid (Amicar)
o Syrup (1.25 gm/5cc) , 5-10 mL QID X 7 days
o Use either as mouthwash or as a soak for the pressure gauze
* Tranexamic acid (Cyklokapron)
o Used topically as 10 mL of a 4.8% -5% weight/volume solution as a mouthwash for 2 minutes, QID, for 7 days
o Unfortunately, the 4.8% elixir is not FDA approved for use in the USA market

Additional Postoperative Measures

Management Considerations for Patients on Anticoagulants.ppt

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Epidermal Nevi, Neoplasms, and Cysts

Epidermal Nevi, Neoplasms, and Cysts

Syringoma
* Small translucent papule
* Commonly on eyelids or upper cheeks
* Axilla, abdomen, forehead, penis, vulva
* Develop slowly and persist indefinitely
* Asymptomatic
* 18% of adults with Down’s syndrome
* Dilated cystic sweat ducts
* Treatment
o Electrodessication
o Laser ablation
o cryotherapy

Variants of Syringoma
* Clear cell syringoma
o Associated with diabetes mellitus
o Identical lesions, histological difference
* Other clinical variants
o Limited to the scalp causing alopecia
o Unilateral linear or nevoid distribution
o Limited to vulva and penis
o Limited to distal extremities

Eruptive syringoma
* Numerous lesions on the neck, chest, axilla, upper arms and periumbilically
* Young persons
* Histologically identical
* Reported in Down’s syndrome
* Clinically may be confused with reticulated papillomatosis of Gougerot-Carteaud

Eccrine hidrocystomas
* Translucent papules 1-3mm
* May have bluish tint
* Usually solitary, however, multiple lesion may be seen
* Occur on the face
* May become more prominent in hot weather
* Treatment – excision
* Topical atropine or scopolamine

Eccrine poroma
* Benign, slow-growing, slightly protruding, sessile, soft, reddish tumor
* Most commonly occur on the sole or the side of the foot. May occur anywhere
* Bleeds with slight trauma
* Frequent cup-shaped shallow depression from which the tumor grows
* Benign – simple excision
* Eccrine poromatosis

Malignant eccrine poroma (porocarcinoma)
* Most arise from longstanding eccrine poromas (50%)
* Clinically similar
* May also manifest as a blue or black nodule, plaque or ulcerated tumor
* M=F, avg 70 yrs
* Legs 30%, feet 20%, face 12%, thighs 8%
* If metastatic, 70% mortality
* Mohs MS TOC

Chondroid Syringoma and Malignant Chondroid Syringoma
* Firm intradermal or subcutaneous nodule
* Most commonly located on the nose or cheeks
* 80 % involving the head and neck
* Symptomatic 5-30mm
* Felt to be of eccrine origin
* Malignant mixed tumor of the skin
* Most occur on extremities. Reported on face, scalp, back, buttocks
* Grow rapidly. Metastasis more the 50%
* Aggressive surgical excision, Adjuvant radiation therapy w/wo chemotherapy

Clear cell hidradenoma (nodular hidradenoma)
* Classified as an eccrine sweat gland tumor
* Single nodular, solid or cystic, occasionally protruding mass
* Flesh colored or reddish
* Anywhere. Most common site is the head
* 20% c/o pain on pressure
* Multiple lesions reported
* Women 2X men
* Extirpation is TOC

Malignant clear cell hidradenoma (hidradenocarcinoma)
* Extremely rare
* Presents as a solitary nodule
* Lower extremity 32.9 %, upper extremity 27.6 %, trunk 11.9 %, head 26.3 %
* Metastasis occurs 60%
* Tx wide local excision, radiation and chemotherapy

Eccrine spiradenoma
* Solitary, 1cm, deep-seated nodule
* Most frequently seen on the ventral surface
* Especially upper half of the body
* Skin-colored, blue or pink with normal overlying skin
* Multiple lesions, linear pattern may be seen
* Paroxysmal pain
* Benign clinical course
* Simple excision
* DDX may include
* A - angiolipoma
* N - neuroma
* G - glomus tumor
* E
* L – leiomyoma

Malignant eccrine spiradenoma
* In long standing lesions malignant degeneration may occur and my be lethal. Malignant Eccrine Spiradenoma

Papillary eccrine adenoma
* Uncommon benign lesion
* Dermal nodules
* Extremities of black patients
* Tendency to recur
* Complete surgical excision

syringoacanthoma
* Extremely rare (21 cases)
* Seborrheic keratosis-like neoplasm
* Significant tissue destruction if left untreated
* Classification remains controversial

Eccrine syringofibroadenoma
* Most presentations are a solitary, hyperkeratotic nodule or plaque involving the extremities
* Characteristic marker of Schopf syndrome
o Hydrocystomas of the eyelids, hypotrichosis, hypodontia, and nail abnormalities

cylindroma
* Dermal eccrine cylindroma, Spiegler’s tumor, turban tumor, and tomato tumor
* benign
* Predominately on scalp and face
* Solitary, firm but rubber-like nodule
* Pinkish to blue
* Few mm to several cm
* Women chiefly affected
* Grow slowly
* Rarely undergo malignant degeneration
* May be mistaken for epidermoid cyst
* excision
* Dominantly inherited form
* Numerous rounded masses of various sizes on the scalp
* Appears soon after puberty
* Resembles bunches of grapes or small tomatoes

Sweat gland carcinoma
* Eccrine carcinoma
o No characteristic clinical appearance
o High incidence of metastatic spread
* Mucinous eccrine carcinoma
o Commonly a round, elevated, reddish, and sometimes ulcerated mass
o Usually head and neck (75%)
o Slow growth and asymptomatic
o 11% incidence of metastasis
o Local excision

Aggressive digital papillary adenocarcinoma
* Aggressive malignancy involving the digit between the nail bed and the distal interphalangeal joint spaces in most cases
* Presents as a solitary nodule
* 50% recurrence rate
* Just under 50% develop metastasis
* All patients should have CXR
* Complete excision TOC
* Amputation may be required

Primary cutaneous adenoid cystic carcinoma
* Rare
* Presents usually on the chest or scalp
* Mohs MS TOC

Microcystic adnexal carcinoma (sclerosing sweat duct carcinoma)
* Generally a very slow-growing plaque or nodule
* Occurs most commonly on the upper lip of women
* Perineural infiltration is common and may be extensive
* TOC Mohs
* No reports of metastases

APOCRINE GLANDS
ceruminoma
* Rare apoeccrine tumor that rarely becomes malignant
* Firm nodular mass in the EAC
* Ulceration and crusting may occur
* Obstruction
* Questionable true entity
* Treatment - excision

Hidradenoma papilliferum
* Benign solitary tumor
* Almost exclusively on the vulva
* Bleeding, ulceration, discharge, itching and pain
* Firm nodule few mm
* excision

Syringadenoma papilliferum (syringocystadenoma papilliferum)
* Most commonly develops in a nevus sebaceous of Jadassohn
* Scalp or face
* Firm rose red papules
* Groups
* Vesicle-like inclusions are seen
* May simulate MC
* Transition to carcinoma is rare
* Excision is advised

Apocrine hidrocystoma/cystadenoma (apocrine retention cyst)
* Benign tumor
* Occurs chiefly on the face. solitary
* Penile shaft- median raphe cyst
* Dome-shaped, smooth-surfaced translucent nodule
* Bluish or brownish
* Simple excision

Apocrine gland carcinoma
* Rare
* Axilla is the most common site
* May be seen in the nipple, vulva and EAC
* May originate from aberrant mammary glands
* Widespread metastases may occur

HAIR FOLLICLE NEVI AND TUMORS
Pilomatricoma (calcifying epithelioma of Malherbe)
* Usually a single tumor
* Most commonly on the face, neck or arms
* Deeply seated firm nodule, covered with normal or pink skin
* Asymptomatic
* Stretching may show “tent sign”
* Derived from hair matrix cells
* Clinical DDX is impossible
* Simple excision
* Familial patterns do occur
* Multiple in Rubinstein-Taybi and Gardner syndrome

pilomatricoma
Malignant pilomatricoma
* Extremely rare
* Do not behave aggressively

Trichofolliculoma
* Benign, highly structured adenoma of the pilosebaceous unit
* Small dome-shaped nodule on the face or scalp
* A small wisp of fine, immature hairs protrude from a central pore
* Simple excisional bx

Trichoepithelioma (epithelioma adenoides cysticum, multiple familial trichoepitheliomas)
* Occur as multiple cystic and solid nodules typically on the face
* Small, rounded, smooth, shiny,slightly translucent and firm.
* Flesh colored or slightly reddish
* Slightly depressed center
* Often grouped and symmetrical
* benign
* Solitary trichoepithelioma
o Nonhereditary
o Mostly on face
* Giant solitary trichoepithelioma
o May reach several cm
o Mostly on thigh and perianal
* Desmoplastic trichoepithelioma
o Difficult to differentiate from morphea-like BCC
o Solitary or multiple on the face

trichoblastoma
* Benign neoplasms of follicular germinative cells
* Asymptomatic
* Scalp and face
* Surgical excision

Trichilemmoma and Cowden’s disease (multiple hamartoma syndrome)
* Benign neoplasm of the hair follicle
* Small solitary papule on the face
* Nose and cheeks
* Multiple
o Marker for Cowden,s syndrome
* Generally limited to the head and neck
* 87% of patients with Cowden’s
* 38% develop malignancies
o Breast 25-36%
o Thyroid 7%
o Colon adenocarcinoma
* Tumor suppressor gene

Trichilemmal carcinoma
* Sun exposed areas
* Face and ears
* Slow growing epidermal papule, indurated plaque or nodule with tendency to ulcerate
* Surgical excision

Trichodiscoma and fibrofolliculoma
* Hundreds of flat or dome-shaped, skin-colored asymptomatic papules
* Face, trunk and extremities
* Autosomal dominant trait
* Controversial entity
* 2-4 mm skin-colored to white papules
* Solitary, more commonly multiple
* Scattered over the face, trunk and extremities

Proliferating trichilemmal cyst
* Large exophytic neoplasms
* Almost exclusively confined to scalp and back of neck
* May ulcerate
* Ass with nevus sebaceous
* Metastasis may occur
* Most respond to surgical excision

Dermoid cyst
* Congenital in origin
* Chiefly along lines of cleavage
* Result from improper embryologic development
* Potential for intracranial communication
* CT or MRI scan is required to rule this out prior to BX over cranial cleavage planes
* Freely mobile and not attached to the skin

Pilonidal cyst
* Midline hairy patch or pit in the sacral region with a sinus orifice in the bottom, or a cyst beneath it
* Usually becomes symptomatic during adolescence
* Opening cyst widely, debriding it, and packing it with silver nitrate crystals
* More advanced surgical intervention may be required
* SCC has been reported to arise from chronic inflammatory pilonidal disease

Pilonidal sinus
Steatocystoma simplex
* Noninheritable counterpart to the more familiar steatocystoma multiplex
* Face limbs or chest
* Simple excision

Steatocystoma multiplex
* Multiple, small, yellowish, cystic nodules 2-6 mm
* Principally on the upper anterior trunk, upper arms, axillae and thighs
* Lesions may be generalizes
* High familial tendency
* Contain a syruplike, yellowish, odorless oily material
* Likely autosomal dominant inheritance
* Tx- excision of individual lesions
* Incision and expression or aspiration

Eruptive vellus hair cysts
* Autosomal dominant inheritance
* Yellowish to reddish brown, small papules of the chest and proximal extremities
* Disseminated lesions reported

Pigmented follicular cysts
* Face or neck
* Suggested to be a variant of multiple pilosebaceous cysts

milia
* White keratinous cysts, 1-4 mm
* Chiefly on the face esp under eyes
* May occur in great numbers
* Occur in up to 50 % of newborns
* Primarily develop without a predisposing condition
* Can develop in inflammatory conditions and skin diseases such as epidermolysis bullosa, pemphigus, bullous pemphigoid, PCT, herpes zoster, contact dermatitis, and after prolonged use of NSAIDS
* Variants include MEM (multiple eruptive milia)
* MEP (milia en plaque)
* Tx- incision and expression
* Tretinoin and minocycline for MEP

Pseudocyst of the auricle
* Fluctuant, tense, noninflammatory swelling of the upper ear
* Believed to be ass with trauma
* Tx – drainage
* ILI steroid

Cutaneous columnar cysts
* Four types of cyst that occur in the skin are lined by columnar epithelium
* Branchiogenic cyst
o Small solitary lesions just above the sternal notch
* Thyroglossal duct cysts
o Anterior aspect of the neck
o Malignancies reported 1%
* Cutaneous ciliated cysts
o Usually located on the legs of females
o Perineum vulva and foot regions
* Median raphe cyst
o Developmental defects lying in the ventral midline of the penis, usually on the glans
o Surgical intervention is standard therapy


Epidermal Nevi, Neoplasms, and Cysts.ppt

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