Dermatoses of Pregnancy: Key Points and Clinical Pearls

Ted Rosen, MD

1. There are physiologic cutaneous changes associated with pregnancy. These include: linea nigra, melisma, striae, faster growing and harder nails, faster growing hair (followed by telogen effluvium 3 months or so post-partum).

2. Treatments for the physiologic changes of pregnancy rarely work well.

  • Melasma: Combination of retinoid, hydroquinone, glycolic acid peels
  • Striae: Perhaps Fraxel laser or Needling device

3. The immune system changes during pregnancy

  • TH1 cell-mediated immunity decreases: EGW may worsen
  1. Imiquimod appears safe
  2. Thermotherapy is safe
  3. Cryotherapy is safe
  4. CO2 laser is treatment of choice
  • TH2 humoral immunity increases: Lupus may worsen or appear for first time

4. Specific dermatoses of pregnancy have been consolidated into just a few entities:

5. Intrahepatic cholestasis of pregnancy

  • Risk to mother: None (itches)
  • Risk to fetus: Stillbirth, Premature birth, intra-cranial hemorrhage
  • Therapy: Oral ursodeoxycholic acid 15mg/kg/day in QID divided doses

6. Herpes (Pemphigoid) Gestationis

  • Risk to mother: Autoimmune disorders: vitiligo, Grave’s disease, alopecia areata, IBD
  • Risk to fetus: Small for gestational age, premature delivery, blisters (10%)
  • Therapy: Systemic steroids

7. Pruritic Urticarial Papules & Plaques of Pregnancy (PUPPP)

  • Risk to mother: None (itches severely)
  • Risk to fetus: None
  • Therapy: Topical steroids, UVB (sunlight)

8. Prurigo of Pregnancy (PP)

  • Risk to mother: None
  • Risk to fetus: None
  • Therapy: Topical steroids

9. Impetigo herpetiformis (Now considered pustular psoriasis of pregnancy)

  • Risk to mother: Electrolyte abnormalities, especially calcium homeostasis
  • Risk to fetus: Spontaneous abortion, Stillbirth
  • Therapy: Systemic steroids or cyclosporine

10. Excellent review: Dermatol Ther 26:274-84, 2013

10 Pearls from the Basic Structure of Skin

Whitney A. High, MD, JD, MEng

Dr High provided the MauiDerm NP+PA Fall 2014 audience with a comprehensive presentation on the basic structure of skin. Here’s what you need to know…

1. The skin consists of “three layered cake.”  The epidermis an outer protective outer layer.  The dermis is a middle layer that provides “tensile” strength.  The deeper subcutis is insulating fat.

2. The epidermis gets all its nutrition and sustenance from the dermis.  The dermis contains all the “supportive” structures of the skin, such as blood vessels, nerves, and many “adnexal structures.”

3. The epidermis consists chiefly of keratinocytes (“skin cells”).  These cells are arranged in layers to form a “maturing” protective layer that replaces itself every ~28 days:

  • stratum basal = the germinative layer of the skin that divides to regenerate the epidermis
  • stratum spinosum = names for the intraspinous properties that bind the keratinocytes
  • straum granulosum = the granular layer where keratohyaline granules are produced
  • stratum corneum = the “dead” outer layer the provides the most barrier function

4. The dermis is comprised of three main building blocks: collagen, elastic fibers, and “ground substance.  Collagen is the material that provides the tensile strength to the skin.  Elastic fibers provide skin resiliency.  Ground substance facilitates the diffusion of nutrients and oxygen.

5. The “dermoepidermal junction” is where the epidermis attaches to the dermis.  This is also the location of melanocytes that make protective melanin for the skin.  The DEJ is where most nonmelanoma skin cancer invades the dermis, the place where nearly all melanoma originates, and the place where many bullous and “interface” diseases transpire.

6. When confronted with a skin disease, one must ask themselves, “where do I believe that that pathology is occurring?” For example, the pathologic process might be:

  • epidermal – such as the spongiosis (intraepidermal edema) and weeping of dermatitis, or the yeast/hyphae of tinea versicolor/pityriasis versicolor growing in the stratum corneum
  • dermal – such as the histiocytic/macrophagic infiltrate of granuloma annulare, or the neutrophilic inflammation of small blood vessels in leukocytoclastic vasculitis
  • subcuticular – such as the panniculitis of erythema nodosum

7. Being able to predict where the likely pathology is occurring also facilitates the securing of a “representative” biopsy, which is always the responsibility of the clinician.

8. Adnexal structures may be the site of inflammatory pathologic processes (acne, hidradenitis), may be the site of neoplastic processes (sebaceous carcinoma), or these structures may simply behave in an undesired way (seborrhea, hyperhidrosis).

9. Uncontrolled and unchecked growth of certain components of the skin leads to cancer, such as basal cell carcinoma (from basilar keratinocytes), squamous cell carcinoma (also from keratinocytes) and melanoma (from melanocytes).

10. Skin structure and function changes with age, such as dyspigmentation and facial wrinkling, formation of “solar elastosis” (damaged elastic), and increased water loss to the environment.

Genital Ulcers

Ted Rosen, MD

What causes genital ulcers? Are you treating patients who present with genital ulcers? Dr Rosen provides us with his clinical pearls from MauiDerm NP+PA Fall 2014…

  1. Ulceration is defined as loss of epidermis and then some or all of dermis and subcutaneous tissue leading to an “open sore.”
  2. There are many general reasons for ulcers to occur. They include: atherosclerotic vascular disease, non-atherosclerotic vascular disease, infections, inflammation of unknown etiology, neoplasms, and exogenous causes
  3. It is often necessary to use ancillary aids to diagnose genital ulcers; these may include serologic tests (eg. RPR), cultures, and biopsy with molecular technique analysis.
  4. STDs commonly cause genital ulcers. You are NOT likely to see the minor STDs in the USA (eg. Donovanosis, chancroid or LGV). However you may see syphilis and herpes. STDs can be distinguished by lesion size, number, degree of pain, presence or absence of inguinal adenopathy.
  5. Genital herpes due to HSV-2 continues to shed virus for at least a decade after initial infection. Genital herpes should prompt an investigation for other STDs (10+% will be HIV+)
  6. Amebiasis of the genitalia may result from anal intercourse with an individual with amoebic dysentery. Or, it may ensue from fecal contamination of the genital skin.
  7. Neoplasms which cause genital ulcers are >90% likely to be squamous cell carcinoma
  8. Multi-system disease which may be associated with genital ulcerations include Behcet’s Syndrome and extra-intestinal Crohn’s disease. Pathergy helps confirm the diagnosis of Behcet’s disease; biopsy confirms cutaneous Crohn’s disease. Topical TCI may help the latter.
  9. Lichen planus is typically the cause of painful erosions in women, but not in men. Treatment is with ultrapotent topical steroids until healing (~75% of women will heal totally). Alternate treatments include topical TCIs and oral cyclosporine-A
  10. Zoon balanitis is a superficially eroding disorder of men with sheets of plasma cells on biopsy. (Hence the name: balanitis plasmacellularis). Topical steroids treat this.
  11. Unusual causes of genital ulceration can be diagnosed by PE and historical data. These include ecthyma gangrenosum, pyoderma gangrenosum, and calciphylaxis. Beware of EG in neutropenic patients, PG in those with RA or IBD, and calciphylaxis in those with CRF on dialysis.
  12. Exogenous factors causing genital ulcers: self-mutiliation, drugs, vacuum erection device and genital bite wounds. The latter respond best to amoxicillin-clavulanate in high dose.

Dermatology In Review: Part 2

Matthew Zirwas, MD

At the MauiDerm NP+PA Fall 2014 conference, Dr Zirwas reviewed with us some of the key findings in dermatology from 2014…

  1. Coconut oil may help atopic dermatitis
  2. “Supplementing the diet of well-nourished adults with mineral or vitamin supplements has no clear benefit and might even be harmful
  3. UV exposure may reduce all-cause mortality!
  4. Metformin 500mg TID helped 18/25 hidradenitis patients
  5. Rifampin 10 mg/kg once daily + Moxifloxacin 400 mg daily + Metronidazole 500 mg tid for hidradenitis?
  6. Fexofenadine 240 mg bid + Montelukast 10 mg qd helped about ½ prurigo nodularis patients
  7. Is post-op pain due to allergic reaction to metal in implants? Maybe. But not commonly.
  8. Probable efficacy of gabapentin in the improvement of pruritus and quality of life of patients with nostalgia paresthetica (max dose 900mg TID)

Vasculitis and Vascular Lesions Part 1: Clinical Pearls

Ted Rosen, MD

1. Vasculitis is a clinicopathologic process characterized by inflammation of and damage to blood vessels
2. Heterogeneous group of disorders leading to a broad group of named diseases due to….  Different sizes, types and locations of the affected blood vessels and variable tissue response to injury
3.  Basic principles:

  • All age groups (Some types have preference)
  • Caucasians (But other ethnic groups, too)
  • Genetic predisposition (But not strictly inherited)
  • Chronic, relapsing (But may go into remission)
  • Think vasculitis when faced with an…..unexplained multi system disease or progressive organ dysfunction
  • Team approach: Early consultations

4. Classification: best done by size of blood vessel affected

5. A wide variety of tissues can be affected. Scoring charts exist which are helpful to systematically asses these patients.

6. Constitutional signs and symptoms may be seen: fever, chills, sweats, weight loss, fatigue

7. Involvement of, damage to and symptoms relating to: eyes, upper or lower airway, joints, kidneys, lungs, central/peripheral nervous system,  heart and clotting mechanisms

8. Morphology of skin lesions is suggestive but virtually never diagnostic of histologic type!

9. Absence of skin lesions does not rule out any variant of vasculitis, while the presence of any specific type of skin lesion does not necessarily predict the subtype of vasculitis present!

10. There are many clinical mimics to vasculitis. These include embolic phenomenon, exposure to certain drugs, cryptogenic infections, Vitamin C deficiency, and cardiolipin antibody syndrome

11. When biopsy is done, try to utilize a lesion less than 72 hours old to get the most representative histology.

12. Therapy may include: NSAIDS, Dapsone, Colchicine, Steroids, Immunosuppressives: Methotrexate, Mycophenolate, Azathioprine, Cyclophosphamide and Rituximab

Infectious Disease Update: Clinical Pearls

Ted Rosen, MD

At MauiDerm Fall NP+PA 2014, Dr Rosen provides us with an update on infectious diseases and his clinical pearls…

  1. STDs are globally epidemic. In the US, 50% of those 15-25 have or have had an STD
  2. STDs are so common due to the “multiplier” effect of sex partners of sex partners
  3. Syphilis is on the rise last three years in USA, now at 5.3/100,000 population
  4. Multi-drug resistant GC (including resistance to drugs of choice, cephalosporins) is here
  5. Topical three months regimen of 4% zinc sulfate soaks for active genital herpes benficial
  6. External genital warts: NEW treatment ideas
    • 5% KOH daily x 3 months
    • Single application of ingenol mebutate (either strength)
    • Thermotherapy with 440C for 30 min x 3 days, each of two consecutive weeks
  7. Leishmaniasis being brought back to USA from Iraq and Afghanistan
    • Rx: Pentavalent antimonial IV, IM from CDC; Quite toxic.
    • Thermotherapy (ThermoMed device): 1300F; Painful and blisters
    • New drug: Miltefosine 100-150mg/day PO (Impavido™) available 2015
      • Lecithin derivative
      • Safe and effective for Old and New World Leishmaniasis
  8. Treatments for MRSA have expanded with three new drugs
    • All new drugs have LONG T1/2 which allows less frequent dosing
    • Oritivancin: Single 1200mg dose
    • Dalbavancin: 1000mg, then 500mg a week later
    • Tedizolid: 200mg QD x 5-7 days
  9. Chikungunya virus
    • Used to be Africa/Asia, Now worldwide
    • Most cases imported from trip (especially from Caribbean)
    • Now, virus-carrying mosquitoes in Caribbean and USA
    • Fever, arthralgia, myalgia, headache, petechial to purpuric rash
    • Like Dengue but not as bad
    • No vaccination, No specific Rx. Supportive therapy, as needed.

Cutaneous Oncology: Clinical Pearls

George Martin, MD

How are you managing your cutaneous oncology patients? Dr Martin provides us with his clinical pearls…

  • Remember that AK patients are not just Medicare patients, we see patients 30-40 years old as well. Also remind older patients that actinic damage is chronic disease and no one therapy will result in a long lasting or permanent cure.
  • When treating AKs, expect side effects based on the MOA of the active ingredient.
  • Treating AKs on the chest? Therapeutic considerations include:  Topical 5-FU cream 0.5/1.5%; Ingenol Mebutate gel 0.5%; and Diclofenac gel 3%., Expect a significant skin reaction to ingenol mebutate 0.05% (not .5%) within 24 hrs that will include blistering and discomfort requiring analgesia when large areas are covered.. 5-FU can be “titrated” and can be used for 7-10  days, discontinued for a month and re-started in a month and used for 2-3 weeks with less of a reaction. DO NOT USE IMIQUIMOD on the chest as it is not FDA approved for the chest and  an result in permanent depigmentation.
  • Managing reactions is key! Utilize analgesia as needed; sunscreen to reduce potential for dyschromia; moisturizers; topical antibiotics as needed; and weekly follow-up.
  • Imiquimod can trigger flu-like symptoms including myalgias and fever before a significant skin reaction such as erosions and ulceration may occur.
  • Ingenol Mebutate has two mechanisms of action: an immediate cytotoxic effect initiated via the PKC pathway which causes swelling  and edema even blistering and weeping and a second MOA involving IL-8 production by rapidly proliferating ketatinocytes and endothelial cells which recruits neutrophils and in vigorous responses can result in sterile pustules.
  •  Counsel patients on anticipated responses and set expectations.
  • Have patients fill prescriptions between Monday to Thursday—less likely to be switched than Fridays or weekends.
  • Have patients start treatments on Sundays, for ingenol mebutate during Mon-Thurs as the immediate reaction to ingenol mebutate may trigger a phone call within 24 hours; this way, reactions occur mid week rather than on weekends.
  • Make sure that surgical sites are well healed and that cryotherapy sites have had a week or two after healing before initiating therapy.
  • Use every adjunct possible except steroids as the immune system plays a role in each modality used.

Dermatology Year In Review: Part 1 Clinical Pearls

Ted Rosen, MD

What’s new in dermatology?

1. Excessive tanning associated with alcohol and drug use, as well as various psychological problems.

2. Increased risk of skin cancer:

  • BCC: Large number of benign moles
  • Melanoma: non-ASA NSAIDs and Viagra ingestion

3.  New genital (and labial) HSV treatment: thermotherapy with Herpotherm device. Applied even a single time shortens outbreak. Heat: about 500C for 4 seconds.  
4. Psoriatic nail dystrophy complicated by concomitant dermatophyte infection 10-20%
5. Tattoo problems

  • Risk of nontuberculous mycobacterial infection
  • Risk of hiding a melanoma
  • Risk of pigment in regional lymph nodes, complicating sentinel node biopsy if needed

6. Clarithromycin and other macrolides have potential to cause fatal arrhythmia

7. Doxycycline 200mg/d plus adapalene/BPO can do almost as well as isotretinoin over 20 weeks in nodulocystic acne. The combo Rx is “noninferior” when safety is combined with efficacy

8. Psoriasis information

  • Risk of Crohn’s disease in US women (RR 4.0)
  • Severe psoriasis associated with increased risk of renal disease (RR 2.0)
  • Increased risk of various solid organ cancers (RR 1.5+)
  • Lindioil application found beneficial for nail psoriasis
  • Frequent telephone positive motivational interviews enhance adherence to Rx regimen

9. Vitiligo associated with cochlear dysfunction (60%!!!) Hearing loss or ringing in the ears

10. Hair dyes contain a variety of potential sensitizers, not just p-Phenylenediamine

Psoriasis and Other Papulosquamous Eruptions: Clinical Pearls

Bruce Strober, MD, PhD

  1. The severity of psoriasis is based on BSA, location, impact on quality of life and presence of psoriatic arthritis.
  2. Patients diagnosed with psoriasis should also be assessed for psoriatic arthritis and other comorbidities.
  3. Psoriasis treatment is not stepwise.
  4. Choice of therapy depends on individual patient characteristics.
  5. Combination therapy may be desirable in some patients.
  6. Topical therapies are appropriate initial step for patients with MILD psoriasis.
  7. Patients failing to response to treatment or worsening symptoms, RETHINK the psoriasis diagnosis.
  8. Erythrodermic or exfoliative dermatitis needs aggressive therapeutic intervention.
  9. 90% of psoriasis patients with nail involvement also have psoriatic arthritis and may require systemic therapy.
  10. Monotherapy is easier, but combination therapy is more effective for patients with moderate to severe psoriasis.