eMedicine Specialties > Dermatology > Bullous Diseases

Pemphigus Vulgaris: Treatment & Medication

Author: Bassam Zeina, MD, PhD, Consulting Staff, Department of Dermatology, Milton Keynes Hospital, UK
Coauthor(s): Sohail Mansoor, MBBS, MSc, Dermatologist and Lead Physician in Dermatologic Surgery, Department of Dermatology, Barnet Hospital, UK
Contributor Information and Disclosures

Updated: Aug 14, 2009

Treatment

Medical Care

The aim of treatment in pemphigus vulgaris (PV) is the same as in other autoimmune bullous diseases, which is to decrease blister formation, promote healing of blisters and erosions, and determine the minimal dose of medication necessary to control the disease process. Therapy must be tailored for each patient, taking into account preexisting and coexisting conditions. Patients may continue to experience mild disease activity while under optimal treatment.

Erosions and healing areas on the back.

Erosions and healing areas on the back.

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Erosions and healing areas on the back.

Erosions and healing areas on the back.



Healing areas on the chest and abdomen.

Healing areas on the chest and abdomen.

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Healing areas on the chest and abdomen.

Healing areas on the chest and abdomen.

Corticosteroids have improved overall mortality, but now much of the mortality and morbidity in these patients relates to the adverse effects of therapy. Whether massive doses of steroids have any advantage over doses of 1 mg/kg/d is unclear. Immunosuppressive drugs are steroid sparing and should be considered early in the course of the disease. Epidermal growth factor may speed healing of localized lesions.21 Amagai et al reported on the successful use of intravenous immunoglobulin in pemphigus patients who did not fully respond to systemic steroids.22

Consultations

Management of patients with PV requires coordination of care between the dermatologist and the patient's primary care physician.

  • An ophthalmologist should evaluate patients with suspected ocular involvement and those requiring prolonged high-dose steroids.
  • Patients with oral disease may require a dentist and/or an otolaryngologist for evaluation and care.
  • Patients on systemic steroids should maintain adequate vitamin D and calcium intake through diet and supplements. Patients with a history of renal calculi should not receive calcium carbonate.
  • Patients receiving long-term systemic corticosteroids should be evaluated by a rheumatologist within the first 30 days of treatment for osteoporosis risk assessment and consideration of a bisphosphonate for prophylaxis against osteoporosis.

Diet

No dietary restrictions exist, but patients with oral disease may benefit from avoiding foods, such as spicy foods, tomatoes, orange juice, and hard foods that may traumatize the oral epithelium mechanically, such as nuts, chips, and hard vegetables and fruit.

Activity

  • Advise patients to minimize activities that traumatize the skin and that may precipitate blistering, such as contact sports. Nontraumatic exercises, such as swimming, may be helpful.
  • Dental plates, dental bridges, or contact lenses may precipitate or exacerbate mucosal disease.

Medication

The aim of treatment is to reduce inflammatory response and autoantibody production. While target-specific therapy is not available, non-target–specific treatments currently are used. The most commonly used medications are corticosteroids.

The introduction of corticosteroids has reduced mortality greatly, but significant morbidity remains. Immunosuppressants should be considered early in the course of disease, as steroid-sparing agents. Mycophenolate mofetil and azathioprine are the usual first-line agents. Rituximab and intravenous immunoglobulin have also proved useful alone or in combination.23 Cyclophosphamide is used for refractory disease. The role of biologic agents is being investigated. Each of these agents should be prescribed and monitored by physicians familiar with them. Wound care of erosions includes daily gentle cleaning, application of topical agents to promote wound healing, and use of nonadhesive dressings. The goal of wound care is to promote healing, minimize trauma to the surrounding skin, and diminish scarring.

Anti-inflammatory agents

Inhibit the inflammatory process by inhibiting specific cytokine production.


Prednisone (Deltasone, Meticorten, Orasone, Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production. For treating PV, administered PO and used alone or in combination with topical or intralesional steroids or in conjunction with other immunosuppressives.
In pediatric patients, disease management with this medication in consultation with the patient's pediatrician is advised.

Adult

1-1.5 mg/kg/d PO initial every am or in divided doses; titrate dose to clinical response; 0.5-2 mg/kg/d; taper as condition improves; single morning dose is safer for long-term use, but divided doses have more anti-inflammatory effect

Pediatric

Administer as in adults

Coadministration with estrogens may decrease prednisone clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; peptic ulcer disease, hypokalemia, hyperglycemia, osteonecrosis, myopathy, osteoporosis, edema, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur; qod therapy does not prevent bone loss

Immunosuppressive agents

Useful adjuvants in patients with PV with generalized disease unresponsive to steroids and/or other anti-inflammatory agents or in patients unable to tolerate prednisone.


Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity. In conjunction with prednisone, it is more effective than prednisone alone. May be an effective monotherapy in mild cases, although the therapeutic effect is delayed 3-5 wk.
Consider withdrawal if no improvement within 3 mo.

Adult

1 mg/kg/d qd/bid (empiric) or based on TPMT level (see Precautions); increase dose by 0.5 mg/kg/d after 6-8 wk if necessary; increase q4wk; 2 mg/kg/d maximum dose for most dermatologic purposes

Pediatric

Not established

Allopurinol increases risk of pancytopenia; captopril/ACE inhibitors may increase risk of anemia and leukopenia; warfarin dose may need to be increased; pancuronium may need to be increase to achieve adequate paralysis; live virus vaccines, co-trimoxazole may increase risk of hematologic toxicity; rifampicin may cause transplant rejection; clozapine may increase risk of agranulocytosis

Absolute: Allergy to azathioprine, pregnancy or attempting pregnancy, clinically significant active infection
Relative: Concurrent use of allopurinol, prior treatment with alkylating agents (cyclophosphamide, chlorambucil, melphalan, others) because of high risk of neoplasia; pediatric patients (safety and efficacy in pediatric population not established)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

TPMT testing is not entirely reliable but it involves testing activity of TPMT activity in RBCs, which correlates with systemic TPMT activity; functional enzyme test has been shown to have variability between test sites and the kits may contain varying amounts of enzyme inhibitor; starting at low doses, monitoring for pancytopenia, then increasing dose is an alternative; if clinical response is not good, patient may be homozygote for high activity and may need an increased dose; Wolverton Comprehensive Dermatologic Drug Therapy; other references recommend checking before treatment in all patients
TPMT <5 U: No treatment with azathioprine
TPMT 5-13.7 U: Dose not to exceed 0.5 mg/kg
TPMT 13.7-19 U: Dose not to exceed 1.5 mg/kg
TPMT >19 U: Dose not to exceed 2.5 mg/kg

More on Pemphigus Vulgaris

Overview: Pemphigus Vulgaris
Differential Diagnoses & Workup: Pemphigus Vulgaris
Treatment & Medication: Pemphigus Vulgaris
Follow-up: Pemphigus Vulgaris
Multimedia: Pemphigus Vulgaris
References
Further Reading
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References

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Keywords

pemphigus vulgaris, PV, bullous disease

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Contributor Information and Disclosures

Author

Bassam Zeina, MD, PhD, Consulting Staff, Department of Dermatology, Milton Keynes Hospital, UK
Bassam Zeina, MD, PhD is a member of the following medical societies: British Association of Dermatologists, British Medical Association, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Sohail Mansoor, MBBS, MSc, Dermatologist and Lead Physician in Dermatologic Surgery, Department of Dermatology, Barnet Hospital, UK
Sohail Mansoor, MBBS, MSc is a member of the following medical societies: American Academy of Anti-Aging Medicine, American Academy of Dermatology, American Society for Dermatologic Surgery, Royal College of Physicians and Surgeons of Glasgow, and Royal College of Physicians of the United Kingdom
Disclosure: Nothing to disclose.

Medical Editor

Abby S Van Voorhees, MD, Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania
Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, National Psoriasis Foundation, Phi Beta Kappa, Sigma Xi, and Women's Dermatologic Society
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Genentech Honoraria Consulting; Incyte Grant/research funds Other; Warner Chilcott Honoraria Consulting; Merck Salary Management position; Abbott  Speaking and teaching

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Medicis Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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