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Treatment of Linear IgA Bullous Dermatosis of Childhood With Mycophenolate Mofetil FREE

Jeanne Farley-Li, MD; Anthony J. Mancini, MD
[+] Author Affiliations

Section Editor: George J. Hruza, MD
Assistant Section Editor: Dee Anna Glaser, MD
Assistant Section Editor: Elaine Siegfried, MD

More Author Information
Arch Dermatol. 2003;139(9):1121-1124. doi:10.1001/archderm.139.9.1121.
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A 27-month-old girl presented with a 5-week history of blistering that was initially localized to the popliteal fossae and face but subsequently progressed to involve the majority of her extremities, her genitals, and portions of her trunk. Treatments initiated prior to dermatologic evaluation included amoxicillin and betamethasone dipropionate and resulted in no improvement. Her medical history was significant for asthma, α thalassemia trait, and neonatal ocular chlamydia infection. She was taking no oral medications and had no known history of drug allergies.

Examination revealed a quiet girl in obvious discomfort. There were numerous tense bullae on an inflammatory base, many with an annular configuration and central crusting, distributed on her extremities (Figure 1), labia majora, ears, and face. There were fewer lesions on her trunk. Involved areas also revealed multiple crusted erosions, and she had hypopigmented annular patches on her upper inner thighs. The oral and ocular mucosae were uninvolved.

Place holder to copy figure label and caption
Figure 1.

The patient at presentation. Bilaterally, ankles and feet reveal annular bullous plaques ("cluster of jewels") with erosions and crusting.

Graphic Jump Location

The patient was clinically diagnosed with linear IgA bullous dermatosis (LABD) of childhood. Treatment was begun with prednisolone at a dose of 12 mg/d (1 mg/kg per day) while a baseline laboratory evaluation was initiated. Hydroxyzine and cephalexin were also prescribed for pruritis and secondary superinfection, respectively.

A 4-mm punch biopsy specimen of a skin lesion revealed a subepidermal bulla containing neutrophils, supporting the clinical diagnosis of LABD of childhood. Direct immunofluorescence confirmed the diagnosis, revealing linear immunoglobulin deposition, primarily IgA, at the dermoepidermal junction. A baseline laboratory evaluation at this time included a glucose-6-phosphate dehydrogenase (G6PD) level, hepatic panel, renal panel, and complete blood cell and reticulocyte counts. The results were notable for a hemoglobin level of 10.7 g/dL, hematocrit of 32.6%, mean corpuscular volume of 73 fL, and a reticulocyte count of 0.4%. The G6PD level and findings of the renal panel were within normal limits. The hepatic panel results were also normal except for a mildly elevated aspartate aminotransferase level of 45 IU/L and an alkaline phosphatase value of 204 IU/L.

Treatment with dapsone was begun at an initial dose of 6.25 mg/d (0.5 mg/kg per day). At the same time, a prednisolone taper was begun. The patient was closely monitored with weekly, biweekly, and eventually monthly blood examinations including a complete blood count, reticulocyte count, and hepatic and renal panels. Over the course of the next 6 months, the dapsone dose was gradually increased to 25 mg/d (2 mg/kg per day) in an attempt to gain better control of her disease. Her laboratory parameters remained stable, with an expected drop in her hemoglobin to as low as 9.2 g/dL and a corresponding increase in the reticulocyte count (maximum of 1.8%). The patient tolerated the treatment well and experienced some improvement in her condition, but she never experienced a complete remission and required numerous bursts of oral prednisolone (1 mg/kg of Prelone syrup; Muro Pharmaceuticals, Tewksbury, Mass) with a 3-week taper for flares. These episodes were only partially controlled with the combined dapsone and corticosteroid-burst therapy. Her energy level was consistently low, her affect depressed, and her disease a source of much emotional and financial distress (due to lost work time) for her family. The patient also began to exhibit signs of developmental delay.

After 8 months of treatment with dapsone and intermittent pulsed corticosteroids, the patient began treatment with mycophenolate mofetil (CellCept; Roche Pharmaceuticals, Nutley, NJ) at 310 mg/m2 per day (100 mg twice daily) and continued dapsone therapy at 25 mg/d. After 10 days of treatment, she experienced some lethargy with decreased oral intake and mild fevers. At this time, out of concern for possible mycophenolate mofetil toxic effects or a superimposed viral illness, the dose was decreased to 155 mg/m2 per day (50 mg twice daily). She rapidly improved over a few days, with resolution of the constitutional symptoms and significant improvement in her skin disease. After 6 weeks of combined dapsone–mycophenolate mofetil therapy, she had nearly complete resolution of the blistering (Figure 2) and experienced only 1 episode of mild blistering around her ankles during the course of the next 8 months. She did not require any pulsed steroid therapy, and there were no adverse effects either clinically or in her laboratory parameters. She subsequently discontinued treatment with mycophenolate mofetil (after 8 months of therapy), and her dapsone dose was tapered with continued excellent control of her disease, which may be naturally regressing 19 months after her diagnosis.

Place holder to copy figure label and caption
Figure 2.

The patient after 6 weeks of combined dapsone–mycophenolate mofetil therapy. Note the marked resolution of blistering with residual postinflammatory hyperpigmentation and hypopigmentation.

Graphic Jump Location

Linear IgA bullous dermatosis of childhood, also known as chronic bullous dermatosis of childhood, is a rare, acquired, self-limited autoimmune subepidermal bullous disease. Skin manifestations include large tense bullae as seen in bullous pemphigoid and/or vesiclular lesions characteristic of dermatitis herpetiformis. The lesions are typically most prominent on the abdomen and perineum but may also involve the trunk, extremities, face, and mucous membranes.1,2 It is also common to see new lesions at the periphery of older blisters forming a configuration known as a "cluster of jewels." The target antigen of the IgA autoantibodies in LABD is a 120-kd secreted portion of the BP180 antigen.3 However, there have been reports of cases where other antigens are recognized, including antigens with molecular weights of 285, 230, 180, 145, 100, and 97 kd.410

Diagnosis of LABD requires 3 criteria:11 (1) a vesicular or bullous eruption, usually confined to the skin and occasionally involving the mucous membranes; (2) a subepidermal vesicle with a predominantly neutrophilic infiltrate on histologic examination; and (3) basement membrane zone–specific IgA antibody deposited in a linear pattern in the absence of other immunoglobulins under direct immunofluorescence examination of perilesional skin. Although these criteria are required to meet the strict definition of LABD, in the research setting there have been several cases of LABD with IgG antibody deposits in a linear fashion at the basement membrane zone in addition to the IgA antibodies.12 Pathologically, these cases represent an overlap of LABD and bullous pemphigoid. Clinically, however, the patient is usually treated in accordance with which antibody response predominates.

The most well-recognized treatment for LABD is dapsone or, if that fails, sulfapyridine. Other corticosteroid-sparing agents that may be beneficial include azathioprine, cyclosporine, and colchicine, but the risk-benefit profile for some of these therapies may not justify their use. Dapsone is an antimicrobial agent indicated for the treatment of all forms of leprosy as well as for dermatitis herpetiformis and Pneumocystis carinii pneumonia prophylaxis. It has traditionally proven very beneficial and well tolerated in the treatment of LABD in children. The main adverse effects of treatment with dapsone include hemolysis, methemoglobinemia, agranulocytosis, and peripheral neuropathy. It is therefore recommended that a complete blood count with differential and a reticulocyte count be done every 2 weeks for the first 3 months of therapy and then every subsequent 3 months.13 Due to the risk of hemolysis, extremely close monitoring is indicated if the drug is used in G6PD-deficient patients. In patients who do not tolerate dapsone, sulfapyridine is an alternative, with the addition of low-dose prednisone bursts traditionally being the next step for those whose disease remains uncontrolled with monotherapy.2,11,14,15 Dicloxacillin has also been advocated as a possible therapy, which if effective, might be a safe and inexpensive alternative for some patients.16

Recently, the newly developed immunosuppressive agent mycophenolate mofetil has been found to be a corticosteroid-sparing agent that is useful in the treatment of some blistering conditions. Mycophenolate mofetil is a new formulation of an old drug, mycophenolic acid, which was investigated in the 1970s as an oral agent for psoriasis.1722 The drug was subsequently rediscovered in its new form, the prodrug of mycophenolic acid, and approved by the Food and Drug Administration in 1997 for the prevention of renal allograft rejection. Once mycophenolate mofetil is absorbed, it is rapidly converted to mycophenolic acid, which acts by noncompetitively binding to inosine monophosphate dehydrogenase and thus blocking steps critical for de novo purine biosynthesis.23 Furthermore, it is relatively specific for lymphocytes, since they rely on the de novo pathway of purine synthesis rather than the salvage pathway. When the proliferative response of T and B lymphocytes is blocked, there is a reduction in antibody formation and the generation of cytotoxic T cells. It is likely that this decrease in antibody production is the mechanism of action for mycophenolate mofetil in the autoimmune blistering diseases. Mycophenolate mofetil is available in 250- or 500-mg capsules and a 200-mg/mL suspension.

Although mycophenolate mofetil is generally well tolerated, adverse effects of gastrointestinal disturbance (diarrhea, nausea, vomiting, anorexia, and abdominal cramping) occur in up to 50% of patients. Other observed effects include reversible dose-dependent anemia, neutropenia, leukopenia, and an increased risk of infections including herpes zoster, herpes simplex, and flulike viral syndromes.24 Neurologic adverse effects include weakness, headache, tinnitus, and sleep disturbances.25 These hematologic, infectious, and neurologic complications of treatment are most often seen in patients concurrently receiving other immunosuppressant therapies and taking adult doses of mycophenolate mofetil greater than 2 g/d.26

The recommended dosage, monitoring regimen, and exact role of mycophenolate mofetil in the treatment of autoimmune and inflammatory cutaneous diseases remain anecdotal. Reports of mycophenolate mofetil being used in the treatment of skin disease have been published for psoriasis,18,27,28 bullous pemphigoid,2831 pemphigus vulgaris,28,29,32 dyshidrotic eczema,33 arthritis,34 atopic dermatitis,3538 and pyoderma gangrenosum39,40 in adults. These patients typically received doses between 2 and 3 g/d. This dose is comparable with that of adult organ-transplant recipients who receive 2 g/d for kidney and 3 g/d for heart transplants, in combination with other immunosuppressive therapy. To date, there are no published reports of children treated for blistering diseases with mycophenolate mofetil.

Our patient began treatment with mycophenolate mofetil at a dose of 310 mg/m2 per day (100 mg twice daily), which is approximately one quarter of the 1.2 g/m2 per day maximum dose recommended in pediatric renal transplantation patients.41,42 The dose was subsequently reduced to 155 mg/m2 day (50 mg twice daily) when the patient developed potential symptoms of toxic effects or a viral infection. The choice and initial dosing regimen of mycophenolate mofetil was based on the recommendation of a dermatologist (Grant J. Anhalt, MD) very experienced in the care of patients with autoimmune blistering diseases.

Cost analysis for treatment of a 15-kg child reveals that 2 daily doses of 100 mg of mycophenolate mofetil (CellCept suspension) costs $12.60 per month, while each monthly prednisolone burst (Prelone syrup) of 1 mg/kg day with a taper over 3 weeks costs $17.40. These costs are fairly cost competitive, although other factors would influence this calculation, including the cost of necessary laboratory monitoring.

Our patient responded rapidly and quite well to the regimen of mycophenolate mofetil in combination with dapsone, experiencing only 1 episode of mild blistering over the course of 8 months. Prior to this, the patient required on average 1 steroid burst per month for disease control. Under our treatment, her laboratory parameters were consistently stable, and her overall status improved with gains in her energy level and catch-up in development.

Mycophenolate mofetil may be a useful adjunct in the treatment of LABD in childhood when monotherapy with dapsone fails, and it may hold promise for other autoimmune blistering diseases of childhood as well. Further clinical observations will clarify the potential roles of this steroid-sparing immunosuppressive agent.

Corresponding author: Anthony J. Mancini, MD, Division of Dermatology No. 107, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614 (e mail: amancini@northwestern.edu).

Accepted for publciaton May 16, 2002.

The authors have no relevant financial interest in this article.

We thank Grant J. Anhalt, MD, for his invaluable input and review of the manuscript.

Esterly  NBFurey  NLKirschner  BSKretshmer  RRSepton  RM Chronic bullous dermatosis of childhood. Arch Dermatol. 1977;11342- 46
PubMed
Chorzelski  TPJablonska  S IgA linear dermatosis of childhood (chronic bullous disease of childhood). Br J Dermatol. 1979;101535- 541
PubMed
Zone  JJTaylor  TBMeyer  LJPetersen  MJ The 97 kDa linear IgA bullous disease antigen is identical to a portion of the extracellular domain of the 180 kDa bullous pemphigoid antigen, BPAg2. J Invest Dermatol. 1998;110207- 210
PubMed
Schumann  HBaetge  JTasanen  K  et al.  The shed ectodomain of collagen XVII/BP180 is targeted by autoantibodies in different blistering skin diseases. Am J Pathol. 2000;156685- 695
PubMed
Arechalde  ABraun  RPCalza  AM  et al.  Childhood bullous pemphigoid associated with IgA antibodies against BP180 or BP230 antigens. Br J Dermatol. 1999;140112- 118
PubMed
Zone  JJTaylor  TBKadunce  DP  et al.  IgA antibodies in chronic bullous disease of childhood react with 97 kDa basement membrane zone protein. J Invest Dermatol. 1996;1061277- 1280
PubMed
Kanitakis  JMauduit  GCozzani  E  et al.  Linear IgA bullous dermatosis of childhood with autoantibodies to a 230 kDa epidermal antigen. Pediatr Dermatol. 1994;11139- 144
PubMed
Wojnarowska  FWhitehead  PLeigh  IM  et al.  Identification of the target antigen in chronic bullous disease of childhood and linear IgA disease of adults. Br J Dermatol. 1991;124157- 162
PubMed
Yamane  YSato  HHigashi  K  et al.  Linear immunoglobulin A (IgA) bullous dermatosis of childhood: identification of the target antigens and study of the cellular sources. Br J Dermatol. 1996;135785- 790
PubMed
Zhou  SFerguson  DJAllen  J  et al.  The localization of target antigens and autoantibodies in linear IgA disease is variable: correlation of immunogold electron microscopy and immunoblotting. Br J Dermatol. 1998;139591- 597
PubMed
Egan  CAZone  JJ Linear IgA bullous dermatosis. Int J Dermatol. 1999;38818- 827
PubMed
Miyagawa  SKiriyama  YShirai  TOhi  HSakamoto  K Chronic bullous disease with coexistent circulating IgG and IgA anti-basement membrane zone antibodies. Arch Dermatol. 1981;117349- 353
PubMed
Zhu  YIStiller  MJ Dapsone and sulfones in dermatology: overview and update. J Am Acad Dermatol. 2001;45420- 434
PubMed
Schiffner  JH Therapy of childhood linear IgA dermatitis herpetiformis. J Am Acad Dermatol. 1982;6403- 404
PubMed
Jablonska  SChorzelski  TPRosinska  DMaciejowska  E Linear IgA bullous dermatosis of childhood (chronic bullous dermatosis of childhood). Clin Dermatol. 1992;9393- 401
Siegfried  ECSirawan  S Chronic bullous disease of childhood: successful treatment with dicloxacillin. J Am Acad Dermatol. 1998;39797- 800
PubMed
Jones  ELEpinette  WWHackney  VCMenendez  LFrost  P Treatment of psoriasis with oral mycophenolic acid. J Invest Dermatol. 1975;65537- 542
PubMed
Epinette  WWParker  CMJones  ELGreist  MC Mycophenolic acid for psoriasis: a review of pharmacology, long-term efficacy, and safety. J Am Acad Dermatol. 1987;17962- 971
PubMed
Gomez  ECMenedez  LFrost  P Efficacy of mycophenolic acid for the treatment of psoriasis. J Am Acad Dermatol. 1979;1531- 537
PubMed
Spatz  SRudnicka  AMcDonald  CJ Mycophenolic acid in psoriasis. Br J Dermatol. 1978;98429- 435
PubMed
Lynch  WSRoenigk  HH  Jr Mycophenolic acid for psoriasis. Arch Dermatol. 1977;1131203- 1208
PubMed
Marinari  RFleishmajer  RSchragger  AHRosenthal  AL Mycophenolic acid in the treatment of psoriasis: long term administration. Arch Dermatol. 1977;113930- 932
PubMed
Allison  ACKowalski  WJMuller  CDEugui  EM Mechanisms of action of mycophenolic acid. Ann N Y Acad Sci. 1993;69663- 87
PubMed
Pirsch  JDSollinger  HW Mycophenolate mofetil: clinical and experimental experience. Ther Drug Monit. 1996;18357- 361
PubMed
Kitchin  JEPomeranz  MKPak  GWashenik  KShupack  JL Rediscovering mycophenolic acid: a review of its mechanism, side effects, and potential uses. J Am Acad Dermatol. 1997;37445- 449
PubMed
Becker  BN Mycophenolate mofetil. Transplant Proc. 1999;312777- 2778
PubMed
Haufs  MGBeissert  SGrabbe  SSchutte  BLuger  TA Psoriasis vulgaris treated successfully with mycophenolate mofetil. Br J Dermatol. 1998;138179- 181
PubMed
Nousari  HCSragovich  AKimyai-Asadi  AOrlinsky  DAnhalt  GJ Mycophenolate mofetil in autoimmune and inflammatory skin disorders. J Am Acad Dermatol. 1999;40265- 268
PubMed
Grundmann-Kollmann  MKorting  HCBehrens  S  et al.  Mycophenolate mofetil: a new therapeutic option in the treatment of blistering autoimmune diseases. J Am Acad Dermatol. 1999;40957- 960
PubMed
Bohm  MBeissert  SShwarz  TMetze  DLuger  T Bullous pemphigoid treated with mycophenolate mofetil [letter]. Lancet. 1997;349541
PubMed
Nousari  HCGriffin  WAAnhalt  GJ Successful therapy of bullous pemphigoid with mycophenolate mofetil. J Am Acad Dermatol. 1998;39497- 498
PubMed
Enk  AHKnop  J Mycophenolate is effective in the treatment of pemphigus vulgaris. Arch Dermatol. 1999;13554- 56
PubMed
Picknacker  ALuger  TASchwarz  T Dyshidrotic eczema treated with mycophenolate mofetil. Arch Dermatol. 1998;134378- 379
PubMed
Goldblum  R Therapy of rheumatoid arthritis with mycophenolate mofetil. Clin Exp Rheumatol. 1993;11S117- S119
PubMed
Grundmann-Knollmann  MKorting  HCBehrens  S  et al.  Successful treatment of severe refractory atopic dermatitis with mycophenolate mofetil. Br J Dermatol. 1999;141175- 176
PubMed
Neuber  KSchwartz  IItschert  G  et al.  Treatment of atopic eczema with oral mycophenolate mofetil. Br J Dermatol. 2000;143385- 391
PubMed
Benez  AFierlbeck  G Successful long-term treatment of severe atopic dermatitis with mycophenolate mofetil. Br J Dermatol. 2001;144638- 639
PubMed
Grundmann-Kollmann  MPodda  MOchsendorf  FBoehncke  WHKaufmann  RZollner  TM Mycophenolate mofetil is effective in the treatment of atopic dermatitis. Arch Dermatol. 2001;137870- 873
PubMed
Hohenleutner  UMohr  VDMichel  SLandthaler  MS Mycophenolate mofetil and cyclosporine treatment for recalcitrant pyoderma gangrenosum. Lancet. 1997;3501748
PubMed
Nousari  HCLynch  WAnhalt  GJ  et al.  The effectiveness of mycophenolate mofetil in refractory pyoderma gangrenosum. Arch Dermatol. 1998;1341509- 1511
PubMed
Jacqz-Aigrain  EKhan Shaghaghi  EBaudouin  V  et al.  Pharmokinetics and tolerance of mycophenolate mofetil in renal transplant children. Pediatr Nephrol. 2000;1495- 99
PubMed
Nevins  TE Overview of new immunosuppressive therapies. Curr Opin Pediatr. 2000;12146- 150
PubMed

Figures

Place holder to copy figure label and caption
Figure 1.

The patient at presentation. Bilaterally, ankles and feet reveal annular bullous plaques ("cluster of jewels") with erosions and crusting.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

The patient after 6 weeks of combined dapsone–mycophenolate mofetil therapy. Note the marked resolution of blistering with residual postinflammatory hyperpigmentation and hypopigmentation.

Graphic Jump Location

Tables

References

Esterly  NBFurey  NLKirschner  BSKretshmer  RRSepton  RM Chronic bullous dermatosis of childhood. Arch Dermatol. 1977;11342- 46
PubMed
Chorzelski  TPJablonska  S IgA linear dermatosis of childhood (chronic bullous disease of childhood). Br J Dermatol. 1979;101535- 541
PubMed
Zone  JJTaylor  TBMeyer  LJPetersen  MJ The 97 kDa linear IgA bullous disease antigen is identical to a portion of the extracellular domain of the 180 kDa bullous pemphigoid antigen, BPAg2. J Invest Dermatol. 1998;110207- 210
PubMed
Schumann  HBaetge  JTasanen  K  et al.  The shed ectodomain of collagen XVII/BP180 is targeted by autoantibodies in different blistering skin diseases. Am J Pathol. 2000;156685- 695
PubMed
Arechalde  ABraun  RPCalza  AM  et al.  Childhood bullous pemphigoid associated with IgA antibodies against BP180 or BP230 antigens. Br J Dermatol. 1999;140112- 118
PubMed
Zone  JJTaylor  TBKadunce  DP  et al.  IgA antibodies in chronic bullous disease of childhood react with 97 kDa basement membrane zone protein. J Invest Dermatol. 1996;1061277- 1280
PubMed
Kanitakis  JMauduit  GCozzani  E  et al.  Linear IgA bullous dermatosis of childhood with autoantibodies to a 230 kDa epidermal antigen. Pediatr Dermatol. 1994;11139- 144
PubMed
Wojnarowska  FWhitehead  PLeigh  IM  et al.  Identification of the target antigen in chronic bullous disease of childhood and linear IgA disease of adults. Br J Dermatol. 1991;124157- 162
PubMed
Yamane  YSato  HHigashi  K  et al.  Linear immunoglobulin A (IgA) bullous dermatosis of childhood: identification of the target antigens and study of the cellular sources. Br J Dermatol. 1996;135785- 790
PubMed
Zhou  SFerguson  DJAllen  J  et al.  The localization of target antigens and autoantibodies in linear IgA disease is variable: correlation of immunogold electron microscopy and immunoblotting. Br J Dermatol. 1998;139591- 597
PubMed
Egan  CAZone  JJ Linear IgA bullous dermatosis. Int J Dermatol. 1999;38818- 827
PubMed
Miyagawa  SKiriyama  YShirai  TOhi  HSakamoto  K Chronic bullous disease with coexistent circulating IgG and IgA anti-basement membrane zone antibodies. Arch Dermatol. 1981;117349- 353
PubMed
Zhu  YIStiller  MJ Dapsone and sulfones in dermatology: overview and update. J Am Acad Dermatol. 2001;45420- 434
PubMed
Schiffner  JH Therapy of childhood linear IgA dermatitis herpetiformis. J Am Acad Dermatol. 1982;6403- 404
PubMed
Jablonska  SChorzelski  TPRosinska  DMaciejowska  E Linear IgA bullous dermatosis of childhood (chronic bullous dermatosis of childhood). Clin Dermatol. 1992;9393- 401
Siegfried  ECSirawan  S Chronic bullous disease of childhood: successful treatment with dicloxacillin. J Am Acad Dermatol. 1998;39797- 800
PubMed
Jones  ELEpinette  WWHackney  VCMenendez  LFrost  P Treatment of psoriasis with oral mycophenolic acid. J Invest Dermatol. 1975;65537- 542
PubMed
Epinette  WWParker  CMJones  ELGreist  MC Mycophenolic acid for psoriasis: a review of pharmacology, long-term efficacy, and safety. J Am Acad Dermatol. 1987;17962- 971
PubMed
Gomez  ECMenedez  LFrost  P Efficacy of mycophenolic acid for the treatment of psoriasis. J Am Acad Dermatol. 1979;1531- 537
PubMed
Spatz  SRudnicka  AMcDonald  CJ Mycophenolic acid in psoriasis. Br J Dermatol. 1978;98429- 435
PubMed
Lynch  WSRoenigk  HH  Jr Mycophenolic acid for psoriasis. Arch Dermatol. 1977;1131203- 1208
PubMed
Marinari  RFleishmajer  RSchragger  AHRosenthal  AL Mycophenolic acid in the treatment of psoriasis: long term administration. Arch Dermatol. 1977;113930- 932
PubMed
Allison  ACKowalski  WJMuller  CDEugui  EM Mechanisms of action of mycophenolic acid. Ann N Y Acad Sci. 1993;69663- 87
PubMed
Pirsch  JDSollinger  HW Mycophenolate mofetil: clinical and experimental experience. Ther Drug Monit. 1996;18357- 361
PubMed
Kitchin  JEPomeranz  MKPak  GWashenik  KShupack  JL Rediscovering mycophenolic acid: a review of its mechanism, side effects, and potential uses. J Am Acad Dermatol. 1997;37445- 449
PubMed
Becker  BN Mycophenolate mofetil. Transplant Proc. 1999;312777- 2778
PubMed
Haufs  MGBeissert  SGrabbe  SSchutte  BLuger  TA Psoriasis vulgaris treated successfully with mycophenolate mofetil. Br J Dermatol. 1998;138179- 181
PubMed
Nousari  HCSragovich  AKimyai-Asadi  AOrlinsky  DAnhalt  GJ Mycophenolate mofetil in autoimmune and inflammatory skin disorders. J Am Acad Dermatol. 1999;40265- 268
PubMed
Grundmann-Kollmann  MKorting  HCBehrens  S  et al.  Mycophenolate mofetil: a new therapeutic option in the treatment of blistering autoimmune diseases. J Am Acad Dermatol. 1999;40957- 960
PubMed
Bohm  MBeissert  SShwarz  TMetze  DLuger  T Bullous pemphigoid treated with mycophenolate mofetil [letter]. Lancet. 1997;349541
PubMed
Nousari  HCGriffin  WAAnhalt  GJ Successful therapy of bullous pemphigoid with mycophenolate mofetil. J Am Acad Dermatol. 1998;39497- 498
PubMed
Enk  AHKnop  J Mycophenolate is effective in the treatment of pemphigus vulgaris. Arch Dermatol. 1999;13554- 56
PubMed
Picknacker  ALuger  TASchwarz  T Dyshidrotic eczema treated with mycophenolate mofetil. Arch Dermatol. 1998;134378- 379
PubMed
Goldblum  R Therapy of rheumatoid arthritis with mycophenolate mofetil. Clin Exp Rheumatol. 1993;11S117- S119
PubMed
Grundmann-Knollmann  MKorting  HCBehrens  S  et al.  Successful treatment of severe refractory atopic dermatitis with mycophenolate mofetil. Br J Dermatol. 1999;141175- 176
PubMed
Neuber  KSchwartz  IItschert  G  et al.  Treatment of atopic eczema with oral mycophenolate mofetil. Br J Dermatol. 2000;143385- 391
PubMed
Benez  AFierlbeck  G Successful long-term treatment of severe atopic dermatitis with mycophenolate mofetil. Br J Dermatol. 2001;144638- 639
PubMed
Grundmann-Kollmann  MPodda  MOchsendorf  FBoehncke  WHKaufmann  RZollner  TM Mycophenolate mofetil is effective in the treatment of atopic dermatitis. Arch Dermatol. 2001;137870- 873
PubMed
Hohenleutner  UMohr  VDMichel  SLandthaler  MS Mycophenolate mofetil and cyclosporine treatment for recalcitrant pyoderma gangrenosum. Lancet. 1997;3501748
PubMed
Nousari  HCLynch  WAnhalt  GJ  et al.  The effectiveness of mycophenolate mofetil in refractory pyoderma gangrenosum. Arch Dermatol. 1998;1341509- 1511
PubMed
Jacqz-Aigrain  EKhan Shaghaghi  EBaudouin  V  et al.  Pharmokinetics and tolerance of mycophenolate mofetil in renal transplant children. Pediatr Nephrol. 2000;1495- 99
PubMed
Nevins  TE Overview of new immunosuppressive therapies. Curr Opin Pediatr. 2000;12146- 150
PubMed

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