Case Studies:

• No cure
• Patients need to be educated
• No clear cut standard therapeutic approach
• Responses to treatments vary with individuals

• Reduce signs and symptoms
• Obtain remission of the disease
• Obtain optimum benefits from treatment without inducing morbidity and mortality
• Improve the quality of life of patients
  

• TCSs continue to be the mainstay of atopic dermatitis treatment1,2.
• Mechanism of action : anti-inflammatory and immunosuppressive
  Direct regulatory effect on gene transcription and indirect blocking effect on
  transcription factors at cellular level25,26.
  Reduces the colonization of Staph aureus on the skin.12,13
• The market is saturated with different strengths and formulations of TCSs However there are no adequate trials to suggest superiority of one over the other.
• Potency of TCS is classified by the potential for vasoconstriction4 . Efficacy of TCS can be enhanced by halogenation of the 9-alpha position which enhances potency and removing the hydrophilic 17dihydroxy acetone side chain or the 16-alphahydoxy group which will increase lipophilicity.
• Guidelines for prescribing TCS are well-described16,17 .In general only preparations that have very weak or moderate strength are used on the face and genital area, whereas those that have moderate or potent strength are used on other areas of the body 5. Patients should be educated about the different steroid potencies in order to minimize untoward side effects6.
• The vehicle through which the active steroid is delivered plays an important role in absorption and can enhance its efficacy. Generally ointments are more effective than creams, as the emollient action and occlusive effect results in better penetration. Ointments also require fewer preservatives so the potential for irritant and allergic reactions is lower. Wet wraps and application under occlusion also enhance absorption of topical steroids. A novel foam vehicle independent of relying on the hydration of the stratum corneum ( which traditional vehicles depend on ) for drug delivery is available in the United States24 .
• The British Association of Dermatologists recommend using topical steroids for 10-14 days when the eczema is active, followed by “holidays ” with just emollients. The National Prescribing Centre recommends that steroids be used in bursts of three to seven days to treat exacerbations. This rationale can be extended to using potent TCS for a few days to initiate control followed by use of a milder potency TCS and or emollient 7,8. Another strategy to taper the use of TCS is to reduce the frequency of application .
• In a study using fluticasone propionate in adults with moderate to severe eczema, twice-weekly application to affected and non-active skin sites significantly prevented relapses once the flare settled 9. For chronic lichenified eczema, however, frequent potent steroids are required for much longer periods 8.
• The BNF also gives a rough guide as to how much TCS to use which is a frequent practical problem with patients. The finger tip unit: index finger: from distal crease to finger tip = 0.5 g. This aids monitoring compliance and usage. There is no clear RCT (randomized controlled trials) to suggest that the application of TCS twice a day is better than a once daily application. Based on this it would be justifiable to use once – daily corticosteroids as a first step in all patients with AD. Such a policy would reduce cost, improve compliance and reduce side effects.
• No convincing evidence to demonstrate superior clinical efficacy of combination antibiotic / corticosteroid to corticosteroid alone.
• There is no RCT evidence to support the notion that diluting TCS reduces adverse effects while maintaining efficacy in AD.
• The reduced efficacy of TCS is thought to be related to disease severity rather than glucocorticoid resistance 4, 21.
• There are many challenges on the subject of TCS use, especially in the light of steroid abuse, steroid misuse , steroid phobia and side effects. There are as a result many publications addressing these issues and certain recommendations as already discussed have been suggested 14.
• Adverse effects are well documented but it is important to recognize the side effects of skin atrophy, telangiectasia, hypopigmentation, steroid acne, hirsutism, rosacea and contact sensitization to the steroid itself. There is no RCT evidence to suggest that skin thinning is a problem for correct use of topical steroids.
• Systemic effects though uncommon are the suppression of the hypothalamic-pituitary –adrenal axis, growth retardation, tachyphylaxis, glaucoma and cataract formation and Cushing’s syndrome15.
• Over recent years the risk of adverse effects of TCS has been reduced by optimizing application protocols and using newer steroid preparations with improved risk/benefit ratios eg. Prednicarbate, mometasone furoate, fluticasone and methylprednisilone aceponate 10,11. To optimize the beneficial effects of TCS different therapeutic schemes have been established: intermittent use might be as effective as an initial therapy with a high potent steroid followed by a time dependant dose reduction or change over to a lower potent preparation. A recent systematic review identified 83 randomized controlled trials of the use of TCS in atopic dermatitis 3. Vehicle controlled studies lasting less than one month indicated that approximately 80 % of people report good, excellent, or clear responses with TCS, whereas 38% of persons whereas 38% of persons in control groups reported such responses.
• The ideal TCS is difficult to create because the intracellular receptors that are responsible for corticosteroid efficacy are also responsible for the adverse side effects.18,19 However, recent findings that glucocorticoids mediate their therapeutic effects through gene expression by transrepression and transactivation has led to novel research which awaits clinical testing20.
• The judicious use of TCS would be short-term appropriate application as initial monotherapy or in combination with other therapeutic agents that ideally possess complementing mechanisms of action. These drugs could be either systemic or topical agents such as newer topical calcineurin inhibitors 23.

1. Hanifin JM, Cooper KD, Ho VC et al . Guidelines of care for atopic dermatitis, developed in accordance with the American Academy of Dermatology. J Am Acad Dermatol 2004;50:391-404
2. Korting HC , Kerscher M J ,Schafer –Korting M. topical glucocorticoids with improved benefit/risk ratio: do they exist? J Am Acad Dermatol 1992:27:87-92
3. Hoare C, Li Wan Po A, Williams H. Systemic review of treatments for atopic eczema. Health Technol Assess 2004;4:1-191
4. Hywel C Williams. N Eng J Med 2005;352:2314-24
5. McHenry PM , Williams HC , Bingham EA . Management of atopic eczema : Joint Workshop of the British Association of Dermatologists and the Research Unit of the Royal College of Physicians of London Br Med J 1995;310:843-7
6. Management of atopic eczema in primary care, Prodigy, 2004. www.prodigy.nhs.uk
7. Thomas KS, Armstrong S ,Avery A etal. Randomized control trial of short bursts of a potent topical corticosteroid versus prolonged use of a mild preparation for children with mild or moderate atopic eczema . Br Med J 2002;324-768
   
8. Joanne Hague and John Berth-Jones. Current management of atopic eczema in primary care www.escriber.com Prescriber 5 September 2005 ,50-57
9. Berth Jones J, Damstra RJ, Golsch S et al. Twicw weekly fluticasone propionate added to emollient maintenance treatment to reduce risk of relapse in atopic dermatitis: randomized , double blind, parallel group study. Br Med 2003;326:1367
10. Van Der Meer JB, Glazenburg EJ, Mulder PG et al. The management of moderate to severe atopic dermatitis in adults with topical fluticasone proprionate. The Netherlands Adult Atopic Study Group. Br J Dermatol 1999;140:1114-21
11. Kerscher MJ ,Hart H, Korting HC. In vivo assessment of the atrophogenic potency of mometasone furoate. Int J Clin Pharmacol Ther 1995;33:187-9
12. Stalder J F ,Fleury M, Sourisse M et al . Local steroid therapy and bacterial skin flora in atopic dermatitis. Br J Dermatol 1994;131:536-40
13. Nilsson EJ, Henning CG, Magnusson J . Topical corticosteroids and Staph aureus in atopic dermatitis Jam Acad Dermatol 1992;27:29-34
14. Sidbury R, Hanifin JM . Old,new and emerging therapiesfor atopic dermatitis Dermatol Clin 2000:18;1-11
15. Hengge UR, Ruzicka MD ,Robert A et al. Adverse effects of topical glucocorticosteroids. J Am Acad Dermatol 2006;54:1-15
16. Sulzberger MB. Witten VH . Effect of topically applied compound in selected dermatoses. J Invest Dermatol 1952;19:101-2
17. Ayres PJ , Hooper G . Assessment of the skin penetration properties of different carrier vehicles for topically applied cortisol. Br J Dermatol 1978;99:307-17
18. Smith EW . Do we need new and different glucocorticoids? . Curr Probl Dermatol 1993;21:1-10
19. Bodor N . Design of novel soft corticosteroids. Curr Probl Dermatol 1993;21:11-9
20. Schacke H , Schottelius A, Docke WD et al. Dissociation of transactivation from transrepression by a selective glucocorticoid receptor agonist leads to separation of therapeutic effects from side effects. Proc Natl Acad Sci U S A 2004;101:227-32
21. Ellison JA ,Patel L, Ray DW et al . Hypothalamic-pituitary -adrenal function and glucocorticoid sensitivity in atopic dermatitis. Pediatrics 2000;105:794-9
22. Charman C, Williams H . The use of corticosteroids and corticosteroid phobia in atopic dermatitis . Clinics Dermatol 2003;21 : 193-200
23. Del Rosso J, Friedlander S F . Corticosteroids: options in the era of steroid sparing therapy. J Am Acad Dermatol 2005;53:S50-8
24. Huang X, Tanojo H, Lenn J et al . A novel foam vehicle for delivery of topical steroids J Am Acad Dermatol 2005;53: S26-38
25. Hughes J ,Rustin M. Corticosteroids. Clin Dermatol 1997;15: 715-21
26. Norris D . Mechanisms of action of topical therapies and the rationale for combination therapy. J Am Acad Dermatol 2005;53:S17-25

• TCIs are complex macrocyclic compounds that bind to the intracellular protein macrophilin-12 ( previously known as FK506-binding proteins) and function as macrolactam immunomodulators, thereby inhibiting the activity of the phosphorylase enzyme, calcineurin 15 . This results in selective inhibition of cytokine transcription in activated T cells without suppressing Langerhans cells 15,16.
• Pimecrolimus and tacrolimus are safe and effective in reducing the severity of AD symptoms in children and adults.
• At present in South Africa we have pimecrolimus and not tacrolimus. Evidence of the safety and efficacy of pimecrolimus was derived from studies primarily in patients with mild to moderate atopic dermatitis; tacrolimus data was derived from moderate to severe patients.
• Pimecrolimus has been studied in clinical trials in infants as young as 3 months, as compared with tacrolimus from 2 years. Pimecrolimus binds to cytoplasmic proteins and the resulting complex binds calcineurin, inhibiting its ability to dephosphorylate the nuclear factor of activated T-Cells (NF-AT). The ligand for cyclosporin is cyclophilin, whereas pimecrolimus and tacrolimus bind macrophilin-12 also known as FK506 binding protein. Pimecrolimus selectively targets T cells and mast cells; it inhibits T-cell proliferation as well as production and release of IL2, IL4, Interferon gamma and TNF-alpha. Moreover pimecrolimus inhibits mast cell degranulation. In contrast to tacrolimus, pimecrolimus has no effects on the differentiation, maturation and function of dendritic cells. In contrast to corticosteroids, pimecrolimus does not affect endothelial cells and fibroblasts and does not induce skin atrophy. Clinical trial data 43-45 have proven that pimecrolimus reduces incidence of flares and has a significant effect on reducing pruritus; these trials have not been performed for tacrolimus.
• TCIs provide a steroid free, anti-inflammatory topical therapy for atopic dermatitis. In both animal and human studies both pimecrolimus and tacrolimus demonstrated immunomodulatory activity 1. The anti-inflammatory potency of 0.1% tacrolimus ointment is similar to a corticosteroid with moderate potency 2 whereas 1% pimecrolimus cream is less active 3. Thus far no trials have been published comparing pimecrolimus 1% with a mild topical steroid. Both agents proved to be effective with a good safety profile for a period of up to 2 years with pimecrolimus and up to 4 years with tacrolimus4,5.
• TCIs are frequently associated with a transient burning sensation of the skin. A recent study showed pimecrolimus to show better tolerability than tacrolimus especially with regards this topical effect 6 . TCIs are not associated with skin atrophy and are therefore a useful treatment for the face and intertriginous areas7 . This property can be an advantage for the drug to be used long term. A long term study confirmed this benefit and also concluded that prolonged use (at least a year ) of tacrolimus ointment therapy is nonatrophogenic and additionally reverses corticosteroid-induced skin atrophy 9 .
• Another randomized double blind study comparing pimecrolimus with topical steroids in adults showed long-term safety and tolerability. Comparative study between pimecrolimus and topical corticosteroids showed that in patients requiring more extensive medication the incidents of overall skin infections in the group receiving corticosteroids was double that in the pimecrolimus group.
• Pimecrolimus was found to a safe drug with none of the side effects seen with topical steroids and was also found to reduce the dependency of patients to topical steroids10 .The percutaneous absorption of TCIs was found to be low. A significant proportion of patients could also be maintained without topical steroids for a year. Pimecrolimus is currently approved by the FDA and the European medicines agency for short term and intermittent use in mild to moderate atopic dermatitis.
• Few long term studies compare intermittent use of TCIs with intermittent use of topical steroids. A 12 month vehicle controlled study of children showed that early use of pimecrolimus reduced the frequency of flares although early use of topical steroids might have shown similar benefits 11 .
• In the United Kingdom the national institute of clinical excellence approves the use of topical tacrolimus for children older than two years of age with moderate to severe dermatitis not controlled by topical corticosteroids, and of topical pimecrolimus as a second line option for resistant dermatitis of the head and neck12 . In the United States both of these agents are approved as second line treatments, and the site of application is not restricted for pimecrolimus.
• Tacrolimus has a favourable safety profile for up to four years.
• Generalised herpetic and molluscum infection have been observed with TCIs but it is unclear whether there is an increased susceptibility to viral infections with TCIs 8. TCIs are not safe to use in pregnancy and during breast-feeding.
• Both drugs are a welcome addition to the treatment armamentarium of atopic eczema. Both are useful for maintenance therapy after establishing acute control of disease flares with topical steroids. On the basis of the information available the American Academy of Dermatology Association Task force recommends that TCIs remain available for patients with atopic dermatitis and other inflammatory skin diseases 17 .
• The recent alert emphasizes the importance of using these preparations only as labeled with patients well informed and when first line treatment has failed or cannot be tolerated. Their drawbacks are expense, a burning sensation on application, a slight increase in herpes labialis and a lack of long term data and studies 14 . There is also a need for studying the efficacy of TCIs in combination with other standard modalities of eczema treatment
  

• Continuous long-term use of these agents in any age group should be avoided
• Application should be limited to areas of involvement only
• Pimecrolimus cream is not indicated for use in children less than 2 years of age.
• Tacrolimus ointment is not indicated for use in children less than 2 years of age.
• Only 0.03% tacrolimus ointment is indicated for use in children 2-15 years of age.

1. Hultsch T, Kapp A , Spergel J. Immunomodulation and safety of topical calcineurin
   inhibitors for the treatment of atopic dermatitis. Dermatol 2005;211:174-87
2. Ashcroft DM, Dimmock P ,Garside R at al. Efficacy and tolerability of topical
   pimecrolimus and tacrolimus in the treatment of atopic dermatitis ; meta-analysis of
   randomized controlled trials. Br Med J 2005; 330-516
3. Luger T, Van Leent EJ, Graeber M et al . SDZ ASM 981 : an emerging safe and
   effective treatment for atopic dermatitis Br J Dermatol 2001;144:788-94
4. Paul C, Cork M, Rossi AB et al. Safety and tolerability of 1% pimecrolimus cream
   among infants. Pediatrics 2006;117:118-28
5. Breuer K, Werfel T, Kapp A. safety and efficacy of topical calcineurin inhibitors in the
   treatment of childhood eczema. Am J Clin Dermatol 2005;6:65-77
6. Kempers S, Boguniewicz M, Carter E et al . A randomized investigator – blinded study
   comparing pimecrolimus cream with tacrolimus in the treatment of pediatric patients
   with moderate atopic dermatitis. J Am Acad Dermatol 2004;51:515-25
7. Queille –Roussel C, Paul C, Duteil L et al. The new topical ascomycin derivate SDZ
   ASM 981 does not induce skin atrophy. Br J Dermatol 2001;144:507-13
8. Wollenburg A ,Zoch C, Wetzel S et al. Predisposing factors and clinical features of
   eczema herpeticum ; a retrospective analysis of 100 cases J Am Acad Dermatol 2003:
   49; 198-205
9. Kyllonen H , Remitz A, Mandelin JM et al . Effects of I year intermittent treatment
   with topical tacrolimus monotherapy on skin collegen synthesis in patients with atopic
   dermatitis. Br J Dermatol 2004;150:1174-81
10. Luger TA , Lahfa R, Folster –Holst R et al. Long term safety and tolerability of
    pimecrolimus cream 1% and topical steroids in adults with moderate to severe atopic
    dermatitis . J Dermatological Treatment 2004;15,169-78
11. Wahn U , Bos JD, Goodfield M et al . Efficacy and safety of pimecrolimus cream in
    the long term management of atopic dermatitis in children. Pediatrics 2002;110:2
12. National Institute for clinical excellence . Final appraisal determination: tacrolimus
    and pimecrolimus for atopic eczema. http: // www.nice.org.uk/pdf/P&T FAD . Pdf
13. center for drug evaluation and research.
    http://www.fda.gov/cder/drug/infoSheets/hcp/elidelHCP.htm
    
14. Kristian Thesstrup – Pedersen . Treatment strategies and compliance for the adult patient with atopic eczema. Acta Derm Venereol 2005;Suppl 215:36-40
15. Bornhovd E , Burgdorf WH ,Wollenberg A . Macrolactam immunomodulators for topical treatment of inflammatory skin diseases . J Am Acad Dermatol 2001;45:736-43
16. Zuberbier T, Chong S. The ascomycin macrolam pimecrolimus is a potent inhibitor of mediator release from human dermal mast cells and peripheral blood basophils. J Allergy Clin Immunol 2001;108:275-80
17. Berger T . Report of the American Academy of Dermatology Association Task Force
    on the safety concerns of the use of TCI in dermatology. J Am Acad Dermatol 54(5):818-23

1. Klein P , Clark R An evidence –based review of the efficacy of antihistamines in relieving pruritus in atopic dermatitis. Arch Dermatol 1999;135:1522-25
2. Munday J , Bloomfield R, Goldman M etal . Chlorpheniramine is no more effective than placebo in relieving the symptoms of childhood atopic dermatitis with a nocturnal itching and scratching component. Dermatology 2002;205:40-5
3. Wahlgren C F , Hagermark O, Bergstrom R . The antipruritic effect of a sedative and a non-sedative antihistamine in atopic dermatitis. Br J Dermatol 1990;122:545-51
4. Kawashima M ,Tango T, Noguchi T et al . Addition of fexofenadine to a topical steroid reduces the pruritus associated with atopic dermatitis in a 1 week randomized, multicenter, double-blind, placebo-controlled parallel-group study. Br J Dermatol 2003;148:1212-21
5. Langelnd T, Fagertun H E ,Larsen S. Therapeutic effect of loratadine on pruritus inpatients wuth atopic dermatitis. Allergy 1994;49:22-6
6. Berth – Jones , Graham- Brown RA. Failure of terfenadine in relieving the pruritus of atopic dermatitis: Br J Dermatol 1989;121:635-7
7. Doherty V , Sylvester DG, Kennedy CT et al. Treatment of itching in atopic eczema with antihistamines with a low sedative profile . Br Med J 1989;298-86

• Cyclosporine is a oral calcineurin inhibitor available as 25 or 100mg soft gelatin capsules. Cyclosporine prevents T lymphocyte activation and the transcription of IL2, which blocks the proliferation of other T lymphocytes10.
• Efficacy in treating mild to moderate eczema is well established but is restricted to case reports 7.
• The American academy of dermatology guidelines recommend the use of cyclosporine for the treatment of severe atopic dermatitis on the basis of the results of well designed randomized controlled trials although the agent is not approved by the FDA for treating atopic dermatitis1.
• In general cyclosporine should be used on a short-term basis for severe refractory atopic dermatitis 2. Maximal efficacy is observed within two weeks, but relapses following cessation of treatment are common3.
• An open study in adults found that one to two six week courses of cyclosporine resulted in long term remission of atopic eczema at one year 4 but open trials in children found that continuous rather than intermittent usage achieved better control 5.
• The starting dose is usually 5mg/kg daily in divided doses tapering down to 2-3mg/kg daily in divided doses6.
• Careful monitoring is essential with cyclosporine use. Documented side effects include nephrotoxicity, immunosuppression, and predisposition to cancer, particularly cutaneous non-melanoma skin cancer and lymphoma 1. Cyclosporine also interacts with a variety of commonly used blood pressure medications, statins, antibiotics, antifungals, antiepileptics, and HIV protease inhibitors 1,8,9.

1. Hanifin J M, Cooper K D ,Ho VC et al. Guidelines of care for atopic dermatitis,
   developed in accordance with the AAD. J Am Acad Dermatol 2004;50:391-404.
2. Naeyaert JM , Lachapelle JM, Degreef H et al Cyclosporine in atopic dermatitis, review
   of the literature and outline of a Belgian consensus. Dermatology 1999;198:142-52
3. Granlund H, Erkko P, Sinasalo M. Cyclosporin in atopic dermatitis: time to relapse and
   effect of intermittent therapy. Br J Dermatol 1995;132:106-12
4. Grandlund H, Erkko P, Reitamo S . Long term follow up of eczema patients treated
   with cyclosporine. Acta Derm Venereol 1998;78(1);40-3
5. Harper JI, Ahmed I, Barclay G et al . Cyclosporin for severe childhood atopic
   dermatitis. Short course versus continuous therapy. Br J Dermatol 2000;142:52-8


6. Sowden JM , Berth-Jones J, Ross JS et al. Double-blind, controlled, crossover study
   of cyclosporine in adults with severe refractory atopic dermatitis. Lancet 1991;338:
   137-40
7. Leung DY, Bieber T. Atopic dermatitis. Lancet 2003:361;151-60
8. Thompson PD ,Clarkson P, Karas RH . Statin associated myopathy. J Am Med Ass
   2003: 289:1681-90
9. Akhavan A , Rudikoff D . The treatment of atopic dermatitis with systemic
   immunosuppressive agents. Clinics Dermatol 2003;21:225-40
10. Sauder D N . Mechanism of action and emerging role of immune response modifier
    therapy in dermatological conditions. J Cutan Med Surg 2005;3-12

• Often used after cyclosporine in treating moderate to severe atopic eczema.
• Very little scientific data except for two recent randomized controlled trials 1,2 . The results of a crossover trial using 2.5 mg/kg azathioprine showed a 25% improvement in disease activity , but 35% of the participants withdrew owing to side effects. Using a parallel group design and using doses of azathioprine according to thiopurinemethyl transferase ( TPMT ) , a key enzyme in thiopurine metabolism status , Meggitt et al observed a larger mean improvement in disease activity (37%) and a lower dropout rate of 15% .Sustained improvement for at least three months after stopping azathioprine may also occur 2 . In a retrospective open study , Murphy et al found that azathioprine resulted in a good or excellent response in 41/48
  ( 85% ) children with atopic eczema 3.
• Treatment with azathioprine as systemic monotherapy is a cost effective adjunctive treatment in moderate to severe atopic eczema that does not respond despite optimum therapy with topical corticosteroids 4, 5. Optimal use is achieved when combined with systemic steroids, providing a steroid sparing effect.
• Dose: 2.5mg per kilogram per day. Can start with 50mg a day increasing it gradually. Onset of effect is slow and therapeutic effects are not dramatic which is discouraging to patients.
• In the randomized controlled trials no participants developed serious laboratory abnormalities, although hypersensitivity reactions occurred in two patients 2. Long term risks are unknown 6.

1. Berth-Jones J, Takwale A, Tan E et al . Azathioprine in severe adult atopic eczema; a double blind , placebo controlled ,crossover trial . Br J Dermatol 2002; 147;324-30
2. Meggitt S J, Gray JC , Reynolds NJ . Azathioprine dosed by thiopurine methyltransferase activity for moderate to severe atopic eczema: a double –blind , randomized controlled trial . Lancet 2006;367 : 839-46
3. Murphy LA , Atherton D . A retrospective evaluation of azathioprine in
   severe childhood atopic eczema using TPMT levels to exclude patients at high risk of myelosuppression. Br J Dermatol 2002;147: 308-15.
4. Get lancet reference
5. Buckley D A , Baldwin P, Rogers S. The use of azathioprine in severe adult atopic eczema. J Eur Acad Dermatol Venereol 1998;11:137-140
6. Kwon JH, Farrel RJ . The risk of lymphoma in the treatment of inflammatory
   bowel disease with immunosuppressive agents. Crit Rev Clin Oncol 2005;56:169-78.
7. Meggit SJ , Reynolds NJ . Azathioprine for atopic dermatitis. Clin Exp Dermatol 2001;26:369-75

• Methotrexate is a folic acid antagonist that prevents the production of tetrahydrofolic acid by binding to dyhydrofolate reductase .
• Methotrexate probably causes a shift from TH1 to TH2 responses by both suppressing the stimulating the production of natural cytokine inhibitors such as IL-1 receptor antagonists 1.
• There are no evidence based RCTs to support its use in AD. 2,3.
  

1. Rothe MJ, grin-Jorgensen C, Ramsey WH ,et al : Monitoring patients taking methotrexate J Am Acad Dermatol 1995;32: 680
2. Egan CA, Rallis TM , Meadows KP. Low dose oral methotrexate treatment for recalcitrant palmoplantar pompholyx. J Am Acad Dermatol 1999;40:612-4
3. Shaffrali FC, Colver GB , Messenger AG. Experience with low dose methotrexate for the treatment of eczema in the elderly J Am Acad Dermatol 2003;48:417-9

• Recently re-introduced to the dermatological world 6. The literature based uses range from various inflammatory to autoimmune disorders6. However only anecdotal case reports are found in the literature and larger studies are therefore required.
• The standard dosage in adults for most dermatological conditions appears to be 1 gram per os BD. It is available as a 250mg (cellcept) capsule and its absorption is enhanced on an empty stomach.
• Severe refractory atopic dermatitis was documented to be responsive to MMF in two patients1. A larger trial of ten patients treated with MMF ( 2g/d ) demonstrated improvement in their atopic dermatitis severity scores as measured by SCORAD indices, and without major side effects2. These two open trials using 2.0g MMF daily reported improvement in disease activity
  ( 68% median reduction and 55% mean reduction ) 1,2 .whereas a third study using 2.0 to 2.5 g daily reported no clinically relevant effect in five patients.
  A recent retrospective study on 20 patients showed MMF to be effective and well tolerated . 17 patients improved within 4 weeks . 10 patients had disease remission and 7 patients attained satisfactory control of their atopic dermatitis using MMF as maintenance therapy3. The success of this study was limited by there being no control group and the lack of a standardized scoring index to assess improvement. Also the concomitant use of adjuvant therapies made the contribution of MMF alone difficult to assess.
• The safety profile in long term usage of MMF also needs to be evaluated. The current concerns with MMF therapy are the induction of neutropenia in the development of lymphomas and other malignancies7,8.

1. Neuber K , Schwartz I, Itschert G. Treatment of atopic eczema with oral mycophenolate mofetil. Br J Dermatol 2000;143:385-91
2. Grundmann-Kollman M, Podda M , Ochsendorf F. Mycophenolate mofetil is effective in the treatment of atopic dermatitis. Arch Dermatol 2001;137:870-3
3. Murray M L and Cohen JB . Mycophenolate mofetil therapy for moderate to severe
   atopic dermatitis. Clinical Exp Dermatol 2006;2:1-5
4. Jones EL , Epinette WW , Hackney VC et al . Treatment of psoriasis with oral
   mycophenolic acid . J Invest Dermatol 1975;65:537-42
5. Alsberg CL, Black OF . Contribution to the study of maize deterioration . US Dept
   Agr Plant Industry Bull 1913;270:7-48
   
6. Liu V and Mackool BT . Mycophenolate in Dermatology. Jnl Dermatological
   Treatment 2003;14:203 - 210
7. Stern DK , Tripp JM , Ho VC , Lebwohl M. Use of systemic immune modulators in
   dermatology : an update . Dermatol Clin 2005;23:259-300
8. Heymann WR . Mycophenolate mofetil J Am Acad Dermatol 2005;53:1045-6