Advertisement

Erythroderma

  • Katrina Harper-KirkseyEmail author
Chapter
  • 476 Downloads

Abstract

Erythroderma, often described as generalized exfoliative dermatitis, is a condition in which erythema involves greater than 90% of the body surface, often as a result of an underlying inflammatory skin condition, which can result in a variety of systemic manifestations and potentially lead to life-threatening complications.

Keywords

Erythema Scaling Exfoliation Hypersensitivity Vasodilation Edema Systemic Drug reaction 

Background

Erythroderma is a severe and potentially life-threatening dermatitis described as an intense and widespread erythema typically involving greater than 90% of the body surface area, with a variable degree of exfoliative skin scaling (see Figs. 19.1 and 19.2) [1, 2]. It is a manifestation of a wide range of cutaneous and systemic diseases including infection, malignancy, and drug hypersensitivity reactions [3].
Fig. 19.1

Widespread erythema and areas of sparing in a patient with unclear etiology of erythroderma. (Used with permission from Rothe et al. [3])

Fig. 19.2

Diffuse erythema and scaling of a 14-year-old girl with erythroderma of unknown etiology. (Source (open access): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2800861/)

There are numerous systemic and cutaneous diseases known to be associated with erythroderma (Tables 19.1 and 19.3). The most common trigger of erythroderma is an exacerbation of an underlying dermatitis, most commonly psoriasis (Fig. 19.3 ) (23%), atopic dermatitis, and contact dermatitis [4, 5, 6, 7]. Drug reaction is another important cause of erythroderma, implicated in 20% of cases, with at least 135 drugs suspected as potential causative agents [58, 10]. A common malignancy associated with erythroderma is cutaneous T-cell lymphoma (CTCL) [3, 7, 9]. Idiopathic erythroderma, where no cause can be elucidated despite thorough serial investigations, occurs in approximately 30% of cases. “Red man’s syndrome” associated with rapid vancomycin infusion is considered to be an example of idiopathic erythroderma [35, 8, 10, 11].
Table 19.1

Common causes of erythroderma (remembered by mnemonic IDSCALP) [54]

I

Idiopathic – 30%

Infections (HIV, HSV, dermatophytosis, scabies)

D

Drug allergy – 20%

S

Seborrheic dermatitis – 2%

Sarcoidosis

C

Contact dermatitis – 3%

Connective tissue diseases

A

Atopic dermatitis – 10%

Autoimmune (systemic lupus/dermatomyositis/bullous pemphigoid/pemphigus foliaceus/lichen planus/graft vs host disease)

L

Lymphoma and leukemia – 14% (including Sezary syndrome)

P

Psoriasis – 23% (including reactive arthritis/pityriasis rubra pilaris)

Fig. 19.3

Patient with erythrodermic psoriasis and classic plaques on elbows. (Used with permission from Rothe et al. [3])

Because erythroderma is often associated with scaling and extensive erythema, it is often difficult to discern the typical features characteristic of the preexisting, underlying condition. For this reason, diagnosis and management strategies can be challenging [1, 2].

Erythroderma is thought to be mediated by a complicated process of inflammatory cell interactions, resulting in a dramatic turnover of epidermal cells [12]. It is a rare condition, with an incidence rate of approximately 1 per 100,000 adults [13]. Erythroderma is rare in children and occurs at an average age of 42–61 years [14]. When age of onset is less than 40 years, the condition is typically a result of atopic dermatitis, seborrheic dermatitis, staphylococcal scalded skin syndrome, or a hereditary ichthyosis [14, 15]. It is more common in males and has no racial predilection [3, 4, 5, 6, 7, 9, 16].

Classic Clinical Presentation

The typical presentation of erythroderma is characterized by erythematous patches which progressively increase in size and coalesce to cover most of the body’s surface, with occasional islands of sparing [17]. Scaling can occur as large sheets or small flakes and generally erupt 2–6 days after the onset of erythema. Pruritus is common and is most severe in patients with atopic dermatitis and Sezary syndrome (a leukemic variant of cutaneous T-cell lymphoma where atypical lymphocytes known as Sezary cells are found in peripheral blood; see Fig. 19.4) [50]. The skin may feel leathery secondary to excessive scratching and there may be eyelid and periorbital involvement [18].
Fig. 19.4

Patient with Sezary and skin fissuring. (Used with permission from Rothe et al. [3])

Especially in chronic conditions, patches of hypopigmentation can be observed, and hair and nails may shed [19]. Nails may also become ridged, thickened, and brittle [9, 17, 20, 21]. Individuals with long-standing erythroderma may present with cachexia, vitiligo, diffuse alopecia (see Fig. 19.5), and thickened palms and soles (Table 19.2) [18, 22].
Fig. 19.5

Diffuse alopecia in a patient with chronic idiopathic erythroderma. (Used with permission from Rothe et al. [3])

Table 19.2

Classic features of erythroderma

Skin

Widespread erythema

Variable degree/character of scaling (2–6 days after erythema)

Pruritus (can lead to lichenification)

Eyes

Eyelid swelling may lead to ectropion (eyelid eversion), blepharitis, epiphora (excessive tearing), ectropion (eyelid eversion)

Palms/soles

May develop yellowish, diffuse keratoderma

Nails

Dull, ridged, thickened

May develop onycholysis and shed (onychomadesis)

Lymph nodes

Generalized lymphadenopathy which may be reactive or suggestive of lymphoma

Hair

Telogen effluvium (scaling of the scalp) leading to varying degrees of hair loss

Atypical Presentation

Table 19.3

Uncommon causes of erythroderma

Stevens-Johnson syndrome

Toxic epidermal necrolysis

Toxic shock syndrome

Stasis dermatitis (venous eczema)

Seborrheic dermatitis

Staphylococcal scalded skin syndrome

Blistering diseases including pemphigus and bullous pemphigoid

Sezary syndrome

Rare congenital ichthyotic conditions

Associated Systemic Symptoms

Systemic symptoms related to erythroderma itself or to the primary disease can be observed. Many of these features can lead to serious sequelae and are discussed further in the complications section. Patients often are unwell appearing and report chills, fever, fatigue, and malaise. Lymphadenopathy and (rarely) splenomegaly can be observed. Hepatomegaly is seen in 1/3 of cases and is most common in drug-induced erythroderma [7, 22]. Significant protein loss exceeding 9 g/m2 body surface per day as a consequence of skin exfoliation can lead to hypoalbuminemia, edema, and muscle wasting [12]. As a result, patients may experience loss in temperature regulation and up to 50% of patients develop pretibial and pedal edema [2, 3].

When erythroderma occurs secondary to drug reaction, eosinophilia can be observed along with systemic symptoms characteristic of DRESS (drug reaction and systemic symptoms; see Chap.  20) [2].

Time Course of Disease

Erythroderma may develop rapidly over hours to days or more gradually over weeks to month (see Table 19.4) [22]. Patients may initially present as medically stable or with life-threatening complications [3].
Table 19.4

Typical course of disease according to etiology [22]

 

Onset

Features

Duration

Primary cutaneous

Slower/indolent

Erythematous patches of increasing size with variable islands of sparing

Subsequent scaling

Variable

Drug-induced

Abrupt

Morbilliform or urticarial followed by erythematous patches which increase in size

Comparatively quick resolution

Systemic

Gradual

Initially characteristic of disease before patches form and coalesce

Variable

Idiopathic

  

Unpredictable

The duration of erythroderma is highly variable and is determined by the underlying cause. Erythroderma as a result of primary skin disease is typically a gradual course with a median duration of 10 months but can go on to last years [7].

The disease evolves more rapidly when it is a result of drug hypersensitivity reaction, lymphoma, or leukemia. In the setting of systemic disease, symptoms may persist from weeks to years – dependent on the course of the underlying disorder. Conversely, in the case of drug-induced erythroderma, resolution of disease can occur in as little as 2–6 weeks after discontinuation of the offending agent [3]. Patients with DRESS, however, may take longer to recover – over weeks to months with possible relapse (see Chap.  20).

Common Mimics and Differential Diagnosis

The diagnosis of erythroderma is difficult given it is usually a manifestation of an underlying diagnosis or exacerbation of primary disorder (Table 19.5). Additionally, the characteristic physical findings of erythroderma generally obscure underlying disease features.
Table 19.5

Common mimics of erythroderma, often implicated as precipitating factors

Acanthosis nigricans

Allergic contact dermatitis

Bullous pemphigoid

Contact dermatitis

Cutaneous T-cell lymphoma

Familial benign pemphigus (Hailey-Hailey disease)

Graft-versus-host disease

Lichen planus

Malignancy

Pediatric atopic dermatitis

Pemphigus foliaceus

Pityriasis rubra pilaris

Plaque psoriasis

Reactive arthritis

Rapid vancomycin infusion

Sarcoidosis

Seborrheic dermatitis

Stasis dermatitis

Key Physical Exam Findings and Diagnosis Features

As the list of causative factors of erythroderma continues to expand, it becomes more difficult to pinpoint the precipitating diagnosis [22]. Because of this, a thorough history of presenting illness is of utmost importance in diagnosing erythroderma [23]. Patients must be asked about all medications, preexisting medical conditions, allergies, and previous diagnoses of rash and skin disorders [7, 22].

Physical examination is crucial in attempts to detect an underlying etiology as well as to evaluate for systemic involvement and potential complications (i.e., organomegaly, lymphadenopathy, peripheral edema, infection, heart failure, and potential respiratory compromise) [7, 18, 24].

Following a detailed history and physical, a skin biopsy, laboratory studies, imaging, and histology may useful adjuncts to derive a definitive diagnosis and exclude clinical mimics (see Fig. 19.6). These ancillary studies are often nonspecific, although with repeat testing the diagnosis may become apparent over time (Table 19.6) [11, 15, 16].
Fig. 19.6

Elderly patient with near erythroderma. Microscopy confirmed scabies infestation. (Used with permission from Rothe et al. [3])

Table 19.6

Diagnostic features of underlying disorders

Skin exam features [3, 18, 26]

Blisters and crusting: secondary infection, autoimmune blistering disorders (bullous pemphigoid, pemphigus foliaceus

Large scales: psoriasis

Fine scales: atopic dermatitis/dermatophyte infection

Burn-like scale: seborrheic dermatitis

Islands of sparing/yellow tinge to the skin/hyperkeratosis of the palms and soles: pityriasis rubra pilaris (PRP)

Laboratory testing

Leukocytosis, increased ESR, anemia, hypoalbuminemia, and hyperglobulinemia are frequent findings in all causes

Eosinophilia in patients with DRESS

Increased IgE may be noted in atopic dermatitis

Consider peripheral blood smears and bone marrow examination if leukemia is considered

Skin biopsy

Consider if cause unknown although tend to be nonspecific

Repeated biopsies may be necessary

Skin scrapings may show hyphae or mites

Imaging [22]

If cause is unknown, imaging may be performed as a survey for occult malignancy

Chest radiograph can identify infections, inflammatory disorders such as sarcoidosis with hilar lymphadenopathy, and congestive heart failure

Cultures/PCR

Evaluation for suprainfection, fungal infections, herpes simplex virus, and varicella zoster virus

Histological [27, 28, 29, 30]

In all comers, hyperkeratosis, acanthosis, spongiosis, and perivascular inflammatory infiltrate are frequent findings in general

May otherwise be nonspecific

Immunofluorescence [22, 31]

Of benefit in autoimmune blistering disease or connective tissue disease (i.e., immunoglobulins at the dermal-epidermal junction)

Management

Erythroderma is a dermatologic emergency which requires a dermatology consultation and hospital admission for severe cases to avoid potentially catastrophic complications. The principle management consists of discontinuation of all offending medications, maintaining skin moisture and integrity (through aggressive wound care), adequate hydration and nutrition, electrolyte repletion, and antibiotics for secondary infection (Table 19.7). Erythroderma as an isolated process will persist until the underlying condition is addressed, and the primary etiology may impact disease course and management options. Therefore, once the underlying diagnosis is established,targeted therapy should be administered promptly (Table 19.8).
Table 19.7

Initial management

Systemic symptoms [3]

Replacement of fluid and electrolytes

Monitoring hemodynamic status

Monitoring and regulation of body temperature

Nutritional support

Treatment of skin inflammation and pruritus

Discontinuation of all offending/unnecessary medications

Diuretics for refractory edema

Skin inflammation and pruritus [3, 22, 32]

Topical corticosteroids and oral antihistamines

Oatmeal baths or warm wet compresses (no more than a quarter of the body at a time)

Bland emollients or petrolatum for patient comfort

Infections

Blood cultures

Broad-spectrum antibiotic coverage (to include MRSA)

Antiviral medications where appropriate

Table 19.8

Targeted treatment modalities

Atopic dermatitis [22, 33, 34, 35, 36]

Avoiding allergens

Topical and systemic steroids

In refractory cases: cyclosporine, methotrexate, azathioprine, mycophenolate mofetil, and/or interferon

Psoriasis [37, 38, 39, 40, 51, 52, 53]

Topical steroids

Phototherapy

Methotrexate

Retinoids (i.e., acitretin)

Cyclosporine

In refractory cases: tumor necrosis factor (TNF) inhibitors, interleukin (IL) inhibitors, phosphodiesterase type 4 [PDE-4] inhibitors (i.e., infliximab, adalimumab, etanercept, ustekinumab, secukinumab) *this therapy can cause mycosis fungoides to progress

Mycosis fungoides [41, 42, 43, 44, 45]

Topical corticosteroids

Topical chemotherapy

Topical retinoids

May consider phototherapy and radiotherapy

In refractory cases: interferon, oral retinoids, histone deacetylase inhibitors, monoclonal antibodies, photopheresis, and chemotherapy

Rarely stem cell transplantation considered

Cutaneous T-cell lymphoma [25]

Methotrexate

Potent topical steroids

Chemotherapy

UV light

Sezary syndrome [46]

Extracorporeal photochemotherapy

Systemic retinoids

Interferon

Pityriasis rubra pilaris (PRP) [22, 47]

Systemic retinoids as first line

Topical steroids as adjunct to palms, soles, face, skin folds, and extremities

May consider methotrexate, TNF-alpha inhibitors, cyclosporine, and azathioprine

Drug induced [2, 7, 35]

Discontinue causative agents

Short-course oral steroids or pulse intravenous IV steroid therapy

Idiopathic erythroderma [1, 5, 9, 11]

Low to mid-potency topical corticosteroids

Oral antihistamines

In refractory cases: systemic corticosteroids

If a cause can be identified, then specific treatment should be initiated. Notably, systemic steroid should be avoided in psoriasis and staphylococcal scalded skin syndrome.

Complications

While the physiologic demands of erythroderma are tolerated by many patients, those at the extremes of age and patients with multiple comorbidities may suffer life-threatening consequences (see Table 19.9). The shunting of blood through the skin due to peripheral vasodilation can result in high-output heart failure [3]. These patients can present with tachycardia and pulmonary edema. Increased skin perfusion also results in temperature dysregulation and fluid and electrolyte imbalance. Exfoliation and protein loss result in edema and leave patient’s susceptible to secondary infections [12]. Acute respiratory distress syndrome (ARDS) is also a common complication.
Table 19.9

Physiologic derangements

Protein loss

Edema

Hypoalbuminemia

Fluid loss

Temperature dysregulation

Electrolyte and metabolic disturbances

High output cardiac failure

Sepsis from superinfection

End-organ damage may develop such as hepatitis, myocarditis, and/or interstitial nephritis [2].

Mortality rates range between 4 and 64% depending on the patient population [7, 22].

Bottom Line: Erythroderma Clinical Pearls

In the majority of cases, erythroderma results from an underlying condition and cannot itself be prevented [22]. Individuals who develop erythroderma as a result of drug hypersensitivity should be instructed to avoid the offending agent in the future. Erythroderma as a result of underlying inflammatory skin condition will usually abate with treatment but may recur at any time. Idiopathic erythroderma is characterized by a more unpredictable course. Overall, prognosis of erythroderma is dependent on the underlying cause and is generally favorable if the underlying disease can be effectively treated [48, 49, 50].

References

  1. 1.
    Khaled A, Sellami A, Fazaa B, Kharfi M, Zeglaoui F, Kamoun MR. Acquired erythroderma in adults: a clinical and prognostic study. J Eur Acad Dermatol Venereol. 2010;24:781–8.CrossRefPubMedGoogle Scholar
  2. 2.
    Usatine RP, Smith MA, Chumley HS, Mayeaux EJ Jr. Erythroderma. In: Usatine RP, Smith MA, Chumley HS, Mayeaux Jr EJ, editors. The color atlas of family medicine. 2nd ed. New York: McGraw-Hill; 2013.Google Scholar
  3. 3.
    Rothe MJ, Bernstein ML, Grant-Kels JM. Life-threatening erythroderma: diagnosing and treating the “red man”. Clin Dermatol. 2005;23:206–17.CrossRefPubMedGoogle Scholar
  4. 4.
    Pal S, Haroon TS. Erythroderma: a clinico-etiologic study of 90 cases. Int J Dermatol. 1998;37:104.CrossRefPubMedGoogle Scholar
  5. 5.
    Akhyani M, Ghodsi ZS, Toosi S, Dabbaghian H. Erythroderma: a clinical study of 97 cases. BMC Dermatol. 2005;5:5.CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    Rym BM, Mourad M, Bechir Z, et al. Erythroderma in adults: a report of 80 cases. Int J Dermatol. 2005;44:731.CrossRefPubMedGoogle Scholar
  7. 7.
    Grant-Kels JM, Fedeles F, Rothe MJ. Exfoliative dermatitis. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, editors. Fitzpatrick’s dermatology in general medicine. 8th ed. New York: McGraw Hill Medical; 2012.Google Scholar
  8. 8.
    Sheen YS, Chu CY, Wang SH, Tsai TF. Dapsone hypersensitivity syndrome in non-leprosy patients: a retrospective study of its incidence in a tertiary referral center in Taiwan. J Dermatol Treat. 2009;20:340.CrossRefGoogle Scholar
  9. 9.
    Li J, Zheng HY. Erythroderma: a clinical and prognostic study. Dermatology. 2012;225:154–62.CrossRefPubMedGoogle Scholar
  10. 10.
    Sigurdsson V, Toonstra J, van Vloten WA. Idiopathic erythroderma: a follow-up study of 28 patients. Dermatology. 1997;194:98.CrossRefPubMedGoogle Scholar
  11. 11.
    Thestrup-Pedersen K, Halkier-Sørensen L, Søgaard H, Zachariae H. The red man syndrome. Exfoliative dermatitis of unknown etiology: a description and follow-up of 38 patients. J Am Acad Dermatol. 1988;18:1307.CrossRefPubMedGoogle Scholar
  12. 12.
    Kanthraj GR, Srinivas CR, Devi PU, et al. Quantitative estimation and recommendations for supplementation of protein lost through scaling in exfoliative dermatitis. Int J Dermatol. 1999;38:91.CrossRefPubMedGoogle Scholar
  13. 13.
    Sigurdsson V, Steegmans PH, van Vloten WA. The incidence of erythroderma: a survey among all dermatologists in the Netherlands. J Am Acad Dermatol. 2001;45:675.CrossRefPubMedGoogle Scholar
  14. 14.
    Sarkar R, Garg VK. Erythroderma in children. Indian J Dermatol Venereol Leprol. 2010;76:341. Sarkar R, Basu S, Sharma RC. Neonatal and infantile erythrodermas. Arch Dermatol. 2001;137:822CrossRefPubMedGoogle Scholar
  15. 15.
    Fraitag S, Bodemer C. Neonatal erythroderma. Curr Opin Pediatr. 2010;22(4):438–44.CrossRefPubMedGoogle Scholar
  16. 16.
    Sigurdsson V, Toonstra J, Hezemans-Boer M, van Vloten WA. Erythroderma. A clinical and follow-up study of 102 patients, with special emphasis on survival. J Am Acad Dermatol. 1996;35:53.CrossRefPubMedGoogle Scholar
  17. 17.
    Sehgal VN, Srivastava G, Sardana K. Erythroderma/exfoliative dermatitis: a synopsis. Int J Dermatol. 2004;43:39–47.CrossRefPubMedGoogle Scholar
  18. 18.
    Sterry W, Steinhoff M. Erythroderma. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology.3rd ed. Philadelphia: Elsevier Saunders; 2012:171–181.Google Scholar
  19. 19.
    Bi MY, Curry JL, Christiano AM, et al. The spectrum of hair loss in patients with mycosis fungoides and Sézary syndrome. J Am Acad Dermatol. 2011;64:53.CrossRefPubMedGoogle Scholar
  20. 20.
    Klein A, Landthaler M, Karrer S. Pityriasis rubra pilaris: a review of diagnosis and treatment. Am J Clin Dermatol. 2010;11:157.CrossRefPubMedGoogle Scholar
  21. 21.
    Rosenbach M, Hsu S, Korman NJ, Lebwohl MG, Young M, Bebo BF Jr, et al. Treatment of erythrodermic psoriasis: from the medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62(4):655–62.CrossRefPubMedGoogle Scholar
  22. 22.
    Mistry N, Gupta A, Alva A, Sibbald G. A review of the diagnosis and Management of Erythroderma (generalized red skin). In: Advances in skin and wound care: Woltkers Kluwer Health; 2015. p. 228–36. www.woundcarejournal.com.
  23. 23.
    Yuan XY, Guo JY, Dang YP, Qiao L, Liu W. Erythroderma: a clinical-etiological study of 82 cases. Eur J Dermatol. 2010;20(3):373–7.PubMedGoogle Scholar
  24. 24.
    Lancrajan C, Bumbacea R, Giurcaneanu C. Erythrodermic atopic dermatitis with late onset casepresentation. J Med Life. 2010;3:80–3.PubMedPubMedCentralGoogle Scholar
  25. 25.
    Botella-Estrada R, Sanmartin O, Oliver V, Febrer I, Aliaga A. Erythroderma. A clinicopathological study of 56 cases. Arch Dermatol. 1994;130:1503–7.CrossRefPubMedGoogle Scholar
  26. 26.
    Griffiths WA. Pityriasis rubra pilaris. Clin Exp Dermatol. 1980;5:105. PMID7398119CrossRefPubMedGoogle Scholar
  27. 27.
    Megna M, Sidikov AA, Zaslavsky DV, Chuprov IN, Timoshchuk EA, Egorova U, et al. The role of histological presentation in erythroderma. Int J Dermatol. 2017;56(4):400–4.CrossRefPubMedGoogle Scholar
  28. 28.
    Ram-Wolff C, Martin-Garcia N, Bensussan A, Bagot M, Ortonne N. Histopathologic diagnosis of lymphomatous versus inflammatory erythroderma: a morphologic and phenotypic study on 47 skin biopsies. Am J Dermatopathol. 2010;32(8):755–63.CrossRefPubMedPubMedCentralGoogle Scholar
  29. 29.
    Zip C, Murray S, Walsh NM. The specificity of histopathology in erythroderma. J Cutan Pathol. 1993;20:393.CrossRefPubMedGoogle Scholar
  30. 30.
    Vasconcellos C, Domingues PP, Aoki V, et al. Erythroderma: analysis of 247 cases. Rev Saude Publica. 1995;29:177.CrossRefPubMedGoogle Scholar
  31. 31.
    Armstrong AW, Bagel J, Van Voorhees AS, Robertson AD, Yamauchi PS. Combining biologic therapies with other systemic treatments in psoriasis: evidence-based, best-practice recommendations from the medical Board of the National Psoriasis Foundation. JAMA Dermatol. 2015;151(4):432–8.CrossRefPubMedGoogle Scholar
  32. 32.
    Bruno TF, Grewal P. Erythroderma: a dermatologic emergency. CJEM. 2009;11(3):244–6.CrossRefPubMedGoogle Scholar
  33. 33.
    Guttman-Yassky E, Dhingra N, Leung DY. New era of biologic therapeutics in atopic dermatitis. Expert Opin Biol Ther. 2013;13(4):549–61.CrossRefPubMedGoogle Scholar
  34. 34.
    Shimizu H. Shimizu’s textbook of dermatology. 1st ed. Tokyo: Hokkaido University Press/Nakayama Shoten; 2007. p. 122–5.Google Scholar
  35. 35.
    Katsarou A, Armenaka M. Atopic dermatitis in older patients: particular points. J Eur Acad Dermatol Venereol. 2011;25(1):12–8.CrossRefPubMedGoogle Scholar
  36. 36.
    Gelbard CM, Hebert AA. New and emerging trends in the treatment of atopic dermatitis. Patient Prefer Adherence. 2008;2:387–92.PubMedPubMedCentralGoogle Scholar
  37. 37.
    Strober BE. Successful treatment of psoriasis and psoriatic arthritis with etanercept and methotrexate in a patient newly unresponsive to infliximab. Arch Dermatol. 2004;140:366.CrossRefPubMedGoogle Scholar
  38. 38.
    Barland C, Kerdel FA. Addition of low-dose methotrexate to infliximab in the treatment of a patient with severe, recalcitrant pustular psoriasis. Arch Dermatol. 2003;139:949–50.CrossRefPubMedGoogle Scholar
  39. 39.
    Ladizinski B, Lee KC, Wilmer E, Alavi A, Mistry N, Sibbald RG. A review of the clinical variants and the management of psoriasis. Adv Skin Wound Care. 2013;26:271–84.CrossRefPubMedGoogle Scholar
  40. 40.
    Zattra E, Belloni Fortina A, Peserico A. Alaibac M. Erythroderma in the era of biological therapies. Eur J Dermatol. 2012;22(2):167–71.PubMedGoogle Scholar
  41. 41.
    Rupoli S, Canafoglia L, Goteri G, Leoni P, Brandozzi G, Federici I, et al. Results of a prospective phase II trial with oral low dose bexarotene plus photochemotherapy (PUVA) in refractory and/or relapsed patients with mycosis fungoides. Eur J Dermatol. 2016;26(1):13–20.Google Scholar
  42. 42.
    Sokolowska-Wojdylo M, Florek A, Zaucha JM, Chmielowska E, Giza A, Knopinska-Posluszny W, et al. Polish lymphoma research group experience with bexarotene in the treatment of cutaneous T-cell lymphoma. Am J Ther. 2016;23(3):e749–56.Google Scholar
  43. 43.
    Chung CG, Poligone B. Cutaneous T cell lymphoma: an update on pathogenesis and systemic therapy. Curr Hematol Malig Rep. 2015;10(4):468–76.CrossRefPubMedGoogle Scholar
  44. 44.
    Galper SL, Smith BD, Wilson LD. Diagnosis and management of mycosis fungoides. Oncology (Williston Park). 2010;24(6):491–501.Google Scholar
  45. 45.
    Wilcox RA. Cutaneous T-cell lymphoma: 2016 update on diagnosis, risk-stratification, and management. Am J Hematol. 2016;91(1):151–65.CrossRefPubMedGoogle Scholar
  46. 46.
    Al Hothali GI. Review of the treatment of mycosis fungoides and Sézary syndrome: a stage-based approach. Int J Health Sci (Qassim). 2013;7(2):220–39.CrossRefGoogle Scholar
  47. 47.
    Leger M, Newlove T, Robinson M, Patel R, Meehan S, Ramachandran S. Pityriasis rubra pilaris. Dermatol Online J. 2012;18(12):14.PubMedGoogle Scholar
  48. 48.
    Boyd AS, Menter A. Erythrodermic psoriasis. Precipitating factors, course, and prognosis in 50 patients. J Am Acad Dermatol. 1989;21:985.CrossRefPubMedGoogle Scholar
  49. 49.
    Kubica AW, Davis MD, Weaver AL, et al. Sézary syndrome: a study of 176 patients at Mayo Clinic. J Am Acad Dermatol. 2012;67:1189.CrossRefPubMedGoogle Scholar
  50. 50.
    Kim YH, Bishop K, Varghese A, Hoppe RT. Prognostic factors in erythrodermic mycosis fungoides and the Sezary syndrome. Arch Dermatol. 1995;131:1003.CrossRefPubMedGoogle Scholar
  51. 51.
    Wang J, Wang YM, Ahn HY. Biological products for the treatment of psoriasis: therapeutic targets, pharmacodynamics and disease-drug-drug interaction implications. AAPS J. 2014;16(5):938–47.CrossRefPubMedPubMedCentralGoogle Scholar
  52. 52.
    Cather JC, Crowley JJ. Use of biologic agents in combination with other therapies for the treatment of psoriasis. Am J Clin Dermatol. 2014;15(6):467–78.CrossRefPubMedPubMedCentralGoogle Scholar
  53. 53.
    Zattra E, Belloni Fortina A, Peserico A. Alaibac M. Erythroderma in the era of biological therapies. Eur J Dermatol. 2012;22(2):167–71.PubMedGoogle Scholar
  54. 54.
    Umar, S, Kelly P. Erythroderma (Generalized Exfoliative Dermatitis) clinical presentation. Medscape. (updated June 4 2018). Retrieved 2018 from https://emedicine.medscape.com/article/1106906-overview.

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Emergency Medicine, Department of Anesthesia Critical CareNYU Langone Medical CentersNew YorkUSA

Personalised recommendations