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===Other Diagnostic Studies===
===Other Diagnostic Studies===
There are no other diagnostic studies for seborrheic dermatitis.


==Treatment==
==Treatment==

Revision as of 22:05, 22 August 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2]; Aysha Anwar, M.B.B.S[3]

Synonyms and keywords: Seborrheic eczema

Overview

Seborrheic eczema (also known as Seborrheic dermatitis AmE, seborrhea) is a skin disorder affecting the scalp, face, and trunk. Seborrheic dermatitis causes flaky, itchy, red skin and temporary hair loss. It particularly affects the sebum-gland rich areas of skin. Causes of seborrheic dermatitis include Malassezia furfur (formerly known as Pityrosporum ovale), as well as genetic, environmental, hormonal, and immune-system factors. Medical therapy for seborrheic dermatitis includes antifungal agents, corticosteroids, and lithium salts.

Historical Perspective

  • Seborrheic dermatitis was first described by Unna in 1887.
  • In 1894, a hypothesis was made by Unna and Sabouraud that causative agents responsible for seborrheic dermatitis include yeast Malassezia, bacteria, or both as they were obtained in high quantities in cultures obtained from the affected patients.
  • In 1984, Shuster studied the disease and discovered seborrheic dermatitis can be treated with oral ketoconazole which was further supported by numerous studies.[1].[2]

Classification

There is no established classification system for seborrheic dermatitis. However, it may be classified according to the anatomical location, age group, symptoms, etiology and severity.[3][4][5][6][7]

Classification by Anatomy

Seborrheic dermatitis may be classified on the basis of anatomical location into following types:[8][3][9][10]

Localised

  • Scalp: In infants its called Cradle Cap. Its the most common presentation in infants.
  • Face: It most commonly involves eyelids, eyebrows and nasolabial folds.
  • Retroauricular:
  • Body folds: It usually affects axilla, breast folds, inguinal area and genital area.
  • Upper Chest: It is mostly seen in adults. Affected areas may present with one of the following presentation.
    • Pityriasiform: It is usually in the form oval macules and patches.
    • Petaloid type: It appears as small papules with oily scales which enlarges to become patches giving it an appearance of petals of flower, hence the name.
  • Trunk: It may be seen in severe cases and most common site of involvement is lower abdomen.

Generalized: It is mostly seen in infants associated with leiner's disease and children with severe immunodeficiency.[11]

Classification by Age

  • Infantile: seen in first three months of life.
  • Adults: occurs most commonly between 30-60 years of age.

Classification by Symptomic Presentation

  • Non pruritic: This type is most commonly seen in infants.
  • Pruritic: This type is seen in older children and adults.

Classification by Etiology

Exact cause of seborrheic dermatitis is unknown. However, following causes may be related to pathogenesis of seborrheic dermatitis.

  • Idiopathic
  • Infectious
  • Autoimmune/Inflammatory

Classification by Severity

  • Mild to moderate disease: seen in immunocompetent individuals.
  • Severe disease: seen in immunocompromised individuals.

Pathophysiology

The exact pathogenesis of seborrheic dermatitis remains unclear. However, following proposed mechanisms may play a role in pathogenesis of seborrheic dermatitis.[12] [13][14][15][11]

Pathogenesis

List of hypothesis related to pathogenesis of seborrheic dermatitis are as follows:

Hypothesis related to Malassezia

  • One hypothesis states strong correlation between presence of fungal yeast named Malassezia and response to antifungals in patients with seborrheic dermatitis.[16]
  • Malassezia is a lipophilic yeast found on the skin of both healthy individuals and seborrheic dermatitis patients. It is thought that host reaction to Malassezia or its metabolites causing inflammatory reaction may have a significant role in the process.[13].
  • Another proposed mechanism for seborrheic dermatitis may indicate that lipid layer of fungus Malassezia when disrupted leads to an inflammatory response resulting in increased production of pro inflammatory cytokines such as IL-6 and IL-7 and decreased production of IL-10. [7]

Other Hypothesis

  • Sabaceous gland activity

It is stated that sebum gland activity may correlate with seborrheic dermatitis but increased sebum production does not have a role in seborrheic dermatitis.[15][20]

  • Immune response

Elevated levels of certain HLA antigens such as HLA-AW30, HLA-AW31, HLA-A32, HLA-B12 and HLA-B18 and increased levels of total serum IgA and IgG antibodies have been detected in seborrheic dermatitis patients implying an immune mediated pathological mechanism.[14][21][22]

  • Epidermal barrier dysfunction

Following abnormalities in stratum corneum may be associated with seborrheic dermatitis

  • corneocyte shape
  • corneodesmosomes
  • disrupted lipid lamellar structure [23]
  • Neurogenic and other factors

Patients with parkinsonism may have increase levels of α-melanocyte stimulating hormone (α-MSH) levels and seborrheic dermatitis in these patients respond to L-dopa treatment[22]

Genetics

There is no specific genetic cause for seborrheic dermatitis.[24].[25]

Associated conditions

Gross Pathology

Superficial flaking and redness are characteristic findings of seborrheic dermatitis.[26]

  • Seborrheic dermatitis showing erythema on face
    Seborrheic dermatitis showing erythema on face
  • Scalp showing redness and crusting
    Scalp showing redness and crusting

Microscopic Histopathology

Histopathological findings of seborrheic dermatitis can be divided into following types, [21][27]

  • Acute
  • Focal mild spongiosis with superficial crust containing neutrophils. **Edema of papillary dermis.
  • Dilatation of blood vessels in superficial vascular plexus with infiltration of lymphocytes, histiocytes.
  • Subacute
  • Chronic
  • Minimal spongiosis
  • Follicular crusting
  • Chronic Seborrheic dermatitis.
    Chronic Seborrheic dermatitis.
  • Acute dematitis showing papillary edema with neutrophil infiltration.
    Acute dematitis showing papillary edema with neutrophil infiltration.

Causes

The cause of seborrhoeic dermatitis remains unknown, although following factors may have been implicated.

Differentiating Seborrheic dermatitis from Other Diseases

Differential diagnosis of seborrheic dermatitis can be classified into two types by age group[36][37][38][17][39][40][27]

Differential diagnosis in Infants

Differential diagnosis in Adults

Epidemiology and Demographics

Epidemiology

  • Seborrheic dermatitis is one of the most common skin disorders in general population but prevalence estimate of the condition is difficult due to lack of diagnostic criteria and grading system for severity.[41]
  • Worldwide, the prevalence of seborrheic dermatitis is estimated to be 11000 cases per 100,000.[24] Prevalence rate varies among individuals based on the following factors:
  • The prevalence rate of disease increases when mild cases are also involved.
  • The prevalence of seborrheic dermatitis is higher in patients with HIV with 35000 per 100,000 in early diagnosis and 85000 per 100,000 with full blown AIDS.[42]
  • There is higher prevalence seen among those directly exposed to UV radiation[43]
  • Incidence of seborrheic dermatitis is unknown.[44][42][45]

Demographics

Following demographic factors may significantly affect the incidence and prevalence of seborrheic dermatitis:

Age

Seborrheic dermatitis commonly affects three age groups.[45][46][21]

  • First incidence peak is seen in infants around three to four months of age, which usually resolves in 12 months
  • Second incidence peak seen around puberty.
  • Third incidence peak is seen after age 50 with highest prevalence seen among age group ranging 33-44 years of age.[47]
  • Age groups showing lowest prevalence of clinical disease is seen in individuals younger than 12 years.[48]

Gender

Males are more commonly affected with seborrheic dermatitis than females.[49]

Race

There may be racial predilection for seborrheic dermatitis as only few cases are seen in African Americans. If seborrheic dermatitis is seen in this population, it leads to high suspicion of HIV in affected individuals.[50]

Risk Factors

Most common risk factors for seborrheic dermatitis are[51][17]

Immunosuppression

Neurologic and psychiatric cases

Genetic disorders

Other risk factors

Screening

There are no screening guidelines for seborrheic dermatitis.[59]

Natural History, Complications, and Prognosis

Natural History

  • The symptoms of seborrheic dermatitis usually develop in the first three months in infants. It may resolve without treatment in most cases in few months and rarely presents after 12 months.[60]
  • In adults, symptoms of seborrheic dermatitis usually develop in the second and third decade of life, and start with symptoms such as redness, scaling and crusting on affected areas. However, occurrence of seborrheic dermatitis is highly variable and it may present after 50 years of age.
  • The course of disease is highly variable among individuals even with treatment with some cases presenting with more frequent relapses than others.[45]

Complications

Common complications of seborrheic dermatitis include the following[61][45][62][63][64][11]

Prognosis

  • Prognosis of seborrheic dermatitis is excellent in infants as it is a self limited disease and usually resolves in few months after birth. However, in adults it is a recurrent condition with no permanant cure.[65][66]

Diagnosis

There is no definitive diagnostic criteria for seborrheic dermatitis. Diagnosis of seborrheic dermatitis is primarily clinical, based on history and physical examination findings.[67]

History

Obtaining complete history is important in making diagnosis of seborrheic dermatitis as it will give an insight into cause and associated risk factors for the disease. In addition to symptoms of seborrheic dermatitis, patient may present with symptoms of one of the following conditions[68][69][70][17] [71][72][73]

Symptoms

Symtoms can be divided into following categories based on age[24][74]

Infants

Infants usually present in the first few months of life. Symptoms can be divided into following types depending on extent of involvement.

  • Localised
    • Redness and flaking
    • Pruritis
    • Most common sites involved are scalp and face.
    • Other sites involved include retroauricular area, nasolabial folds, cheeks, eyebrows and eyelids.
    • Napkin or diaper area involvement is not rare in infants.
  • Generalised
    • Few cases may present with generalised involvement such as lower abdomen, groin and pubic area.

Adults

Symptoms of seborrheic dermatitis may overlap with other skin conditions such as psoriasis, candidiasis, contact dermatitis, atopic dermatitis but most common symptoms of seborrheic dermatitis are divided into two types based on extent of involvement.[24]

  • Localised
    • Macules, thin plaques, or red patches(scalp, face, nasolabial folds, anterior hairline, eyebrows, glabella region of the forehead, melolabial folds, ears, central chest, and genital region)
    • Pruritis
    • Fine scaling(mild cases)
    • Redness and yellow to white crusting or scaling( severe disease)
    • Redness, itching and yellow crusting of eye lashes (Blepharitis).
    • Repeated itching of ear causing secondary bacterial infection resulting in fever and ear pain.
  • Generalised
    • Patients with HIV or other immunosupressive conditions such as malignancies usually present with more severe disease involving unusual sites such as extremities.[75][76]

Physical Examination

Age Site involved Local Examination Image[77]
Infants General Appearance Infant looks healthy with good apatite and sleep.
Scalp Fine scaling in mild cases. Thick greasy scales with erythema in severe cases.[78]Thick greasy scales with erythema in severe cases.
Face Face may present with scaly salmon colored scales.
Neck, axilla and body Folds Non scaly moist glistening appearance of lesions which tend to appear confluent.[17]
Trunk Trunk involvement is seen in severe cases. However, diaper area gets commonly involved which presents with erythema and maceration of skin with edema of surrounding skin. Secondary bacterial and candidal infections are common in these cases.[79]
Generalised It is most commonly seen in Leiner's disease which is an immunosuppressive condition. It may involves unusual site such as extremities and trunk with scaling and erythematous red patches. Scaling and crusting usually spreads to involve other parts of the body with extensive peeling of skin.[80][81][82]
Adults General appearance Adults may present with healthy outlook in mild cases or may present in considerable distress due to widespread involvement esp in cases with underlying diseases associated with seborrheic dermatitis such as HIV, malignancy, parkinsonism.[52]
Scalp Mild desquamation to honey coloured crusting of scalp and hair causing alopecia.
Face/Retroauricular

areas

Erythema and scaling may spread to malar region in a butterfly situation. Yellowish scaling between eyelashes and eyelids causing blepharitis with honey colored crusting on free margins.[45]
Upper Chest SD presents as petalloid or pityriasiform.

Petalloid: Small reddish follicular or perifollicular papules that may coalesce forming patches resembling petals of flower. Pityriasiform: Common on skin tension lines and intertriginous areas and presents as oval scaly macules and patches. This type involves extensive involvement of the body.[75]

Body Folds Lesions usually present as moist, macerated and erythematous lesions. May lead to fissuring and secondary infection.[17]
SD in

Immuno suppression

It may presents as extensive scaling and erythema involving unusual sites such as extremities and is refractory to treatment. It is usually seen in children and adults with immunosuppression such as HIV/AIDS.[83][84]


Imaging Findings

There are no imaging findings used to diagnose seborrheic dermatitis. The diagnosis of seborrheic dermatitis is mainly clinical.[40]

Other Diagnostic Studies

There are no other diagnostic studies for seborrheic dermatitis.

Treatment

Medical Therapy

The mainstay of treatment for seborrheic dermatitis is supportive. Depending on age, it can be divided into following types:

Infantile

In infants, seborrheic dermatitis (Cradle Cap) is a self limited disease in most cases and resolves in few months. The mainstay of treatment is supportive and divided into two types depending on severity of disease.[85]

  • Mild
  • Education and reassurance of parents.
  • Use of simple skin measures such as application of emollients such as baby oil or mineral oil to loosen scales and frequent shampooing using non-medicated shampoos and removing scales frequently.
  • Severe and persistant

Adults

There is no curative treatment for seborrheic dermatitis in adults as it is a chronic recurring condition. The mainstay of treatment is supportive to control the acute flares of disease. Supportive treatment includes use of topical and oral glucocorticoids, zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos), or mild detergents.[88][89][90]

Depending on severity of disease, treatment can be divided into following types:

  • Mild
  • Treatment modality for mild cases of scalp disease is topical antifungals such as azoles, zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos. Topical use of (low, moderate and high potency) corticosteroids requiring overnight application, Baker's P&S solution, tar shampoo, or salicylic acid (ointment or shampoo, is usually reserved for thick and severe scaling.[91]
  • Other effective treatments include coconut oil compound (ointment combination of coal tar, salicylic acid and sulfur).
  • Moderate to Severe

Following are the preffered treatment regimens for treatment of seborrheic dermatitis:[102]

  • 1. Antifungal agents
  • Preferred regimen (1): Ketoconazole 2% in shampoo, foam, gel, or cream
  • Scalp: Twice/week for clearance THEN once/week or every other week for maintenance
  • Other areas: From bid to twice/week for clearance THEN from twice/week to once every other week for maintenance
  • Preferred regimen (2): Bifonazole 1% in shampoo or cream
  • Scalp: 3 times/week for clearance
  • Other areas: qd for clearance
  • Preferred regimen (3): Ciclopirox olamine (also called ciclopirox) 1.0% or 1.5% in shampoo or cream
  • Scalp: Twice to 3 times/week for clearance THEN once/week or every 2 week for maintenance
  • Other areas: Twice daily for clearance THEN qd for maintenance
  • 2. Corticosteroids
  • Scalp: Twice weekly in a short- contact fashion (up to 10 min application, then washing)
  • Preferred regimen (5): Desonide 0.05% lotion bid on scalp and other areas
  • 3. Lithium salts

Plant-based treatments

Main article: phytotherapy

The World Health Organization mentions Aloe vera gel as a yet to be scientifically proven traditional medicine treatment for Seborrhoeic dermatitis.[103]

Surgery

Surgical intervention is not recommended for the management of seborrrheic dermatitis.

Prevention

Primary prevention

  • There is no established method for prevention of seborrheic dermatitis.[45]

Secondary prevention

  • Secondary prevention strategies following seborrheic dermatitis include

Related Chapter

External Links

References

  1. ↑ Shuster S (1984). "The aetiology of dandruff and the mode of action of therapeutic agents". Br J Dermatol. 111 (2): 235–42. PMID 6235835.
  2. ↑ Low, R. Cranston, and H. W. Barber. "Discussion on the etiology of seborrhoea and seborrhoeic dermatitis." The British Medical Journal (1922): 752-757.
  3. ↑ 3.0 3.1 Dessinioti C, Katsambas A (2013). "Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies". Clin Dermatol. 31 (4): 343–51. doi:10.1016/j.clindermatol.2013.01.001. PMID 23806151.
  4. ↑ Dessinioti, Clio, and Andreas Katsambas. "Seborrheic dermatitis: Etiology, risk factors, and treatments:: Facts and controversies." Clinics in dermatology 31.4 (2013): 343-351.
  5. ↑ ===Classification by Anatomical Location===Peyri, J., and M. Lleonart. "Clinical and therapeutic profile and quality of life of patients with seborrheic dermatitis." Actas Dermo-Sifiliográficas (English Edition) 98.7 (2007): 476-482.
  6. ↑ name="pmid6220754">Burton JL, Pye RJ (1983). "Seborrhoea is not a feature of seborrhoeic dermatitis". Br Med J (Clin Res Ed). 286 (6372): 1169–70. PMC 1547390. PMID 6220754.
  7. ↑ 7.0 7.1 {{cite journal| author=Thomas DS, Ingham E, Bojar RA, Holland KT| title=In vitro modulation of human keratinocyte pro- and anti-inflammatory cytokine production by the capsule of Malassezia species. | journal=FEMS Immunol Med Microbiol | year= 2008 | volume= 54 | issue= 2 | pages= 203-14 | pmid=: 18752620 | doi=10.1111/j.1574-695X.2008.00468.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?
  8. ↑ Schwartz RA, Janusz CA, Janniger CK (2006). "Seborrheic dermatitis: an overview". Am Fam Physician. 74 (1): 125–30. PMID 16848386.
  9. ↑ Dessinioti, Clio, and Andreas Katsambas. "Seborrheic dermatitis: Etiology, risk factors, and treatments:: Facts and controversies." Clinics in dermatology 31.4 (2013): 343-351.
  10. ↑ ===Classification by Anatomical Location===Peyri, J., and M. Lleonart. "Clinical and therapeutic profile and quality of life of patients with seborrheic dermatitis." Actas Dermo-Sifiliográficas (English Edition) 98.7 (2007): 476-482.
  11. ↑ 11.0 11.1 11.2 Hampshire J, Violaris N (1988). "Oral and oropharyngeal malignancies: the case for early detection". Practitioner. 232 (1452): 766. PMID 3255962.
  12. ↑ name="pmid6220754">Burton JL, Pye RJ (1983). "Seborrhoea is not a feature of seborrhoeic dermatitis". Br Med J (Clin Res Ed). 286 (6372): 1169–70. PMC 1547390. PMID 6220754.
  13. ↑ 13.0 13.1 Tajima M (2001). "Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry". Br J Dermatol. 144 (3): 549–56. PMID 11260013.
  14. ↑ Burton JL, Pye RJ (1983). "Seborrhoea is not a feature of seborrhoeic dermatitis". Br Med J (Clin Res Ed). 286 (6372): 1169–70. PMC 1547390. PMID 6220754.
  15. ↑ 21.0 21.1 21.2 Sampaio AL, Mameri AC, Vargas TJ, Ramos-e-Silva M, Nunes AP, Carneiro SC (2011). "Seborrheic dermatitis". An Bras Dermatol. 86 (6): 1061–71, quiz 1072-4. PMID 22281892.
  16. ↑ 22.0 22.1 Burton JL, Shuster S (1970). "Effect of L-dopa on seborrhoea of parkinsonism". Lancet. 2 (7662): 19–20. PMID 4193751.
  17. ↑ Simon M, Tazi-Ahnini R, Jonca N, Caubet C, Cork MJ, Serre G (2008). "Alterations in the desquamation-related proteolytic cleavage of corneodesmosin and other corneodesmosomal proteins in psoriatic lesional epidermis". Br J Dermatol. 159 (1): 77–85. doi:10.1111/j.1365-2133.2008.08578.x. PMID 18460028.
  18. ↑ 24.0 24.1 24.2 24.3 Dill FJ, Schertzer M, Sandercock J, Tischler B, Wood S (1987). "Inverted tandem duplication generates a duplication deficiency of chromosome 8p". Clin Genet. 32 (2): 109–13. PMID 2888552.
  19. ↑ Birnbaum RY, Zvulunov A, Hallel-Halevy D, Cagnano E, Finer G, Ofir R; et al. (2006). "Seborrhea-like dermatitis with psoriasiform elements caused by a mutation in ZNF750, encoding a putative C2H2 zinc finger protein". Nat Genet. 38 (7): 749–51. doi:10.1038/ng1813. PMID 16751772.
  20. ↑ Warner, Ronald R., et al. "Dandruff has an altered stratum corneum ultrastructure that is improved with zinc pyrithione shampoo." Journal of the American Academy of Dermatology 45.6 (2001): 897-903.
  21. ↑ 27.0 27.1 Druet P, Burtin P (1967). "[On the detection in renal cancers of an antigen not found in normal human kidney]". Eur J Cancer. 3 (3): 237–8. PMID 4318061.
  22. ↑ Hay R, Graham-Brown R (1997). "Dandruff and seborrheic dermatitis: causes and management". Clin Exp Dermatol. 22 (1): 3–6. doi:10.1046/j.1365-2230.1997.d01-231.x. PMID 9330043.
  23. ↑ Nowicki R (2006). "[Modern management of dandruff]". Pol Merkur Lekarski. 20 (115): 121–4. PMID 16617752.
  24. ↑ Am Fam Physician 2000;61:2703-10,2713-4
  25. ↑ Janniger C, Schwartz R (1995). "Seborrheic dermatitis". Am Fam Physician. 52 (1): 149–55, 159–60. PMID 7604759.
  26. ↑ Parry M, Sharpe G (1998). "Seborrheic dermatitis is not caused by an altered immune response to Malassezia yeast". Br J Dermatol. 139 (2): 254–63. doi:10.1046/j.1365-2133.1998.02362.x. PMID 9767239.
  27. ↑ "MedlinePlus Medical Encyclopedia: Hypervitaminosis A". www.nlm.nih.gov. Retrieved 2008-03-19.
  28. ↑ 34.0 34.1 34.2 "Seborrheic Dermatitis: An Overview - July 1, 2006 -- American Family Physician". www.aafp.org. Retrieved 2008-03-19.
  29. ↑ "eMedicine - Nutritional Neuropathy : Article by R Andrew Sewell". www.emedicine.com. Retrieved 2008-03-19.
  30. ↑ Naldi, Luigi, and Alfredo Rebora. "Seborrheic dermatitis." New England Journal of Medicine 360.4 (2009): 387-396.
  31. ↑ Braun-Falco O, Heilgemeir GP, Lincke-Plewig H (1979). "[Histological differential diagnosis of psoriasis vulgaris and seborrheic eczema of the scalp]". Hautarzt. 30 (9): 478–83. PMID 161301.
  32. ↑ Rosina P, Zamperetti MR, Giovannini A, Girolomoni G (2007). "Videocapillaroscopy in the differential diagnosis between psoriasis and seborrheic dermatitis of the scalp". Dermatology. 214 (1): 21–4. doi:10.1159/000096908. PMID 17191043.
  33. ↑ Schwartz, Robert A., Christopher A. Janusz, and Camila K. Janniger. "Seborrheic dermatitis: an overview." Am Fam Physician 74.1 (2006): 125-130.
  34. ↑ 40.0 40.1 Clark GW, Pope SM, Jaboori KA (2015). "Diagnosis and treatment of seborrheic dermatitis". Am Fam Physician. 91 (3): 185–90. PMID 25822272.
  35. ↑ Naldi, Luigi, and Alfredo Rebora. "Seborrheic dermatitis." New England Journal of Medicine 360.4 (2009): 387-396
  36. ↑ 42.0 42.1 Gupta AK, Bluhm R (2004). "Seborrheic dermatitis". J Eur Acad Dermatol Venereol. 18 (1): 13–26, quiz 19-20. PMID 14678527.
  37. ↑ Moehrle M, Dennenmoser B, Schlagenhauff B, Thomma S, Garbe C (2000). "High prevalence of seborrhoeic dermatitis on the face and scalp in mountain guides". Dermatology. 201 (2): 146–7. doi:18458 Check |doi= value (help). PMID 11053918.
  38. ↑ Denton, C. P., et al. "Scleroderma (systemic sclerosis)." Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York, NY: McGraw-Hill Medical Publishing Division (2008): 1553-1562
  39. ↑ 45.0 45.1 45.2 45.3 45.4 45.5 45.6 Okochi T, Seike H, Saeki K, Sumikawa K, Yamamoto T, Higashino K (1987). "A novel alkaline phosphatase isozyme in human adipose tissue". Clin Chim Acta. 162 (1): 19–27. PMID 3100109.
  40. ↑ Sachdeva M, Kaur S, Nagpal M, Dewan SP (2002). "Cutaneous lesions in new born". Indian J Dermatol Venereol Leprol. 68 (6): 334–7. PMID 17656992.
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  42. ↑ Naldi, Luigi, and Alfredo Rebora. "Seborrheic dermatitis." New England Journal of Medicine 360.4 (2009): 387-396.
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