PITYRIASIS RUBRA PILARIS : REPORT OF 16 CASES IN SAUDI ARABIA
Auther:Sahar Hassan Al-Natour, M.D
page: 09-15
ORIGINAL ARTICLEPITYRIASIS RUBRA  PILARIS :  REPORT OF 16 CASES IN SAUDI ARABIA Sahar Hassan Al-Natour, M.D.Department of Dermatology, King Faisal University, Dammam, King Fahd Hospital of the University, Al-Khobar, Saudi Arabia

Correspondence:

Sahar Hassan Al-NatourP.O. Box 2106. Dhahran 31311, Saudi Arabia. Tel : +966-3-8957786,Mobile: +966504845523 / Fax#: +966-3-8944370, Email: saharnatour@yahoo.com
-------------------------------------------------------------------------------------------------------------------------------------------------------
ABSTRACT
Background:
Pityriasis rubra pilaris (PRP) is a rare chronic papulosquamous disorder. There are a few world-wide large scale studies; and no reports of this dermatosis from Saudi Arabia.
Objective: The present study was designed to highlight the main clinical and histological features of PRP as seen in a tertiary health care institution amongst Saudi patients.
Methods:   The diagnosis of PRP was made based on clinico-pathological correlation. The therapeutic response and disease course were evaluated by follow up appointments and re-examination of patients.
Results: A total of 28 patients were reviewed, and the histopathological confirmation of the clinical diagnosis of PRP was in 16 patients.  Griffith type I PRP was found in 12.5 %, type II PRP in 18.75%, type III  in 18.75 % and type IV in 50 %.  Type V was not observed in this case study.   The cardinal clinical feature in this series was palmoplantar keratoderma which occurred in all 16 patients.  In patients with types II PRP and IV PRP, lesions other than those located on the elbows and knees and palmoplantar keratoderma were common. Treatment with systemic Vitamin A, combination of Vitamin A and E, etretinate, acitretin and 13-cis-retinoic acid showed favorable variable response initially, however relapse occurred upon discontinuation of the treatment regimens.  All the clinical types of PRP in this study showed a protracted course of more than 3 years duration.
Limitations:  This study is a retrospective study with high default rates.
Conclusion:  Type IV was the predominant type of PRP amongst Saudi patients.  The diagnosis of PRP should be considered especially when patients present with acute onset keratoderma.
Key words: Pityriasis rubra pilaris, PRP, palmoplantar keratoderma, keratotic follicular papules
--------------------------------------------------------------------------------------------------------------------------


 

Pityriasis rubra pilaris (PRP), a rare chronic papulosquamous dermatosis, was first described by Claudius Tarral 1. First embroiled in the then confused taxonomy of scaly disorders 2, the concept of PRP as a separate entity remained controversial until the Vienna Congress of Dermatology in 1892 3.Subsequent work for over 100 years  has been concerned with proposing and testing various theories on its unknown etiology, establishing clear morphological parameters, determining its distinctive histopathological picture, instituting effective therapeutic regimens and assessing its natural history and prognosis following treatment.Given the considerable heterogenicity in the clinical presentation of this disorder, Griffith suggested a clinical classification of PRP into 5 types based on age of onset, cutaneous features, disease course and prognosis 4   (Table 1).More recently, an additional type VI PRP associated with HIV infection has been proposed and is characterized by a triad of nodulocystic acne, lichen spinulosus and a PRP- like eruption 5.Given the rarity of this disease, the unresolved facets of its nature and heterogenecity of its clinical features, large scale studies are limited.   The author reports a long-term observational study of 16 patients with PRP seen at King Fahd University Hospital, a tertiary service hospital in the Eastern Province of Saudi Arabia.
METHODS
Patients
Patients with the diagnosis of PRP were recruited between 1983-2008 from the Department of Dermatology at King Fahd University Hospital, Al-Khobar, Saudi Arabia. Some patients were still undergoing treatment at the time of this study. The clinical charts and archival photographs of the department were reviewed and used to analyze the clinical features and distribution of the skin lesions, treatment regimens and response. Only those in whom the diagnosis was confirmed histologically were included in this study. Follow up of the disease course and response to treatment was conducted by regular clinical appointments. Out of 28 patients initially diagnosed as PRP, 12 were subsequently excluded based on histological grounds (psoriasis vulgaris in 8 patients, nonspecific dermatitis in 3 patients, keratosis pilaris with atopic dermatitis in 1 patient). Sixteen patients, (7 males and 9 females) ages 6 months to 53.5 years were included in this study. 
PRP diagnosis and classification:
The clinical morphology of PRP was characterized by an erythematous scaly eruption, peri-follicular papules and follicular plugging. The diagnostic histopathological features were irregular hyperkeratosis with alternating parakeratosis and acanthosis, hypergranulosis, follicular plugging and slight to moderate lymphohistiocytic infiltrate 6.The clinical diagnosis was classified according to Griffith’s classification (Table 1).
Determination of clinical course and response to treatment:
The clinical course of the disease was evaluated by calculating the area of involvement at the time of the study and thereafter in follow up appointments, response to treatment was graded as excellent (90 – 100 %   resolution),   moderate (30 – 90 % resolution) and poor (less than 30 % resolution).
RESULTS
The distinctive histological and clinical features of PRP were observed in 16 patients, (9 males and 7 females) out of the initial 28 cases with a provisional clinical diagnosis of PRP.  In 3 of 16 patients more than 1 skin biopsy was performed before the characteristic histological features of PRP were observed. The incidence of PRP at King Fahd Hospital of the University was found to be 0.05% of all new dermatology cases over a period of 25 years. Both adult and juvenile forms of the disease were observed in this study with 5 adults and 11 children.The distribution pattern of the 16 PRP cases was bimodal.  In the juvenile patients (ages of onset 0.5-10 yrs) the   mean age was 5.1 years, while in the adults, the ages of onset were 19 – 53 years (mean of 36.6 yrs) . Amongst the 11 juvenile PRP cases, type III PRP was diagnosed in 3 cases, including one boy, age 3 years and 2 girls at ages 2.2 and 3 years respectively.There were 8 cases  with type IV PRP,  3 males ages 4, 7, 10 years  and 5 females ages 0.5, 4.8, 6, 7.8 and 8 years  respectively.Of the 5 adult PRP group, 2 males were diagnosed with type I PRP; ages 35 and 53.5 years and 3 males with type II ages 19, 23 and 52 respectively.A family history of PRP was not elicited in any of the studied patients.A febrile illness preceding the eruption was found in 2 adult patients( types I and II PRP), with erythroderma, but none in the juvenile group .
Clinical features:
All sixteen cases presented with combinations of several of the classic clinical features:  follicular papules on an erythematous base, palmoplantar keratoderma with fissures, cephalic rash, scaly plaques, erythroderma and nail involvement.Table 2 summarizes the clinical features. All lesions observed were in a bilateral symmetrical distribution.  Palmoplantar keratoderma was present in all 16 cases (100%); the salmon color characteristically demonstrated in the palms and soles in 8 (50%) and erythema in 8 (50%); follicular papules on various parts of the body in 15 cases (93.7%); scaly plaques in 15 (93.7%), cephalic rash in 11 (68.7%); palmoplantar fissures in 10 (62.5%); onychopathy in 10 (62.5 %).   Mucous membrane involvement or ectropian was not observed.   Pruritus with a severity ranging between moderate to severe was present in 10 patients (62.5%). An additional symptom was pain in the fissures in 9 patients (52.25%).Alopecia was observed in 2 patients (type II PRP) and  eruptive seborrheic keratoses was present in one (6.2 %)  patient who presented with fever, erythroderma and marked edema of the face, palm, soles and legs .The classic cephalocaudal progression was observed in 5 patients (31%); one patient with type I PRP, 2 patients with type II PRP and 2 patients with type III PRP.  In the remaining cases, the disease started as a palmoplantar keratoderma which later spread to other parts of the body.Erythroderma with large well demarcated plaques was found in 5 patients (31.25 %); but islands of normal looking skin in erythrodermic areas was found in only 3 patient (18.75%).Lymphadenopathy associated with severe erythroderma was found in two (12%) patients; a 53.5 year old male with type I PRP and a 52 year old male with type II PRP.The natural history of disease was variable.  The onset was acute in 4 cases (25%) and insidious in 12 cases (75%), the duration of disease upon presentation between 2 weeks to 20 years, with an average of 3.44 years.Aggravation of PRP by sunlight was reported by 2 male patients with types I and II PRP associated with severe and generalized erythroderma involving the entire trunk and face.One patient is a 7 yr old male with type IV PRP who experienced seasonal variations with exaccerbations during the winter months.The 16 cases of PRP in this study included 4 of the 5 clinical types based on Griffith’s classification (Table 2).   PRP type V was not observed in this series.The 2 classical adult (type 1 PRP) and 3 classical juvenile (type III PRP) patients were true to type. In the patients with types II and IV PRP, lesions other than those located on elbows and knees were common in addition to the palmoplantar keratoderma.The predominant type of PRP on this study was type IV ( juvenile circumscribed ) occurring in 50 % of the cases.
Histology:The distinctive histopathological features of PRP 6 were well demonstrated in the 16 proven cases of PRP in this study. Hyperkeratosis with alternating orthokeratosis, parakeratosis, psoriasiform acanthosis with a mononuclear cellular infiltrate in the upper dermis or perifollicularly were present in all 16 cases (100%).  Follicular plugging in only 5 patients       (31.25 %) and hypergranulosis, focal or confluent was present in 3 patients (18.75 %).  Acantholysis was not seen in any of the studied patients. Spongiosis was present in 2 patients      (12%).
Response to treatment: 
The therapeutic approach with systemic therapy included 5 protocols and were prescribed based on the availability of the drug at the time of presentation, age of the patient and extent of the eruption.The systemic therapies and results are summarized in table 3.Fourteen of 16 studied patients required systemic therapy; and one patient (type II PRP) received two systemic therapies during the course of disease; etretinate for 8 weeks then Vitamin A for another 14 weeks.Irrespective of the type of PRP, there was response to various protocols of treatment as seen in table 3.  Excellent response with over 90% resolution of the eruption was achieved with 4 of the 5 treatment protocols used. The best response was achieved with etretinate with complete clearing in two patients (type I PRP and type II PRP); one patient (type III PRP) cleared on Vitamin A and one patient (type IV PRP) on acitretin.  Another (type II PRP) patient achieved excellent response with combinations of Vitamin A and E. Isotretinoin outcome was less favorable with only 40–50 % resolution achieved in 2 (type IV PRP) patients.All patients received adjuvant topical treatment, singly or in combination including topical steroids of different potencies, salicylic acid, and 10 % urea and as a maintenance therapy after a remission. Despite an initial response of variable degrees in all treated patients, relapse was the rule irrespective of the clinical type of PRP, treatment modality, duration of disease or age of the patient and occurred as early as 3 weeks after discontinuation of isotretinoin and up to 56 weeks with etretinate requiring re-treatment.
Figure 1.  Patient 1 (Type II PRP: Atypical adult).  Palmar keratoderma, scaling and follicular hyperkeratotic  plaques.

Figure 2. Patient 6 (Type III PRP: Classical juvenile) demonstrating the extensive facial erythema, seborrheiform scaling of the scalp and face and palmar keratoderma with  the typical orange hue.

Figure 3.  Patient 6 (Type III PRP:Classical juvenile) Discrete erythematous accuminate papules mainly over the abdomen and dorsa of the phalanges.
Figure 4.  Patient 1 (Type II PRP: Atypical adult) featuring the scaly circumscribed follicular hyperkeratotic plaques over the knees.
Figure 5. Diffuse hyperkeratosis, parakeratosis, acanthosis and follicular plugging with a mononuclear infiltrate in the papillary dermis.
DISCUSSION
Pityriasis rubra pilaris is a rare scaly erythematous cutaneous disease of unknown etiology. The incidence of PRP at King Fahd University Hospital, Al-Khobar was found to be 0.05% of all new dermatology cases over a period of 25 years. This figure contrasts with that of 0.03% reported by Griffith  7,  but still attests to the rarity of the disease.Interestingly, the data relative to the age of onset of PRP in this study group clearly demonstrated the bimodal distribution pattern of cases as shown in other studies 7,8.  The peak age in childhood was about 5.1 years and in adults 36.6 years.  The peak age in adult cases was earlier in this study than in earlier studies4,8,9 in which the peak was in the age group of 45- 59 years.  The limited number of adult patients in this report may account for this difference.   No significant sex preponderance was found as in most studies 9,10; our finding of 56%  males is in line with the 59% Gross et al found in their series 11. PRP has been reported in all racial groups from all continents4,9,11-14.  The apparent preponderance of cases from Europe and North America reflects the priority in studying the disease and in case reporting.Heredity is controversial.  There are sporadic reports of familial inheritance where an autosomal dominant pattern is shown, but in general there are no consistent familial occurrence nor any genetic studies suggesting a mode of inheritance 15-18.                                       A family history was not elicited in any of the 16 Saudi patients studied in this series, agreeing with Griffith’s conclusion that many of the reported cases of hereditary PRP could in fact, be either psoriasis or  atypical  icthyosis 4.A febrile illness has been reported to precede the onset of PRP in 75% of the patients followed up by Larregue et al 19.  However, in our patients such a history was elicited in only 2 patients (12.5%) patients; both of which it was associated with a serious erythroderma.The predominant clinical type of PRP in our patients was type 1V (circumscribed juvenile) occurring in 8/16 (50%) patients.  This is in line with Yang et al’s and Gelmetti et al’s findings of the predominance of type IV PRP over type III PRP in their report of 28 cases from Taiwan  and 31 cases from Argentina respectively 12,13.  The mean age of onset in our patients was 5.9 years, close to that (6.3 years) reported by Gelmetti.13.    The  mean age of  onset in our type III PRP was found to occur slightly later than the suggested 2 years 4  with a mean of 2.7 years.   Of the 9 patients with type IV PRP, 6 patients had lesions other than those localized to the elbows and knees occurring on the feet, hands, back, scalp, dorsal phalanges, trunk neck and chest.  The remaining 3 patients had lesions localized to the elbows and knees along with palmoplantar keratoderma.   In a study of 104 patients from Thailand diagnosed as PRP based solely on the clinical features without histological assessment, the disease was reported to be focal in 100 out of 104 of their patients.  Of these, 21/100 presented with palmoplantar keratoderma, 59/100 with palmoplantar keratoderma, scaly plaques on face and trunk and            20 /100 with palmoplantar keratoderma and circumscribed lesions on the elbows and knees 2.    The heterogenicity of our findings along with others 12,13  demonstrate the limitations of Griffith’s classification4 for clinical use and can explain the discrepancy in the clinical manifestations and typing of PRP cases in different studies.  Type V is rare and absent even in reports of large scale series.  However, more recently several sporadic cases have been reported 13, 14, 20-22. Type V was absent in this group of patients with PRP as well.Types I and III PRP patients were true to type but in contrast to Griffith’s expected frequency of type I PRP to be greater than 50 % of cases, this type was found to be the least occurring (2/16) 12.5%.   The small number of cases may account for this discrepancy.Our data is in line with the observations of others 12,13,20 who considered palmoplantar keratoderma as one of the primary diagnostic criteria, this feature occurring in all 16 patients in this study. Follicular papules on an erythematous base with a keratotic plug characteristically located on elbows/knees, dorsal aspect of hands and feet and other parts of the body were found in 93.7% also in line with Gelmetti et al 13, who regarded follicular papules as another diagnostic criteria.  The salmon color characteristic of  lesions of PRP was demonstrated in only 50% of cases in this series.  This could be due to the different ethnic background or darker skin color of Saudi patients obscuring the orangish tinge, further demonstrating the heterogenicity of clinical features.  Another clinical feature regarded as a diagnostic criteria 13 is the cephalic rash which was present in 11 out of 16 patients, however, the described geographic borders extending beyond the neck in a cape like formation was not demonstrated in any of our patients.Even though the clinical presentation of PRP is often distinctive enough to allow a diagnosis, a histologic confirmation is still necessary to rule out other papulosquamous disorders.  The descriptions of the histopathological features of PRP are not uniform 6,23 and the prototypical findings of PRP are not always demonstrated in biopsy specimen; the presence of atypical features sometimes seen, emphasize the importance of clinical and histopathological correlation in establishing the diagnosis. Our histological findings of all 16 patients are compatible with Soepronos 23 proposed diagnostic histologic criteria.Acantholysis, a newly added histologic feature of PRP 23, however was not found in any of our patients. Psoriasis has many clinical and histologic features in common with PRP and differentiation between the two conditions is essential. The presence of acantholysis, hypergranulosis, follicular plugging, absence of dilated capillaries and epidermal pustulation and relatively shorter duration of disease help distinguish PRP and psoriasis. The multiplicity of theories on the etiology indicates how uncertain the knowledge is on the cause of PRP.  Postulated causes are Vitamin A deficiency, infections, trauma, physical factors, automimmune disorders and rheumatic associations, and underlying malignancy 3-5, 24-29.Of interest is one patient, a 54 year old male (type II PRP) who presented with a severe erythroderma, edema of entire body, lymphadenopathy and eruptive seborrheic keratoses on the trunk preceding the icthyosiform eruption.  This patient was not a clear cut type II PRP and had overlapping features of both type I and type II PRP. An extensive workup of this patient did not find an underlying systemic or other disease associations and an underlying malignancy was ruled out.  Similar associations of erythrodermic PRP with eruptive seborrheic keratoses have been reported in the literature 30.Photoaggravation of PRP is uncommon but has been reported especially in type I PRP patients12,31.   Two patients who were erythrodermic with type I and III PRP were observed to have aggravation of their PRP by sunlight and a 7 yr old male (type IV PRP) experienced seasonal variation with exacerbations during the winter months.A standard treatment for PRP is lacking and therapy has largely been based on anecdotoal reports as large trials due to the rarity of the disease are sparse.The classic treatments that have been used include vitamins, retinoids, antimetabolites and ultraviolet phototherapy32 ; immunesuppre- ssants and newer therapies like intravenous immunoglobulin (IVIG), biologics and extracorporeal photochemotherapy have been used recently 33-36.                 All treatment regimens instituted in this series yielded initial favorable response of variable degrees as seen in table 3.   In contrast to the study by Dickens 37, in which 10 out of 15 (67%) of patients with adult onset PRP had total clearing after treatment with istotretinoin, both patients who were treated with isotretinoin in this study group achieved only partial clearing of 40-50%.Etretinate showed the best results with 2 of 3 patients clearing and one with partial response.         A longer remission was achieved with etretinate than with the other 4 protocols. Similarly, systemic retinoids have particularly yielded excellent response by several authors and have been used extensively in the treatment of PRP 21,37,14.                       The clinical course of the patients studied was more protracted than those presented by           others 4,13,14 with all types lasting more than 3 years with a high relapse rate after treatment. Yang et al presented similar results 12.   This can be due to several reasons:  the predominance of type IV PRP which has a protracted course , the high default rates of patients in Saudi Arabia, poor compliance, failure to avail to follow up for evaluation of the course or that PRP in Saudi patients does in fact present with a more protracted course than that of Western countries.  The retrospective nature of this study is an additional factor compromising the analysis of the findings.In summary, sixteen patients with adult and juvenile PRP from Saudi Arabia showed a predominance of Griffith type IV PRP with a protracted clinical course of more than 3 years.  The cardinal clinical feature was palmoplantar keratoderma. All 16 showed initial favorable response to the 5 therapeutic regimens used. Relapse was the rule after discontinuation of treatment irrespective of the type of PRP or treatment used.There are so many unknown aspects of PRP that it is essential to have long term multi-center studies on this disease, including possible genetic defects and better therapies.
REFERENCES:
  1. Tarral C. In: Traite theorique et pratique des malades de la peau. Rayer, P. 2nd ed. Bailliere, Paris 1835; 2: 158-9.
  2. Besnier E. Observations pour servir a' l' histoire clinique du pityriasis rubra pilaire. Ann Derm Syph 1889; 10: 253-287, 398-427, 485-544.
  3. Griffith WAD. Pityriasis rubra pilaris – a historical approach. I. Toxonomy and etiology. Trans St. John's Dermatol Soc 1975; 61: 58-69.
  4. Griffith WAD. Pityriasis rubra pilaris. Clin and Exp Dermatol 1980; 5: 105-12.
  5. De D, Dogra S, Narang T, Radotra BD, Kanwar AJ. Pityriasis rubra pilaris (Type 6 PRP) in a HIV-positive patient. Skin Med 2008; 7: 47-50.
  6. Griffith WAD. Pityriasis rubra pilaris. In: Harper J, Oranje A, Prose N, editors. Textbook of Pediatric Dermatology. Malden: Blackwell; 2006. pp 786-92.
  7. Griffith WAD. Pityriasis rubra pilaris: a historical approach II. Clinical features. Clin and Exp Dermatol 1976; 1: 37-50.
  8. Davidson CL, Jr, Winkleman RK, Kierland RR. Pityriasis rubra pilaris: a follow up study of 57 patients. Arch Dermatol 1969;100: 175-178..
  9. Krierland RR and Kulwin MH. Pityriasis rubra pilaris, a clinical study. Arch Dermatol 1950; 61: 925-930.
  10. El Zawahry M. Skin Diseases in Arabian Countries, Cairo: The author, 1964; II: 153-157.
  11. Gross DA, Landau JW, Newcomer VD. Pityriasis rubra pilaris. Arch Dermatol 1969; 99: 710-16.
  12. Yang CC, Shih IH, Lin WL, Yu YS, Chiu HC, et al. Juvenile pityriasis rubra pilaris: Report of 28 cases in Taiwan. J Am Acad Dermatol 2008; 59: 943-948.
  13. Gelmetti C, Schiuma AA, Cerri D, Gianotti F. Pityriasis  rubra pilaris in childhood: a long term study of 29 cases. Pediatr Dermatol 1986; 3: 446-51.
  14. Allison DS, El-Azhary RA, Calobrisi SD, Dicken CH. Pityriasis rubra pilaris in children. J Am Acad Dermatol 2002; 47: 386-9.
  15. Touraine A. L'eredite dans le pityriasis rubra pilaire. Ann Dermatol Venereol 1942; 2: 175-77.
  16. Kint A, De Bie S, Geerdas ML, T'Kint R. Pityriasis rubra pilaris, a familial condition. Arch Delg Dermatol 1972; 158: 371-376.
  17. Vanderhooft SL, Francis JS, Holbrook KA, Dale BA, Fleckman P. Familial pityriasis rubra pilaris. Arch Dermatol 1995; 131: 448-453.
  18. Sehgal VN, Jain S, Kumar S, Bhattacharya SN, Sardana K, Bajaj P. Familial Pityriasis Rubra Pilaris (Adult Classic I): A Report of Three Cases in a Single Family. Skin Med 2008; 1: 161-64.
  19. Larregue M, Champion R, Bressieux JM, Laidet B, Lorette J. Le pityriasis rubra pilaire aigu de l'enfant. Ann Dermatol Venereol 1983; 110: 221-228.
  20. Piamphongsant T, Akaraphant R. Pityriasis rubra pilaris: a new proposed classification. Clin Exp Dermatol 1994; 19: 134-8.
  21. Clayton BD, Jorizzo JL, Hitchcock MG, Fleischer AB Jr, Williford PM.  Adult pityriasis rubra pilaris: a 10 year case series. J Am Acad Dermatol 1997;36: 959-64..
  22. Jacyk WK. Pityriasis rubra pilaris in black South African. Clin Exp Dermatol 1999; 24: 160-3.
  23. Soeprono FF. Histologic criteria for the diagnosis of pityriasis rubra pilaris. J Am Acad Dermatol 1986; 8: 277-83.
  24. Erdem T, Atosoy M, Aliagaoglu C, Melikuglu M, Yildirim U. Pityriasis rubra pilaris in association with hepatitis A. Saudi Med J 2006; 27: 1421-2.
  25. Gül U, Gönül M, Kilic A, Soylu S, Kocak O, Gönen B, Bodur H, Güler S. A case of pityriasis rubra pilaris associated with sacroileitis and autoimmune thyroiditis. J Eur Acad Dermatol Venereol 2008; 889-90.
  26. Orlandini V, Cogrel O, Doutre MS, Beylot C, Beylot-Barry M. Pityriasis rubra pilaris and hypothyroidsm. Efficacy of thyroid hormone replacement therapy in skin recovery. Br J Dermatol 2007; 156:606-7.
  27. Chan H, Liu FT, Naguwa S. A review of pityriasis rubra pilaris and rheumatologic associations. Clin Dev Immunol 2004; 11: 57-60.
  28. Kurzydlo AM, Gillespie R. Paraneoplastic pityriasis rubra pilaris in association with bronchogenic carcinoma. Australas J Dermatol 2004; 45: 130-2.
  29. Sharma S, Weiss GR, Paulger B. Pityriasis  rubra pilaris as an initial presentation of hepatocellular carcinoma. Dermatology 1997; 194: 166-7.
  30. Gleeson C, Chan I, Griffith W, Bunker C. Eruptive seborrheic keratoses associated with erythrodermic pityriasis rubra pilaris. J Eur Acad Dermatol Venereol 2008; May 13. [Epub ahead of print]
  31. Evangelon G, Murdoch SR, Palmara SI, Rhodes LE. Photoaggravated pityriasis rubra pilaris. Photodermatol Photoimmunol Photomed 2005; 21: 272-4.
  32. Cohen RR, Prystowsky JH. Pityriasis rubra pilaris: a review of diagnosis and treatment. J Am Acad Dermatol 1990; 23: 1186-8.
  33. Kerr AC, Ferguson J. Type II adult-onset pityriasis rubra pilaris successfully treated with intravenous immunoglobin. Br J Dermatol 2007; 156: 1055-6.
  34. Seckin D, Tula E, Ergun T. Successful use of etanercept in type I pityriasis rubra pilaris. Br J Dermatol 2008; 158: 642-4.
  35. Liao WC, Mutasim DF. Infliximab for the treatment of adult-onset pityriasis rubra pilaris. Arch Dermatol 2005; 141: 423-5.
  36. Haenssle HA, Bertsch HP, Emmert S, Wolf C, Zult M. Extracorporeal photochemotherapy for the treatment of exanthematic pityriasis rubra pilaris. Clin Exp Dermatol 2004; 29: 244-6.
  37. Dicken CH. Isotretinoin treatment of pityriasis rubra pilaris. J Am Acad Dermatol 1987; 16: 297-301.


 

[PDF]  [ABSTRACT]  

[back]