Erythematotelangiectatic rosacea may be associated with a subclinical stage of demodicosis: a case-control study.

BACKGROUND: Facial densities of Demodex mites have been observed to be greater in patients with demodicosis and papulopustular rosacea than in healthy control patients. In patients with erythematotelangiectatic rosacea (ETR), this density has been observed to be similar to or greater than that of healthy controls. Erythema and telangiectasia, characteristics of ETR, are often observed among patients with pityriasis folliculorum, a discreet demodicosis, suggesting a possible link between these conditions. OBJECTIVES: To compare the facial Demodex densities of patients with clinical ETR and patients with healthy skin, demodicosis, rosacea with papulopustules, and other facial dermatoses. METHODS: In this retrospective study, we recorded Demodex densities measured using two consecutive standardized skin surface biopsies (SSSB1 and SSSB2) in 23 patients with ETR, 20 healthy control patients, 590 patients with demodicosis, 254 with rosacea with papulopustules and 180 with other facial dermatoses. RESULTS: Patients with ETR had higher Demodex densities (D cm-2 ) than did the healthy controls (mean ± SEM; SSSB1: 15·7 ± 6·3 vs. 1·8 ± 1·1 D cm-2 , P = 0·042; SSSB2: 38·0 ± 13·7 vs. 5·1 ± 2·1 D cm-2 , P = 0·026) and patients with other dermatoses (SSSB1: 0·4 ± 0·1 D cm-2 , P = 0·004; SSSB2: 1·3 ± 0·3 D cm-2 , P = 0·004), but lower densities than patients with demodicosis (SSSB1: 82·7 ± 4·2 D cm-2 , P = 0·008; SSSB2: 172·2 ± 7·7 D cm-2 , P = 0·001) or rosacea with papulopustules (SSSB1: 86·6 ± 7·3 D cm-2 , P = 0·027; SSSB2: 197·0 ± 12·1 D cm-2 , P = 0·002). CONCLUSIONS: ETR may be associated with nonvisible Demodex proliferation, possibly corresponding to a subclinical stage of demodicosis. Dermatologists should be aware of this potential association and look for subclinical demodicosis in patients with ETR, so that topical acaricidal treatment can be offered if Demodex density is high.

Subsets of T lymphocytes in the lesional skin of pityriasis rosea.

BACKGROUND: Pityriasis rosea is a common papulosquamous disorder. However, its etiology and pathogenesis remain unclear. OBJECTIVE: We investigate the types of inflammatory cells infiltrating the lesional skin of pityriasis rosea and demonstrate whether T-cell-mediated immunity is involved in the pathogenesis of this condition or not. METHODS: The biopsies were taken from the lesional skin of 35 cases of patients diagnosed with pityriasis rosea. The specimens were prepared in paraffin sections, then submitted to routine immunohistochemistry procedures using monoclonal antibodies directed against CD3, CD4, CD8, CD20 and CD45RO and horseradish peroxidase-labeled goat anti-human antibodies. The positive sections were determined by the ratio and staining intensity of positive inflammatory cells. RESULTS: The mean score of positive CD3, CD4, CD8, and CD45RO staining was respectively 3.74±3.88, 5.67±4.40, 2.94±3.42 and 7.68±4.33 in these pityriasis rosea patients (P<0.001). The percentage of positive staining was 54.29% (19/35), 69.7% (23/33), 40% (14/35) and 79.41% (27/34) (P<0.05). However, the staining of CD20 was negative in all samples. The mean score of CD3 staining in patients with time for remission ≤60 days (4.90±4.21) was higher than that in patients with time for remission >60 days (2.00±2.5) (P<0.05), whereas no statistical difference in the mean score of CD4, CD8 and CD45RO staining was observed. study liMitations: The sample size and the selected monoclonal antibody are limited, so the results reflect only part of the cellular immunity in the pathogenesis of pityriasis rosea. CONCLUSION: Our findings support a predominantly T-cell mediated immunity in the development of pityriasis rosea.

Subsets of T lymphocytes in the lesional skin of pityriasis rosea

Abstract: Background: Pityriasis rosea is a common papulosquamous disorder. However, its etiology and pathogenesis remain unclear. Objective: We investigate the types of inflammatory cells infiltrating the lesional skin of pityriasis rosea and demonstrate whether T-cell-mediated immunity is involved in the pathogenesis of this condition or not. Methods: The biopsies were taken from the lesional skin of 35 cases of patients diagnosed with pityriasis rosea. The specimens were prepared in paraffin sections, then submitted to routine immunohistochemistry procedures using monoclonal antibodies directed against CD3, CD4, CD8, CD20 and CD45RO and horseradish peroxidase-labeled goat anti-human antibodies. The positive sections were determined by the ratio and staining intensity of positive inflammatory cells. Results: The mean score of positive CD3, CD4, CD8, and CD45RO staining was respectively 3.74±3.88, 5.67±4.40, 2.94±3.42 and 7.68±4.33 in these pityriasis rosea patients (P<0.001). The percentage of positive staining was 54.29% (19/35), 69.7% (23/33), 40% (14/35) and 79.41% (27/34) (P<0.05). However, the staining of CD20 was negative in all samples. The mean score of CD3 staining in patients with time for remission ≤60 days (4.90±4.21) was higher than that in patients with time for remission >60 days (2.00±2.5) (P<0.05), whereas no statistical difference in the mean score of CD4, CD8 and CD45RO staining was observed. study liMitations: The sample size and the selected monoclonal antibody are limited, so the results reflect only part of the cellular immunity in the pathogenesis of pityriasis rosea. Conclusion: Our findings support a predominantly T-cell mediated immunity in the development of pityriasis rosea.

Recurrent pityriasis rosea: A case report.

Pityriasis rosea is a papulosquamous skin disorder that occurs most commonly between the ages of 10 and 35 years. Recurrent pityriasis rosea is rare. We report a patient suffering from recurrent pityriasis rosea, whose etiology may be related to either vaccine-induced stimulation of the immune system, or some rare vaccine component(influenza A [H1N1] vaccine, hepatitis B vaccine). We believe that such a case is unique and it has not been reported previously. The patient was successfully treated with a combination of oral cetirizine, a topical steroid cream, and narrowband-ultraviolet B phototherapy. The symptoms of this disorder should be recognized by dermatologists.

The role of interleukin-22 in pityriasis rosea.

BACKGROUND: Pityriasis rosea (PR) is an exanthematous disease related to reactivation of human herpes virus (HHV) types 6 and 7. The pathogenesis and cytokine profile of PR are still poorly understood.There is a large amount of evidence indicating a viral aetiology for PR. AIM: To measure the serum level of interleukin (IL)-22, a cytokine expressed by T helper (Th)17 cells in patients with PR to explore the possible association of IL-22 with the pathogenesis of the disease. METHODS: This case-control study enrolled 25 patients with PR (mean ± SD age 20 ± 12 years) and a control group of 25 apparently healthy individuals (mean age 18 ± 12.1 years). Blood samples were collected from both patients and controls to measure serum IL-22. Scoring of PR was performed using the Pityriasis Rosea Severity Score (PRSS). RESULTS: There was a statistically significant difference in IL-22 serum level between the patient and control groups. The IL-22 serum level increased with increase in disease severity (PRSS), extent and duration. CONCLUSION: Through its proinflammatory cytokines, IL-22 plays a role in the inflammatory process of PR.

Is There a Link between Human Herpesvirus Infection and Toll-like Receptors in the Pathogenesis of Pityriasis Rosea? A Case-control Study.

Human herpesvirus (HHV) 6 and 7 are involved in the pathogenesis of pityriasis rosea (PR). Our aim was to evaluate the role of the innate immune response in PR through the detection of Toll-like receptors (TLR) 2, 3, 4, 7, 8, and 9 expression in the skin of affected patients and to detect the possibility of being induced by HHV-6 and/or HHV-7 viral coexistence in these patients. Twenty-four patients with PR and 24 healthy controls were included in this case-control study. Biopsy was obtained from the PR lesion and from the healthy skin of controls for detection of HHV-6 and 7 as well as TLRs 2, 3, 4, 7, 8, and 9 gene expression using real-time polymerase chain reaction (PCR). Significantly elevated expression of all studied TLRs and significantly higher viral load of HHV-6 and 7 in PR cases were detected. A significant higher expression of TLR2 and 4 in HHV-7 positive cases and a significant positive correlation between TLR9 and HHV-7 viral load were documented. HHV6 and 7 may also be involved in the pathogenesis of PR via TLR pathways.

Persistent pityriasis rosea: an unusual form of pityriasis rosea with persistent active HHV-6 and HHV-7 infection.

Pityriasis rosea (PR) is an acute, self-limiting exanthematous disease, associated with the reactivation of the human herpesvirus 6 (HHV-6) and/or human herpesvirus 7 (HHV-7) that usually lasts 6-8 weeks. We studied, from a clinical and virological point of view, 12 patients in whom the features of PR lasted longer than 12 weeks, defining this form of the disease as persistent PR (PPR). As in typical PR, in most of the PPR patients the disease begins with a herald patch, but compared to typical PR, systemic symptoms and oral lesions are more common. Moreover, in PPR we found a persistent reactivation of HHV-6 and/or HHV-7 with higher viral loads than in typical PR, accounting for the unusual persistence of the illness, the more frequent and severer systemic symptoms and the oral lesions. In conclusion, we describe an unusual persistent form of PR, whose prevalence has probably been underestimated so far and which should be added to the other variants of PR.

Pityriasis rosea of Gibert: immunological aspects.

More than 200 years after first description and 150 years after complete definition by Gibert, pityriasis rosea (PR) is still a clinical entity with many obscure aspects. Although great interest was focused on aetiology, studies on immunological mechanisms associated with this disease were rather discontinuous. We present a review of the literature on immunological features of PR, aimed to outline a unified picture of currently available knowledge in this field and create a useful starting point for future research.

Pityriasis rosea and herpesviruses: facts and controversies.

Pityriasis rosea is an acute exanthem with many clinical and epidemiologic features of an infectious disease. To date, human herpesvirus (HHV)-6 and HHV-7 appear to be the most indicted culprits, and the evidence in favor of this hypothesis and the controversial results produced elsewhere are discussed. The complex pathophysiology of HHV-6 and HHV-7 infection, their diffusion in the population at large, the difficulties of understanding whether the infection is still latent or is clinically manifest, and well as whether pityriasis rosea depends on a reinfection or on a viral reactivation, all make the issue extremely difficult to study and understand.

Characterization of the inflammatory cell infiltrate in herald patches and fully developed eruptions of pityriasis rosea.

BACKGROUND: Pityriasis rosea (PR) is a common cutaneous papulosquamous disorder affecting young adults. Previous studies have suggested possibilities of a viral aetiology and the involvement of cell-mediated immunity, but these remain unproven to date. AIM: To elucidate the possible pathomechanisms in PR by characterizing the inflammatory cellular infiltrate in herald patches and fully developed PR eruptions. METHODS: In total, 12 biopsy specimens from 6 patients diagnosed with PR were examined. For each patient, biopsies were taken from both a herald patch and a secondary patch. Specimens were processed for histopathological examination and immunohistochemical staining with a large panel of monoclonal antibodies. RESULTS: Histopathologically, all specimens showed epidermal changes such as parakeratosis, orthokeratosis, epidermal hyperplasia and spongiosis. Less common results included epidermal exocytosis and focal parakeratosis. In all biopsies, the dermal infiltrate of lymphocytes stained positively for monoclonal antibodies specific for T cells. The ratio of the CD4+ (helper) vs. CD8+ (cytotoxic) T cells in the dermal infiltrate was increased in most specimens. Increased staining for Langerhans cells was seen within the dermis of lesional skin. There were no marked differences found in histopathology and immunohistochemistry between the herald patch and secondary lesions. Overall, there was a lack of natural killer cell and B-cell activities in PR lesions. CONCLUSIONS: Our results support a predominantly T-cell mediated immunity in the development of PR.

Phenotypical characteristics of the immune cells in allergic contact dermatitis, atopic dermatitis and pityriasis rosea.

Allergic contact dermatitis (ACD) is a cell-mediated, delayed type IV immunologic reaction. Atopic dermatitis (AD) is a chronic inflammatory skin disease that results from a complex interaction between immunologic, genetic, and environmental factors. Pityriasis rosea (PR) is a self-limited eruption of unknown etiology. Immune cell infiltrate is a constant feature in the inflammatory skin diseases. Here, we performed phenotypical characterization of the immune cells in ACD, AD and PR (ten cases each). We performed immunohistochemical stains for B cells (CD20), T cells (CD3), histiocytes (CD68) and T cells with cytotoxic activity (granzyme-B). The data were compared with findings in 20 specimens of normal skin. The results were scored as mean values of positively stained immune cells. Immunohistochemistry showed significantly high counts of immune cells in lesional skin (ACD, AD and PR) compared to the normal one (p < 0.05). In the lesional skin, the immune cells were composed predominantly of CD3(+) T lymphocytes and CD68(+) cells (histiocytes). Some of the CD3(+) cells were granzyme B(+). The counts of some immune cells (CD3(+) and CD68(+)) were high in ACD compared to AD and PR. The counts of CD20(+) and granzyme B(+) cells were high in PR compared to ACD and AD. However, these differences did not reach the level of statistical significance. The present data describe the profile of the immune cell infiltrate in AD, ACD and PR. The cell-mediated immunity seems to have critical role in the development of these lesions.

Immune-mediated pathology following hepatitis B vaccination. Two cases of polyarteritis nodosa and one case of pityriasis rosea-like drug eruption.

The association of hepatitis B virus infection and vasculitis or other immune-mediated manifestations is well documented. Reports on such manifestations in relation to hepatitis B vaccination are scarce, however. We report 2 patients who developed polyarteritis nodosa following vaccination against hepatitis B. In one patient this resulted in an ischemic and necrotic digital ulcus, necessitating surgical amputation. The other patient presented with typical cutaneous polyarteritis nodosa which responded well to corticosteroid treatment. A third patient developed a severe pityrias rosea-like eruption. He was treated with topical steroids with healing of the lesions, leaving only post-inflammatory hyperpigmentation. The literature on these associations is reviewed.

Pityriasis rosea Gibert: detection of Legionella micdadei antibodies in patients.

Some epidemiological and clinical characteristics of Pityriasis rosea Gibert has led us to hypothesize that this disease may be the clinical manifestation of an infection caused by legionellas. We have thus tested the sera of 36 patients ill with Pityriasis rosea and 19 controls for Legionella pneumophila serogroup 1-6 and Legionella micdadei antibodies. These, who had the same age and sex distribution as study patients, were receiving treatment for other diseases in the same ward. Also tested were 200 sera from the voluntary blood donors from the same region as study patients. Legionella micdadei antibodies were detected in 12 (33.3%) Pityriasis rosea cases and in one (5.2%) control. They were significantly more common in Pityriasis rosea cases than in either controls or voluntary blood donor population. The findings to date encourage continued research into the causative relationship between the Legionella micddadei infection and the onset of Pityriasis rosea Gibert.

Group A streptococcal antigen-specific T lymphocytes in guttate psoriatic lesions.

A strong association exists between guttate psoriasis and group A, beta-haemolytic streptococcal infections. To demonstrate the presence of streptococcal-specific T cells in psoriatic skin, T-cell lines (TLs) were established from biopsies of lesions from five patients with guttate psoriasis, and compared with TLs from five patients with eczema, five with lichen planus, two with pityriasis rosea and three with nickel contact dermatitis. TLs from purified protein derivative (PPD)-induced delayed hypersensitivity sites in three normal individuals were also studied. All five of the psoriatic TLs responded in a proliferation assay to heat-killed isolates of group A streptococci, compared with only one eczema, two lichen planus and one pityriasis rosea. The response of one nickel contact dermatitis and two PPD TLs to group A streptococci was markedly less than to nickel and PPD, respectively. One of the psoriatic TLs was cloned in the presence of type 5 streptococcal M protein. The nine clones obtained were all CD3+, CD4+, CD45RO+, TCR alpha, beta+, gamma, delta-. However, they were all unreactive with antibodies to TCR V beta 5, 6, 8 or 12. Eight of the nine clones reacted, to a varying extent, to one or two of three preparations of group A streptococci expressing different M proteins. The streptococcal response of four consistently reactive clones from this patient was HLA-DR-restricted and inhibited by anti-HLA-DR antibody in a dose-dependent manner. On stimulation these four clones secreted high levels of gamma-interferon and detectable levels of IL-2, IL-10 and granulocyte/macrophage colony stimulating factor (GM-CSF) depending upon the nature of the stimulus, but no IL-4 or TNF-alpha production was detected. This study has demonstrated, for the first time, that T lymphocytes specific for group A streptococcal antigens can be consistently isolated from guttate psoriatic lesions. The role of streptococcal-specific T cells in the pathogenesis of psoriasis remains to be determined.