AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Gougerot and Carteud originally described confluent and reticulated papillomatosis (CRP) in 1927 under the name papillomatose pigmentée innominée and later renamed it papillomatose pigmentée confluente et réticulée. It was subsequently categorized as a new form of cutaneous papillomatosis and diagnostic criteria were established. Wise described the first case in the United States in 1937 and called it confluent and reticular papillomatosis. Its existence as a distinct entity was argued for many years because of the clinical and histologic similarities between CRP and the different forms of acanthosis nigricans, but the disease is now generally accepted as a distinct entity.

CRP is a rare disease typically affecting young persons. It is characterized by grayish blue hyperkeratotic papules, usually located on the trunk. The lesions coalesce to form confluent plaques centrally and a reticular pattern peripherally. CRP may represent an endocrine disturbance, a disorder of keratinization, an abnormal host reaction to fungi or bacteria, a hereditary disorder, or a variant of amyloidosis. The eruption is chronic with exacerbations and remissions. It is responsive to treatment but frequently recurs after discontinuation of therapy.

Pathophysiology

Both electron microscopy studies and immunohistochemical analysis of lesions of CRP support the concept of abnormal keratinocyte differentiation and maturation. These findings include an increased transition cell layer and increased lamellar granules in the stratum granulosum, along with increased involucrin, keratin 16, and Ki-67 expression. Increased melanosomes in the stratum corneum probably account for the observed pigmentary changes.

Frequency

United States

The frequency in the United States is unknown.

International

The frequency internationally is unknown.

Race

Older reviews report CRP being more common among blacks than other races, with a ratio of 2:1, but more recent surveys, including one survey of 90 cases, show a predominance in whites.

Sex

The proportion of women to men affected has been reported to be as high as 2.8:1, but the ratio is probably closer to 1.4:1. The opposite is true in Japan, where CRP is more common in men than in women.

Age

The onset of CRP usually occurs shortly after puberty. The mean patient age at onset varies from 18.5-21 years, with a range of 5-63 years. Similarly, the average patient age at onset is 17.1 years in Japan, with a range of 3-30 years.

CLINICAL

Section 3 of 11  

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History

Patients with CRP are often asymptomatic, but they may experience mild pruritus. In a study of cases in Japan, 57.1% were asymptomatic, while the rest experienced pruritus.

Physical

Physical findings are limited to the skin.

• Primary lesion
• • Lesions begin as slightly hyperkeratotic to warty papules that are 1-2 mm in diameter. They enlarge to 4-5 mm in diameter and coalesce to form a reticular pattern peripherally and confluent plaques centrally.
  • Skin markings are preserved and sometimes exaggerated, especially in the neck and the axillae, where the skin may be thickened.
  • Atrophic macules rarely may be seen.
  • Scraping of lesions produces a fine powdery scale or mealy deposit.
• Distribution
• • CRP usually begins on the skin of the intermammary or epigastric region, spreading over a period of weeks or months to the breasts, the lower abdomen, the flanks, and the pubic area.
  • In one case, lesions were entirely confined to the cheeks; in another case, lesions were entirely confined to the pubic area.
  • The eruption may be found in the interscapular region, from which it spreads to the shoulders, the nape of the neck, and the gluteal cleft.
  • Involvement of the face and the proximal extremities may be seen.
  • The mucous membranes are spared.
• Color: Early lesions are erythematous and later become grayish brown.

Causes

Theories as to the etiology of CRP include an endocrine disturbance, a disorder of keratinization, and an abnormal host reaction to Pityrosporum organisms or bacteria. Reports also exist of familial cases of CRP and the possibility of CRP representing a variant of amyloidosis.

• Endocrine disturbance
• • Gougerot himself suggested the possibility of an endocrine disturbance having a role in CRP. Others have also advanced this theory in light of the common observation of endocrine disturbances in patients with CRP (eg, Cushing disease, menstrual irregularities, obesity, abnormal glucose tolerance or diabetes mellitus, thyroid disease, pituitary dysfunction, hirsutism or hypertrichosis).
  • In Japan, 76.5% of cases of CRP are associated with obesity or rapid weight gain.
  • In addition, lesions of CRP have been noted to remit during pregnancy or with weight loss.
  • No single endocrine abnormality is seen; however, in many of the cases, no abnormality exists at all.
• Disorder of keratinization
• • Miescher first proposed that CRP is due to a defect in keratinization. This idea is supported by electron microscopic studies, which demonstrate increased lamellar granules in the stratum granulosum, a finding seen in conditions of increased cell turnover and desquamation (eg, psoriasis), and an increased transition cell layer, which represents the zone where granular cells are converted into cornified cells.
  • The above findings are consistent with immunohistochemical studies of lesions of CRP, which demonstrate increased expression of involucrin, keratin 16, and Ki-67—protein markers for keratinocyte differentiation and maturation.
  • Further evidence for the role of a defect of keratinization is the response of CRP to topical and oral retinoids, which are useful in treating such defects. Most recently, CRP has been shown to respond to topical analogues of vitamin D, agents that also regulate cell differentiation and inhibit keratinocyte proliferation.
  • Ultraviolet light exposure and avitaminosis have been associated with the development of CRP, and they may trigger or exacerbate the underlying abnormality.
  • Another interesting association is that of 2 patients with both CRP and atopy, a condition where other disorders of keratinization are found.
• Fungal infection
• • Another theory holds that CRP represents an abnormal host reaction to Pityrosporum orbiculare, either in the yeast or the hyphal form. This theory is based on the observation that CRP is sometimes colonized with Pityrosporum organisms, and clearance occurs with antifungals and the associated eradication of Pityrosporum organisms.
  • Many cases of CRP do not have any evidence of Pityrosporum infection, and they fail to respond to antifungal therapy.
    • In one study, 20 of 31 cases of CRP had negative potassium hydroxide examinations, and 14 of 19 patients treated with topical imidazoles failed to respond, with no correlation between potassium hydroxide (KOH) examinations and response to therapy.
    • In another study, P obiculare was isolated in only 15 of 54 cases, and only 8 of 26 cases improved with antimycotic therapy.
    • Similarly, in Japan, fungus could be detected in only 6 of 44 cases.
  • A genetic or diet-induced abnormal keratinizing response is suggested to be triggered by P orbiculare.
• Bacterial infection
• • The use of antibiotics in the treatment of CRP was introduced after the fortuitous discovery of improvement in a patient who was taking furacycline for arthritis. Since then, an increase has occurred in the number of reports of successful treatment of CRP with antibiotics of the tetracycline, macrolide, cephalosporin and (most recently) steroid classes. This finding has lead to the concept that bacteria, perhaps within the hair follicle, are the etiologic agents.
  • An exciting development in our understanding of the cause of CRP is the report of a newly described dietzia strain of Actinomyces, isolated from a patient with CRP. Antibiotic minimal inhibitory concentrations suggested sensitivity to tetracycline and erythromycin, and the patient responded to treatment with these medications. The authors of this study propose that CRP is probably a reaction pattern to bacterial infection in susceptible individuals, resulting in epidermal proliferation, and have named this A dietzia strain X.
  • Another explanation for the effectiveness of antibiotics may be the anti-inflammatory and antiproliferative actions of these agents; however, some authors argue that CRP is not an inflammatory disorder.
• Heredity: Six familial reports of CRP have raised the possibility of it being a heritable disorder. These cases include 2 sisters and a brother; 2 sisters and 1 of their daughters; a mother, a daughter, and a son; and 3 sets of brothers, including 1 observed by the authors of this article. This small number of reports does not suggest any particular pattern or mode of inheritance.
• Variant of amyloidosis: The report of amyloid in skin lesions of only 3 patients makes this theory unlikely.

DIFFERENTIALS

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Other Problems to be Considered

Benign or juvenile acanthosis nigricans
Dyschromatosis universalis
Epidermal nevus
Pseudoacanthosis nigricans
Verrucae plana

WORKUP

Section 5 of 11  

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Lab Studies

• KOH examination of skin scrapings: P orbiculare or Pityrosporum ovale spores and rarely hyphae may be found.
• Fungal culture: P orbiculare or P ovale may be cultured in some cases. The laboratory needs to be informed to make specific modifications to the media to grow this yeast.

Other Tests

• Wood lamp examination: Yellow fluorescence occurs when Pityrosporum organisms are present.

Histologic Findings

In CRP, the epidermis shows compact hyperkeratosis, often associated with the presence of Pityrosporum yeast. Other features are less consistent and include a decreased or absent granular cell layer, papillomatosis, and a stratum spinosum that varies from acanthotic to atrophic. Because papillomatosis is an inconsistent feature, one paper has proposed changing the name of CRP to confluent and reticulated papulosquamous eruption. This name is also less than perfect because most patients have little-to-no scale associated with the lesions. The dermis may contain a perivascular lymphocytic infiltrate.

On electron microscopy, some lesions demonstrate an alteration in the arrangement and the structure of cornified cells, an increased transitional cell layer, an increase in the number of lamellar bodies in the stratum granulosum, and an increased number of melanosomes in the stratum corneum.

Immunohistochemical analysis shows suprabasal keratin 16 expression with intense focal staining in the stratum granulosum and an increased number of epidermal cells with Ki-67 binding in the basal layer and stratum malpighii.

TREATMENT

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Medical Care

CRP is strictly a disorder of the skin that results in cosmetic disfigurement, with no adverse systemic effects; therefore, no treatment is necessary other than for eradication of the rash (see Medication).

• Many different modalities have been used in the treatment of CRP with variable results. The most consistent results may be seen with minocycline. Other modalities include keratolytics; intramuscular, oral, and topical forms of vitamin A; sodium thiosulphate; ammoniated mercury; oral contraceptives; oral and topical retinoids; thyroid extract; ultraviolet light; propylene glycol; antibiotics; antimycotics; and calcipotriene.
• The most consistently effective treatment and the only one evaluated by retrospective and prospective studies has been oral antibiotics.
• Another therapeutic option may be tazarotene gel (Bowman, 2003). The treatment was well-tolerated and may be an alternative to systemic retinoid therapy.

Surgical Care

Surgical treatment of CRP has been unsuccessful.

Diet

The lesions of CRP may regress with weight reduction.

MEDICATION

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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Antimycotic agents

These agents are directed against Pityrosporum infection. Selenium also has keratolytic properties.

Drug Category: Retinoids

These agents correct disorders of keratinization.

Drug Category: Antibiotics

These agents are antibacterials, and they may have anti-inflammatory or antiproliferative effects.

Drug Category: Antipsoriatic agents

These agents correct disorders of keratinization.

FOLLOW-UP

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Prognosis

• CRP is a chronic disease characterized by exacerbations and remissions. Discontinuation of successful therapy usually results in recurrence.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Failure to distinguish acanthosis nigricans from CRP may result in failure to diagnosis a malignancy. (Some forms of acanthosis nigricans represent a paraneoplastic syndrome.)

MULTIMEDIA

Section 10 of 11  

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Media file 1:  Grayish brown hyperkeratotic papules and plaques in a confluent pattern on the intermammary region with a reticular pattern peripherally.
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Media file 2:  Close-up view of the interscapular area, again demonstrating a confluent pattern centrally and a more reticular pattern peripherally.
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Media type:  Photo

Media file 3:  A biopsy specimen showing hyperkeratosis, papillomatosis, and a mild superficial perivascular inflammation (hematoxylin and eosin, original magnification X125).
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Media type:  Photo

REFERENCES

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Article Last Updated: Mar 21, 2006