Confluent and Reticulated Papillomatosis Clinical Presentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 18, 2012
 

History

Patients with confluent and reticulated papillomatosis 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. Patients observe reticulated and pigmented macules, patches, and plaques most commonly on the chest.[7]

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Physical

Physical findings of confluent and reticulated papillomatosis are limited to the skin, as shown in the images below.

Grayish brown hyperkeratotic papules and plaques iGrayish brown hyperkeratotic papules and plaques in a confluent pattern on the intermammary region with a reticular pattern peripherally. Close-up view of the interscapular area, again demClose-up view of the interscapular area, again demonstrating a confluent pattern centrally and a more reticular pattern peripherally.

Primary lesion in confluent and reticulated papillomatosis

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 of lesions in confluent and reticulated papillomatosis

This autosomal dominant trait is characterized by many asymptomatic oval macules symmetrically distributed on axillae, groin, face, neck, arms, and trunk; scattered comedolike papules (dark dot follicles); and pitted acneiform scars.[8]

Confluent and reticulated papillomatosis 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[9] ; in another case, lesions were entirely confined to the pubic area.[10]

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.[11] It may also occur on the forehead.[12]

The mucous membranes are spared.

Color of confluent and reticulated papillomatosis lesions

Early lesions are erythematous and later become grayish brown.

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Causes

Theories as to the etiology of confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis[13, 14, 15, 16] and the possibility of confluent and reticulated papillomatosis representing a variant of amyloidosis.[17]

Endocrine disturbance in confluent and reticulated papillomatosis

Gougerot himself suggested the possibility of an endocrine disturbance having a role in confluent and reticulated papillomatosis. Others have also advanced this theory in light of the common observation of endocrine disturbances in patients with confluent and reticulated papillomatosis (eg, Cushing disease, menstrual irregularities, obesity, abnormal glucose tolerance or diabetes mellitus, thyroid disease, pituitary dysfunction, hirsutism or hypertrichosis). It has been described in at least one patient with hyperthyroidism.[18]

In Japan, 76.5% of cases of confluent and reticulated papillomatosis are associated with obesity or rapid weight gain.

In addition, lesions of confluent and reticulated papillomatosis 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 in confluent and reticulated papillomatosis

Miescher first proposed that confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis, 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 confluent and reticulated papillomatosis to topical and oral retinoids, which are useful in treating such defects. Most recently, confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis, and they may trigger or exacerbate the underlying abnormality.[19]

Another interesting association is that of 2 patients with both confluent and reticulated papillomatosis and atopy, a condition where other disorders of keratinization are found.[20]

Fungal infection in confluent and reticulated papillomatosis

Another theory holds that confluent and reticulated papillomatosis represents an abnormal host reaction to Pityrosporum orbiculare, either in the yeast or the hyphal form. This theory is based on the observation that confluent and reticulated papillomatosis is sometimes colonized with Pityrosporum organisms, and clearance occurs with antifungals and the associated eradication of Pityrosporum organisms.

Many cases of confluent and reticulated papillomatosis do not have any evidence of Pityrosporum infection, and fail to respond to antifungal therapy.

In one study, 20 of 31 cases of confluent and reticulated papillomatosis 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. However, yeastlike spores were evident in 6 of 10 Lebanese cases, supporting a role for Malassezia furfur in the pathogenesis of confluent and reticulated papillomatosis.[7]

A genetic or diet-induced abnormal keratinizing response is suggested to be triggered by P orbiculare.

Bacterial infection in confluent and reticulated papillomatosis

The use of antibiotics in the treatment of confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis is the report of a newly described dietzia strain of Actinomyces, isolated from a patient with confluent and reticulated papillomatosis.[21] 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 confluent and reticulated papillomatosis 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 confluent and reticulated papillomatosis is not an inflammatory disorder.

Heredity in confluent and reticulated papillomatosis: Six familial reports of confluent and reticulated papillomatosis 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.

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Ponciano D Cruz Jr, MD  Vice-Chair, JB Shelmire Professor, Department of Dermatology, University of Texas Southwestern Medical Center

Ponciano D Cruz Jr, MD is a member of the following medical societies: Texas Medical Association

Disclosure: RCTS Consulting fee Independent contractor; Mary Kay Cosmetics Honoraria Consulting; Galderma Grant/research funds Principal Investigator

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD  Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Glen H Crawford, MD  Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Kenneth A. Becker, MD, to the development and writing of this article.

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Grayish brown hyperkeratotic papules and plaques in a confluent pattern on the intermammary region with a reticular pattern peripherally.
Close-up view of the interscapular area, again demonstrating a confluent pattern centrally and a more reticular pattern peripherally.
A biopsy specimen showing hyperkeratosis, papillomatosis, and a mild superficial perivascular inflammation (hematoxylin and eosin, original magnification X125).
 
 
 
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