Confluent and reticulated papillomatosis (CARP) was first described >60 years ago. It is distinct from acanthosis nigricans. This article presents the results of a review of the literature in MEDLINE through May 2006 using the terms 'confluent and reticulated papillomatosis', 'reticulated and confluent papillomatosis of Gougerot and Carteaud', and 'reticulated papillomatosis'.
A recent report has linked the presence of Dietzia spp. (family: Dietziaceae; suborder: Corynebacterineae; order: Actinomycetales) in the skin to CARP. CARP has also been linked to defects in keratinization. Other possible causes of CARP that have been suggested but seem less likely include endocrine abnormalities, Pityrosporum, a reaction to UV light, and a variation of cutaneous amyloidosis. CARP has been reported worldwide and occurs in both sexes, all age groups, and all races. The disorder can initially manifest as hyperkeratotic or verrucous papules that coalesce to form a reticular pattern peripherally and confluent plaques centrally.
Although a variety of treatments for CARP exist, oral minocycline 50-100mg twice daily has been the preferred treatment. However, recent reports of the effectiveness of azithromycin 250-500mg three times weekly may make azithromycin the preferred treatment for CARP, since it has a more benign adverse effect profile than minocycline. Other effective antibacterial treatments include fusidic acid 1000mg daily, clarithromycin 500mg daily, erythromycin 1000mg daily, tetracycline 500mg twice daily, and cefdinir 300mg twice daily. If a recent finding that CARP is caused by a bacterial microorganism is replicated, treatment should likely be determined by bacterial sensitivities, antibacterial adverse effect profiles, and cost considerations. Other oral treatments of CARP that are effective but currently disfavored because of the effectiveness of minocycline include isotretinoin, acitretin, and etretinate. There have been mixed reports regarding the effectiveness of topical treatments, which include selenium sulfide, ketoconazole cream, tretinoin, tazarotene, tacalcitol, and calcipotriene (calcipotriol).
Contents 1. Etiology 2. Epidemiology 3. Clinical Presentation 4. Differential Diagnosis 5. Histology 6. Treatment 7. Discussion 8. Conclusion
In 1927, Gougerot and Carteaud[l] described the clinical features of confluent and reticulated papillomatosis (CARP). They initially named the condition 'papillomatose pigmentee innominee' but later renamed it 'papillomatose pigmentee confluente et reticulee.' Wise and Sachs  described the first case in the US in 1937 and called it 'confluent and reticular papillomatosis.  CARP has also been referred to as 'reticulated and confluent papillomatosis of Gougerot and Carteaud.' A debate continued for decades as to whether CARP and acanthosis nigricans were the same entity; however, it has now been confirmed that they are distinct. [41 CARP has been reported continually worldwide over the last 60 years. [5-16]
To prepare this article, a review of the literature in MEDLINE through May 2006 was performed using the terms 'confluent and reticulated papillomatosis', 'reticulated and confluent papillomatosis of Gougerot and Carteaud', and 'reticulated papillomatosis'. This search revealed that almost 100 articles have touched on CARP. 
Several causes for CARP have been suggested,  including: (i) a keratinization disorder; (ii) a reaction to Pityrosporum; (iii) an eruption related to an endocrinopathy; (iv) a reaction to bacterial infection; (v) a reaction to UV light; (vi) a process involving amyloidosis; and (vii) a genetic factor. The data supporting these hypotheses are discussed in this section. 
Among the possible causes, the strongest evidence exists for CARP being a disease of keratinization. CARP's histologic features of an increased transition cell layer, increased lamellar granules in the stratum granulosum, and increased involucrin expression support the theory that the disorder results from abnormal keratinocyte differentiation and maturation. Increased numbers of melanosomes in the stratum corneum probably account for the observed pigmentary changes. CARP also responds to treatment with retinoids and vitamin D derivatives, which are treatments for diseases of keratinization. Finally, no bacteria, even in the role of colonizers, are identified when viewing histology specimens diagnosed as CARP. However, this theory does not explain why CARP also resolves with antibacterial treatment, which does not directly affect keratinization.
Many reports have linked CARP with Pityrosporum. [18-21] Some commentators have found yeast forms when scrapings from CARP plaques are analyzed by potassium hydroxide preparations. Topical antifungals are also sometimes effective in treating CARP. However, some of these cases might be the result of tinea versicolor being confused with CARP. Thus, it seems increasingly likely that CARP and infection with Pityrosporum (tinea versicolor) are distinct entities.
CARP has commonly occurred in patients with endocrine abnormalities, such as diabetes mellitus and thyroid disease  Hirokawa et al.  described a 19-year-old Japanese man with CARP and acanthosis nigricans on his axillae and neck. The patient was obese and dark-complexioned and had impaired glucose tolerance and hyperinsulinemia. The clinical and histological findings were consistent with the diagnosis of CARP. Neither spores nor hyphae were detected from scales. Antifungal treatment had no benefit, and weight loss did not change the patient's appearance. The CARP cleared with retinoid therapy, but the acanthosis nigricans did not. It is unclear whether immunosuppression resulting from an endocrine abnormality or the endocrine abnormality itself might be responsible for the apparent increased incidence of CARP in patients with endocrine abnormalities.
Some have suggested that CARP is related to bacterial infection of the follicle  This suggestion is supported by the responsiveness of CARP to a variety of antibacterials.  Furthermore, a recent report has suggested that CARP is, in fact, caused by a bacterium. Natarajan et al.  inoculated skin scrapings on to blood agar, Sabouraud agar, chocolate agar, and Robertson's cooked meat. After 72 hours of incubation at 37[degrees]C in 5% C[O.sub.2], there was moderate growth of small orange colonies of a Gram-positive organism (catalase-positive, oxidase-negative) that macroscopically resembled members of the genus Rhodococcus. Moderate growth of commensal skin flora such as coagulase-negative staphylococci was also observed. On biochemical identification by means of the API[R] Coryne test system (bioMerieux SA, Marcy l'Etoile, France), a dubious profile closest to Rhodococcus sp. resulted. However, by means of 16S rRNA gene sequencing following an established procedure, the organism was provisionally identified as a new Dietzia species. Natarajan et al J141 have placed a specimen of Dietzia in the GenBank database of bacteria under accession number AY643401. Antibacterial minimal inhibitory concentrations (MICs) to eradicate Dietzia were determined by Etest[R] (AB Biodisk, Solna, Sweden). These MICs were 0.75 mg/L for erythromycin and 0.125 mg/L for tetracycline. 
Natarajan et al.  noted that Dietzia spp. (family: Dietziaceae; suborder: Corynebacterineae; order: Actinomycetales) have been isolated mainly from the environment. As of 2006, only D. maris has been associated with catheter-related bacteremia in an immunocompromised patient and with an infection of a prosthetic hip joint. Natarajan et al.  suggested that Dietzia might previously have been missed by investigators and evaluators of CARP because skin scrapings of CARP patients were not routinely cultured for bacteria. Even if the skin scrapings were cultured, it seems likely that Dietzia might have been missed because of slow growth on routine bacterial culture media or because of misidentification as Rhodococcus spp. The biochemical profile of Dietzia using the API[c] Coryne test system, which evaluates bacteria using biochemical reaction evaluation and other differential tests, was also consistent with assignment of Dietzia to the genus Rhodococcus, albeit at a low discrimination level. While the newly isolated Dietzia strain X may also be an unidentified commensal or a contaminant, the proposal of Natarajan et al.  that Dietzia is an etiological agent of CARP was supported by the patient's response to minocycline and the susceptibility of Dietzia to minocycline. Nevertheless, Natarajan et al.  suggestion has not yet been supported by other reports, and when their patient discontinued therapy and his CARP recurred, Dietzia could not be re-isolated from his skin. Thus, the exact role of bacterial infection or colonization in CARP requires more reports to firmly establish the role of bacteria in the etiology of this disorder.
One case report has linked CARP to UV light exposure  in this report, a 16-year-old girl initially had an eruption consisting of dark gray, flat, pin-sized, confluent papules with a slight hyperkeratosis; these appeared after her summer holidays and were restricted to the tanned skin of sun-exposed areas, mainly the abdomen and back. As this is an isolated case report, it is not likely that light exposure is a major cause of CARP.
Groh and Schnyder  detected amyloid in the skin lesions of three patients with CARP, but this should be grouped under the nosologic entity of biphasic primary localized amyloidosis. No other such report exists, and it seems therefore that amyloid is not involved in the etiology of CARP. Confusion might exist when the rippled pattern of lichen or macular amyloid is confused with the reticulated pattern of CARP.
It is possible that there is a genetic component to some cases of CARP. Several reports have noted familial cohorts with CARP J281 Stein et al.  described three teenage siblings with CARP, all presenting during a 6-month period. Two of the three patients had confirmed tinea versicolor with positive potassium hydroxide scrapings in association with this entity. The import of this article is unclear because it might just represent tinea versicolor; however, this is the largest series of siblings with CARP and the only report describing family members having both CARP and tinea versicolor. CARP has also been described in two brothers.  One report has linked CARP and atopy,  a condition with a genetic basis.
CARP has been reported worldwide and in all racial groups.  Worldwide, it also occurs in all age groups, but occurs most commonly shortly after puberty. The mean patient age at onset varies from 18.5 to 21 years, with a range of 5-63 years.  Similarly, in Japan, the average patient age at onset is 17.1 years, with a range of 3-30 years  In the US, the female : male ratio of affected patients has been reported to be as high as 2.8 : 1, but is probably closer to 1.4 : 1.  The opposite is true in Japan, where CARP is more common in men than in women.  Older reviews (consonant with the author's personal experience) have reported that CARP is more prevalent in darker-skinned persons than in lighter-skinned persons, with a ratio of 2: 1. However, more recent surveys, including one survey of 90 cases of CARP, showed a predominance in Whites. [15,17] A more recent study of 39 patients, published in 2006 by Davis et a1.,  noted that the mean age at the onset of the skin eruption was 15 years (range 8-32); 21 patients (54%) were male, most were White, most (33) presented for cosmetic reasons, and eight noted that their eruption was somewhat pruritic. When examined by the diagnosing dermatologist, CARP had manifested for a mean of 3.1 years (range 3 months to 20 years) and had been recalcitrant to therapy, including antifungal treatment. 
3. Clinical Presentation
CARP can have a variety of clinical presentations but is rarely accompanied by symptoms.  It can manifest initially as hyperkeratotic or verrucous papules that are 1-2mm in diameter. These papules can increase in size to 4-5mm in diameter and coalesce to form a reticular pattern peripherally and confluent plaques centrally (figure 1). Early papules are sometimes erythematous and later become dull brown. Skin markings are preserved and sometimes exaggerated, especially on the breasts (figure 2), the neck (figure 3), and the axillae (figure 4), where the skin possesses a velvety quality like acanthosis nigricans. CARP can also manifest as atrophic macules with a shiny quality (figure 4) or with surface change resembling cigarette paper. There can be a marked xerosis.  CARP has been described with coincidental vascular mottling.  Sometimes CARP is described as being mildly pruritic, but, as noted earlier in this paragraph, it often manifests with no symptoms or discomfort. CARP most commonly occurs on the torso. [35,36] CARP often manifests initially on inframammary or epigastric skin (figure 2) and then extends to the back (figure 5) and the chest, upper abdomen, and lower abdomen (figure 6). Sometimes CARP can manifest as rippled reticulated erythema in Caucasians (figure 7 and figure 8). CARP can also begin in the infrascapular region, from which it can spread to the shoulders, the nape of the neck, and the gluteal cleft. In other cases, the eruption initially consists of confluent, flat, brown papules localized primarily to the intermammary and interscapular regions with subsequent spread to the breast and abdomen; at the periphery, the papules spread out, forming a pigmented reticulated pattern. Rare locations of CARP include the cheeks  and the pubic area.  In a 15-year-old girl diagnosed with CARP, patches of the disease first appeared on her knees and elbows when she was 4 years old and on the interscapular area when she was 13. Similar lesions arose on her left hand a few weeks prior to consultation  CARP does not occur on the oral mucosa.
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4. Differential Diagnosis
The differential diagnosis for CARP is wide  and includes acanthosis nigricans, prurigo pigmentosa, erythema dyschromicum perstans, pigmented contact dermatitis, lichen pigmentosus, amyloidosis, dermatopathia pigmentosa reticularis, dyskeratosis congenita, epidermal nevus syndrome or isolated epidermodysplasia verruciformis, erythrokeratodermia variabilis, flat warts, mycosis fungoides, keratosis follicularis (Darier disease), Naegeli-Franceschetti-Jadassohn syndrome, pityriasis rubra pilaris, pseudoatrophoderma colli,  large or widespread seborrheic keratosis, axillary granular parakeratosis, syringomas,  tinea versicolor, axillary granular parakeratosis, and dyschromatosis hereditaria universalis. Other reticulated conditions to be considered in the differential diagnosis include X-linked reticulate pigmentary disorder, Dowling-Degos disease, reticulate acropigmentation of Kitamura, and Revescz syndrome.  Unlike tinea versicolor, from which fine scale can be elicited when the lesion is rubbed with the fingertips, there is no production of scale when plaque or patches of CARP are rubbed.
CARP can be distinguished from the aforementioned conditions by: (i) lack of associated findings; (ii) negative tests for fungus; (iii) reticulated rather than distinctly keratotic or scaly surface change; (iv) biopsy findings of papillomatosis with minimal and never florid inflammatory cell infiltrate; (v) uncertain relationship to genetic factors; (vi) occasional surface change resembling cigarette paper in sun-exposed locations; and, perhaps most definitely, by (vii) response to therapy with minocycline or azithromycin. It can sometimes be difficult to distinguish CARP from the conditions it resembles clinically (in particular, acanthosis nigricans) but, unlike any of the conditions that it resembles, CARP responds to therapy with minocycline or azithromycin in almost every case.
Suggested diagnostic criteria for CARP are similar to, and expand on, those suggested by Davis et al., [151 which include: (i) clinical findings including scaling brown macules and patches, at least some of which appear reticulated and papillomatous; (ii) involvement of the upper trunk and neck; (iii) fungal staining of scales is negative for fungus; (iv) lack of response to antifungal treatment; and (v) excellent response to minocycline.
The histology of CARP demonstrates epidermal undulation with hyperkeratosis, squat papillomatosis, and minimal and occasional acanthotic downward projections from the bases of the dells between the papillomatous areas (figure 9).  There can be a mild or moderate increase in deposition of pigmentation (melanin) and malpighian layer atrophy in focal locations. While these changes resemble those of acanthosis nigricans, they tend to be less pronounced and less florid. In some cases, CARP can be distinguished from acanthosis nigricans because it is sometimes marked by a mild to moderate increase in the lumen size of superficial dermal blood vessels, and it occasionally demonstrates beading of elastic fibers.
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It is important to reiterate, as stated above, that in CARP the epidermis shows undulating compact hyperkeratosis, low papillomatosis, and some acanthotic downgrowths from the base of the 'valley' between papillomatous areas.  Pityrosporum are sometimes present. Other features are less consistent and include a decreased or absent granular cell layer, irregular papillomatosis, and a stratum spinosum that varies from acanthotic to atrophic.  The dermis may contain a perivascular lymphocytic infiltrate, mild dilation of superficial dermal blood vessels, beading of elastic fibers, and hypermelanosis of the basal layer. CARP without papillomatosis has been reported. [44,45] Bacteria are not identified in histological sections of CARP. 
Electron microscopic studies suggest that CARP may involve a defect of keratinization. Lee et al.  found transitional cells between the stratum granulosum and stratum corneum that were increased in CARP. Jimbow et al.  noted that under electron microscopy, the skin eruption of CARP consisted of the following abnormal findings: (i) a marked alteration of cornified cell structures showing snake coil-like or triangle-like stacks; (ii) a marked increase in the number of lamellar granules in the granular layer; (iii) an increased number of melanosomes in the horny layers; and (iv) no significant fine structural changes of epidermal melanocytes.  Involucrin expression is increased in plaques of CARP, providing support for the argument that CARP is a disease of keratinization. 
In 1965, Carteaud  described the successful treatment of CARP with minocycline, the first such report. Since then, many reports have noted that minocycline is an effective treatment for CARP. [50-54] CARP that has not responded to topical treatment with isotretinoin and erythromycin has been successfully treated with minocycline.  In one study, 11 patients with CARP were treated with oral minocycline 50mg twice daily for 6 weeks.  The average follow-up period was 11 months. Nine patients had a 90-100% response to minocycline therapy. Recurrences were noted in three patients, all of whom responded to re-treatment with minocycline. None of the nine patients had an adverse reaction. 
A variety of other antibacterial agents are also effective treatments for CARP. Effective antibacterial treatments include oral fusidic acid 1000mg daily for several weeks, oral clarithromycin 500mg daily for 5 weeks, oral erythromycin 1000mg daily for 6 weeks, and oral azithromycin 500mg daily 3 times per week for 3 weeks.  Several reports have noted that CARP can respond to azithromycin.  A case of CARP that successfully responded to roxithromycin has been noted.  Furacycline, tetracyclines,  and cefdinir  have also been successfully used to treat CARP.
It is not clear whether minocycline or azithromycin is the preferred antibacterial for the treatment of CARP. While there have been many more reports demonstrating the effectiveness of minocycline, the adverse effects of azithromycin seem more benign than those of minocycline. Minocycline has been linked to a lupus-like hypersensitivity syndrome, whereas azithromycin has not. Azithromycin is a pregnancy category B drug, can be administered in the form of one pill every other day, and is not involved in any important drug interactions. Minocycline is a pregnancy category D drug, is associated with many adverse effects (some minor, such as dizziness, and some major, such as hypersensitivity syndrome), is administered once or twice daily, and is involved in more drug interactions. Although azithromycin was previously a more expensive antibacterial than minocycline, its cost has fallen now that it is available generically. While a head-to-head trial is unlikely, if it is indeed borne out that CARP is caused by a bacterium, selection of the optimal therapy should probably take into account the adverse effect profile and antibacterial sensitivity of the drug.
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A variety of treatments that are effective against fungi have been useful for treating CARP. CARP responsive to selenium sulfide has been reported. [62,63] Topical antifungal agents (in particular, topical ketoconazole) have also been reported as effective treatments of CARP. 
Supporting the concept that CARP is a disease of keratinization, retinoids have been shown to effectively treat CARP. CARP responds to high-dose isotretinoin therapy,  and low dose isotretinoin can also be effective. [66,67] Another retinoid, etretinate, is also an effective oral treatment of CARP. [68,69] Oral retinoids are a disfavored treatment because of their adverse effects and the effectiveness and better adverse effect profile of minocycline. Topical tazarotene  and topical tretinoin  have been reported to treat CARP effectively.
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Vitamin D derivatives have been used to treat CARP with mixed effects. Calcipotriene (calcipotriol) in a 0.005% cream or ointment base twice daily has been effectively used to treat CARP. [71-73] A recent report described a case in which CARP failed to respond to 3 months of treatment with a topical vitamin D3 analog (maxacalcitol ointment) but was then subsequently cured with 1 month of treatment with minocycline 100mg daily.  Other failures of calcipotriene have been reported.  Ginarte et al.  reported the case of a 14-year-old girl with CARP in whom Malassezia furfur was found and eliminated with antifungal therapy but without disappearance of the eruption, which was subsequently cleared with treatment with tacalcitol.
CARP remains an enigmatic condition that has long attracted interest. [76-78] It is readily distinguishable from acanthosis nigricans, a condition which it resembles clinically. Until recently, the keratinization theory was the predominant explanation for the etiology of CARP. However, if CARP is a disease of keratinization, it is unclear why it responds so consistently to minocycline. In this regard, the report that linked CARP to a bacterial etiology was tantalizing for students of CARP. However, an isolated case report does not define a disease, and this report needs to be confirmed. A simple way to test the theory of a bacterial etiology for CARP is to treat patients with submicrobial doses of doxycycline. If CARP responds to submicrobial doxycycline, it will be clear that it does not have a primary bacterial etiology.
It should be noted that tetracycline, doxycycline, and minocycline (and, for that matter, erythromycin and azithromycin) have anti-inflammatory properties. Minocycline inhibits the migration and function of neutrophils. Tetracycline, doxycycline, and minocycline have been used effectively to treat bullous pemphigoid (with nicotinamide) and sarcoidosis, conditions for which a causative pathogen has not yet been identified or definitively implicated. In other words, the anti-inflammatory and immunomodulatory effects of these antibacterials might be the basis for their effectiveness in treating CARP. The mechanism that links these effects to aberrant keratinization is unclear, although the effectiveness of retinoid for treating psoriasis shows that this is not an isolated effect. It is a little disconcerting that CARP usually recurs after minocycline is stopped, perhaps making azithromycin a preferable medication because it can be taken almost indefinitely without adverse effects. 
With regard to the use of anti-inflammatory antibacterials to treat skin diseases of unknown etiology that mostly affect the epidermis, it is interesting to assess prurigo pigmentosa, which is a condition that resembles CARP clinically and also responds to tetracycline class drugs. Prurigo pigmentosa is a recurrent pruritic eruption characterized by the rapid manifestation of erythematous papules or urticarial plaques (rarely with scant scale) that coalesce into brown reticulated plaques that can last for months or years.  The distribution of the lesions is on the back and chest with rarer occurrence on the abdomen, lumbosacral regions, antecubital fossae, limbs, and forehead--but, as in CARP, the mucous membranes are spared. Like CARP,  prurigo pigmentosa has been linked to endocrine abnormalities or flux in states that include diabetes mellitus, ketosis, pregnancy, and fasting or dieting.  The histology of prurigo pigmentosa is distinct from that of CARP and involves a variety of inflammatory cells.  The appearance and therapeutic sensitivity of CARP and prurigo pigmentosa are similar, suggesting some common etiology, but this will require further investigation and assessment. It could be that there is some pathogenic stimulus in both diseases that elicits a reaction from keratinocytes.
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While eminently treatable, CARP remains, decades after its first description, an enigma of interest to those who are fascinated by pondering the pathology of the skin.
No sources of funding were used to assist in the preparation of this manuscript. The author has no potential conflicts of interest that are directly relevant to the contents of this manuscript.
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Department of Dermatology, St Luke's-Roosevelt Hospital, New York, New York, USA
Correspondence and offprints: Dr Noah Scheinfeld, Department of Dermatology, St Luke's-Roosevelt Hospital, 1090 Amsterdam Avenue, New York, NY 10025, USA.