Version May 2024
INTRODUCTION — Palmoplantar pustulosis (PPP) is a chronic inflammatory condition characterized by crops of sterile pustules on the palms and soles that erupt repeatedly over time (picture 1A-F). Yellow-brown macules (remnants of resolving pustules), erythema, scale, and fissures are additional frequent findings. Other terms that have been used to refer to PPP are palmoplantar pustular psoriasis, pustulosis palmoplantaris, and pustulosis palmaris et plantaris.
Despite the limited area of skin involvement in PPP, the condition can have a significant negative effect on quality of life. Symptoms of pruritus, burning sensations, or pain are often present. In severe cases, the discomfort associated with skin involvement can cause difficulty with walking or other activities of daily living.
The clinical features and diagnosis of PPP will be reviewed here. Other pustular disorders, including acrodermatitis continua of Hallopeau (an acral variant of pustular psoriasis that primarily involves the digits) are reviewed separately. (See "Palmoplantar pustulosis: Treatment" and "Approach to the patient with pustular skin lesions" and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis" and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Acrodermatitis continua of Hallopeau' and "Neutrophilic dermatoses".)
CLASSIFICATION — The classification of palmoplantar pustulosis (PPP) is controversial. While some authors propose that PPP is a variant of psoriasis [1,2], others consider the disease a separate condition [3-10].
A consensus statement from the European Rare and Severe Psoriasis Expert Network (ERASPEN) recognizes psoriasis vulgaris and pustular psoriasis as distinct phenotypes and classifies PPP as a variant of pustular psoriasis [11]. In the ERASPEN classification scheme, PPP is subclassified as occurring "with or without psoriasis."
Authors who consider PPP a subtype of psoriasis have done so based upon the recognition of similarities between the conditions. As an example, our retrospective study comparing 39 patients with PPP and 51 patients with palmoplantar plaque psoriasis (a nonpustular form of psoriasis characterized by erythematous scaly plaques on the palms and soles) did not find statistically significant differences in age of onset, disease duration, family history of psoriasis, concomitant arthritis, or smoking habits between the two groups [1]. In addition, erythematous, scaly plaques similar to those of palmoplantar plaque psoriasis frequently accompanied pustules in PPP.
Other findings that suggest a direct relationship between PPP and psoriasis include the detection of psoriasis-like plaques on the trunk or extremities of some patients with PPP [12]. Moreover, a family history of psoriasis has been reported in 10 to 43 percent of patients with PPP [1,7]. A Scottish retrospective study of 73 patients with PPP found a family history of chronic plaque psoriasis or PPP in 21 and 3 percent of patients, respectively, a concomitant diagnosis of PPP and chronic plaque psoriasis in 27 percent, and concurrent psoriatic arthritis in 12 percent. These prevalences are 10 to 15 times higher than in the general population and suggest a close association between the two diseases [7].
Observations used to negate the designation of PPP as a variant of psoriasis include the strong association of PPP with smoking (an association much stronger than psoriasis vulgaris), the female predominance in PPP, the lack of an association between PPP and the psoriasis susceptibility locus PSORS1 (the major genetic determinant for psoriasis vulgaris) [13], the association of PPP with metal allergies [8,9,14], and differences in the response of PPP and psoriasis to therapy. Further study of the pathogenic mechanisms of PPP may help to resolve the controversy over the relationship between psoriasis and PPP. (See 'Pathogenesis' below.)
EPIDEMIOLOGY — Epidemiologic data on palmoplantar pustulosis (PPP) are limited. In general, PPP appears to be uncommon in the general population. A review of studies assessing the prevalence of PPP from Sweden, Korea, Germany, and Japan found prevalence rates of 0.05 to 0.12 percent [15]. In our personal experience in an academic dermatology practice, PPP seems to present slightly more often.
PPP usually develops in middle-aged adults. The mean age of onset in a retrospective study that included 39 patients with PPP was 48 years [1]. In the nationwide Japanese study, the highest prevalences for PPP occurred between the ages of 50 and 69 years [6]. PPP occurs more frequently in women than in men; observational studies from various parts of the world have found proportions of female patients ranging from 58 to 94 percent [1,6-10,16,17].
PATHOGENESIS — The pathogenesis of palmoplantar pustulosis (PPP) is not fully understood. Contributions of components of both the innate and adaptive immune systems are proposed. Environmental exposures and genetic susceptibility also may contribute to PPP:
●Mechanism – Studies investigating the mechanisms of PPP have yielded several observations regarding the development of this disease:
•The acrosyringium appears to be the primary site of vesicle/pustule formation and inflammation [18], and an abnormality in sweating may contribute to the formation of vesicles and pustules in PPP [19]. The finding that patients with PPP in Japan increase use of health care services during the hot season compared with the cold season may also support a role for sweating as a contributor to PPP [6].
•The inflammatory process that destroys the acrosyringium involves lymphocytes, neutrophils, eosinophils, and mast cells [20].
•Increased numbers of Langerhans cells have been detected around sweat ducts in PPP skin, suggesting the possibility of an antigen-driven process [20].
•Specific chemotactic factors may contribute to the development or propagation of the inflammatory process in PPP:
-Increased expression of interleukin (IL) 8 (a known neutrophil chemoattractant) and IL-17 related cytokines (eg, IL-17A, IL-17C, IL-17 D, IL-17 F, IL-22, IL-23A, IL-23 receptor) has been detected in PPP tissue [21,22]; in particular, expression of IL-17 has been detected within the acrosyringium [20].
-Increased serum levels of tumor necrosis factor-alpha (TNF-alpha), IL-17, IL-22, and interferon-gamma (IFN-gamma) have been detected in patients with PPP [22].
-A hyperimmune response to group A streptococci in tonsillar mononuclear cells has been described in PPP, and a tonsil-induced, autoimmune/inflammatory response might play a pathogenic role in PPP pathogenesis. In particular, cutaneous lymphocyte antigen (CLA), chemokine receptor CCR6, and integrin beta-1 may play an important role in the recruitment of T cells from the tonsils to the skin lesions of PPP [23].
-Complement pathway activation has been demonstrated inside PPP vesicles containing neutrophil-chemotactic C5a anaphylatoxin; the stratum corneum activates the alternative complement pathway, resulting in neutrophilic chemotaxis [24].
-The antimicrobial peptide LL-37 may contribute to neutrophil recruitment by upregulating IL-8 (neutrophil activation), IL-23, IL-17C, IL-1-alpha, and IL-1-beta [25].
Additional studies are necessary to elucidate how these factors interact in the development of PPP.
●Environmental factors – Clinical observations suggest that smoking, stress, infection, and drugs may contribute to the development or exacerbation of PPP:
•Smoking – There is a strong association between smoking and PPP, suggesting that smoking has a role in the pathogenesis of this disease. The reported prevalences of current or previous smoking among patients with PPP range from 38 to 100 percent [1,7,16,17]. The mechanism through which smoking could contribute to PPP has not been established. Proposed mechanisms have included effects of nicotine on sweat gland function or keratinocyte function (eg, nicotine-induced increase in keratinocyte cornification) [26]. In addition, differences in nicotine acetylcholine receptor staining patterns in PPP skin observed in a study of biopsy specimens taken from patients with PPP, healthy smokers, and healthy nonsmokers prompted consideration that an abnormal response to nicotine could contribute to inflammation [19].
•Stress – The observation that patients with PPP frequently report worsening of symptoms with stress led to a study investigating skin nerve fibers in involved skin [27]. The study found increased numbers of contacts between nerves and mast cells and intense substance P-like immunoreactivity in neutrophils in pustules and the papillary dermis, suggesting a role for neuro-mediation in the inflammatory process of PPP. In addition, a study of 21 patients with PPP and 21 age- and sex-matched controls found a higher rate of moderate to high anxiety among the patients with PPP than in the control population (61 versus 19 percent) [28].
•Infection – Focal infections (eg, acute or chronic tonsillitis, dental infection, chronic sinusitis) may be associated with PPP. Reports from Japan document episodes of PPP that follow infection, worsen in the setting of infection, or improve following treatment of infection [29-31]. One retrospective analysis of outcomes of PPP following dental infection control, tonsillectomy, and dental metal removal found improvement of PPP in 44 of 70 patients (63 percent) after dental infection control, 6 of 6 patients (100 percent) after tonsillectomy, and 3 of 9 patients (33 percent) after dental metal removal [32].
Also, differences in immune responses in tonsillar tissue and differences in oral microbiota that may be related to smoking or other factors have been detected in Japanese patients with PPP [33-40].
•Drugs – There are multiple reports of the development of PPP following treatment with biologic TNF-alpha inhibitors [41-44]. The mechanism behind this occurrence is not definitively known. Paradoxically, biologic TNF-alpha inhibitors have also been used for the treatment of PPP. (See "Palmoplantar pustulosis: Treatment", section on 'Severe recalcitrant disease'.)
•Metal allergy – A role for metal allergy in the development of PPP has been suggested by some authors based upon observations in small numbers of patients [7-9,14,45,46]. One report describes an exacerbation of PPP following a strongly positive nickel patch test [9]. However, sufficient data to confirm an association are lacking.
●Genetics – Although PPP does not appear to be associated with the PSORS1 locus that is strongly associated with psoriasis vulgaris [10,13], other genetic factors common to both diseases may influence an individual’s risk for the development of PPP. The findings of a study of 43 patients with PPP and 149 healthy controls suggest that variations of IL19, IL20, and IL24 genes may influence risk for both PPP and psoriasis vulgaris [47]. In addition, missense variants in the CARD14 gene may be involved in the pathogenesis of PPP as well as psoriasis vulgaris and generalized pustular psoriasis [10].
Other mutations that may play a role include mutations in AP1S3 and ATG16L1, genes also associated with psoriasis. In psoriasis, the ATG16L1 mutation affects the production of antimicrobial peptides and the production of IL-18 and IL-1, propagating systemic inflammation [16,48-50]. Single nucleotide polymorphisms (SNPs) of the ATG16L1 gene have been detected in patients with PPP, supporting a genetic link between PPP and psoriasis [49].
The genetic findings of patients affected by PPP with and without concomitant plaque psoriasis have been compared. A study that used gene expression microarray to compare skin biopsies from PPP with concomitant plaque psoriasis with skin biopsies from PPP without concomitant plaque psoriasis found that these entities could not be distinguished based upon gene expression, suggesting a relationship between these conditions [51]. The same authors found an increase in IL-17 gene expression without an increase in IL-23 in PPP with and without concomitant plaque psoriasis, a feature that may contribute to poor responses of PPP to ustekinumab, an inhibitor of IL-12 and IL-23 [52]. (See "Palmoplantar pustulosis: Treatment", section on 'Severe recalcitrant disease'.)
CLINICAL MANIFESTATIONS — The clinical manifestations of palmoplantar pustulosis (PPP) consist of the classic findings on the palms or soles and associated cutaneous and extracutaneous clinical features.
Cutaneous manifestations — PPP is characterized by the development of recurrent crops of discrete 1 to 10 mm sterile pustules limited to the palms and/or soles (picture 1A-F) [1-3,53-55]. The pustules often coalesce and resolve after several days, leaving brown macules and hyperkeratosis. Well-demarcated erythema, hyperkeratosis, and desquamation often surround the sites of pustulation.
Patients with PPP may have involvement of only the palms or only the soles of the feet; however, involvement of both the palms and soles is most common [1,26]. On the hands, the thenar and hypothenar eminences and central palm are common sites for pustule development [53,56]. The instep, the medial and lateral borders of the foot across from the instep, and the sides or back of the heel are common sites of PPP on the feet. Diffuse involvement of the palms or soles can also occur (picture 1C, 1G-H). The distribution is usually bilateral, but may also be unilateral, particularly at the onset of disease [53].
The impact of PPP on quality of life can be significant and should not be underestimated [57]. Patients frequently experience symptoms of itching and burning in the areas of involvement, and fissures may form, resulting in pain and bleeding. Severe eruptions can inhibit the patient’s ability to walk or perform other activities that require use of the hands or feet.
Associated clinical findings — Patients with PPP may develop additional clinical findings, including nonpustular cutaneous eruptions, nail dystrophy, and arthritis:
●Extra-palmoplantar skin involvement – The development of nonpustular psoriasis-like skin eruptions in other areas, such as the forearms, elbows, dorsal feet, lower legs, knees, or buttocks, has been described in patients with PPP [12]. These extra-palmoplantar skin lesions tend to be less pronounced and less well demarcated than classic plaque psoriasis (picture 2). Other potential findings include scale and erythema on the scalp, and infrequently, solitary pustules in areas other than the hands and feet [12]. Extra-palmoplantar skin changes may be more likely to occur in patients with severe PPP than in patients with milder disease [12].
The proportion of patients with extra-palmoplantar skin involvement is difficult to assess because some studies have intentionally excluded patients with extra-palmoplantar psoriatic lesions and reported estimates for extra-palmoplantar psoriasis in patients with PPP vary widely, ranging from 4 to 73 percent [1].
●Nail abnormalities – Nail abnormalities are common in patients with PPP [17,58,59]. Subungual pustules, onycholysis, pitting, destruction of the nail, or discoloration of the nail plate may be seen (picture 3) [58]. In a series of 50 adults with PPP, nail abnormalities were present in 15 patients (30 percent) and subungual pustulation was the most common nail abnormality seen [58].
●Arthritis – A subset of patients with PPP have concomitant arthritis, arthralgias, or unspecified forms of arthritis. In a retrospective study of 197 patients with PPP, 25 (13 percent) had documentation of arthralgias in the medical record [17].
In our retrospective study of 39 patients with PPP, 10 patients also had arthritis (26 percent), in accordance to other literature reports [1]. None of these patients had SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome. (See 'SAPHO syndrome' below.)
ASSOCIATED DISORDERS — Several systemic abnormalities have been linked to palmoplantar pustulosis (PPP).
Pustulotic arthro-osteitis — Pustulotic arthro-osteitis (PAO) is a common osteoarticular comorbidity of PPP that has been estimated to occur in 20 to 30 percent of patients with PPP in Japan [60]. The condition presents with joint pain, most often involving the anterior chest wall, although other joints may also be affected. PAO primarily occurs in middle-aged females and often develops in association with focal infection [60]. Bone scintigraphy reveals increased uptake in the anterior chest wall [60]. Clinical symptoms may overlap with SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, a much less frequent disorder.
SAPHO syndrome — PPP is one of the cutaneous manifestations that may occur in patients with SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, a rare arthropathy characterized by various presentations of arthropathy and a variety of neutrophilic skin disorders [61]. The arthropathy of SAPHO syndrome commonly involves the anterior chest wall and may present with pain, tenderness, and swelling of the sternum and its articulations. (See "Major causes of musculoskeletal chest pain in adults", section on 'Sternocostoclavicular hyperostosis (SAPHO syndrome)'.)
Osteoarticular features often precede skin findings but may appear concomitantly or subsequent to skin involvement [61]. Other pustular skin disorders that may occur in the setting of SAPHO syndrome are psoriasis, acne conglobata, acne fulminans, dissecting cellulitis of the scalp, and hidradenitis suppurativa.
Psychiatric disorders — Psychiatric disorders may be more prevalent in patients with PPP. In a case-control study, 23 percent of 60 female patients with PPP had psychiatric comorbidity, as depression, anxiety, schizophrenia, and manic-depressive disease, compared with 5 percent of 154 healthy female controls [62]. Age-adjusted odds for psychiatric disorders were greater (odds ratio [OR] 5.6, 95% CI 2.2-14.4) for females with PPP compared with healthy controls.
Systemic diseases — The relationship between PPP and systemic diseases is controversial. Limited data suggest that several systemic abnormalities may occur at increased frequency in patients with PPP, such as thyroid disease [7,63,64], disturbed calcium homeostasis [62], diabetes [7,62], and dyslipidemia [1,7]. Further studies are necessary to confirm a relationship between PPP and these conditions. Increased prevalence of gluten sensitivity was suggested by a Swedish study of 123 patients with PPP [65]; however, a German study did not find an association between PPP and gluten sensitivity, suggesting geographical or ethnic variability [66]. A case report describes a concomitant flare of PPP and new-onset sarcoidosis, which may reflect the role of tumor necrosis factor (TNF) in the pathogenesis of both disorders [67].
DISEASE COURSE — Palmoplantar pustulosis often persists for several years or decades, with frequent periods of disease exacerbation and partial remissions [68]. The severity does not appear to attenuate over time, and the risk of relapses seems to remain unchanged during the patient's lifetime [15].
The disease may significantly impair quality of life secondary to discomfort and resultant functional disability.
DIAGNOSIS — The diagnosis of palmoplantar pustulosis usually can be made based upon recognition of the clinical findings of a pustular eruption limited to the palms and/or soles with associated erythema and hyperkeratosis and a clinical evaluation to rule out other conditions. Performance of a potassium hydroxide (KOH) preparation (or fungal culture) is particularly important to rule out cutaneous fungal infection as the cause of symptoms in patients with plantar involvement.
A skin biopsy is not usually necessary, but can be useful for supporting the diagnosis in patients with atypical presentations or refractory disease. A KOH preparation should be performed prior to a skin biopsy to prevent an unnecessary biopsy.
History and physical examination — Expected physical findings of PPP are multiple pustules on the palms and/or soles, often with surrounding erythema and hyperkeratosis. Brown macules at sites of resolving pustules, fissures, and nail changes also may be present. If vesicles rather than pustules are the primary finding, the possibility of acute palmoplantar eczema (dyshidrotic eczema) should be considered. (See "Acute palmoplantar eczema (dyshidrotic eczema)".)
In addition to a physical examination of the palms and soles, a full examination of the skin and nails is indicated. The full skin examination allows the clinician to rule out generalized pustular psoriasis with palmoplantar involvement, to identify the presence of extra-palmoplantar skin lesions, and to detect additional skin manifestations that might suggest SAPHO syndrome (eg, acne, dissecting cellulitis, hidradenitis suppurativa). (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Generalized pustular psoriasis' and "Major causes of musculoskeletal chest pain in adults", section on 'Sternocostoclavicular hyperostosis (SAPHO syndrome)'.)
The clinical evaluation should also include a review of systems that includes questions about bone or joint pain to identify symptoms suggestive of concomitant arthritis or SAPHO syndrome. Because of the potential association of PPP with thyroid abnormalities and gluten sensitivity, we also question patients about symptoms of thyroid disease or gluten sensitivity (eg, diarrhea, steatorrhea, flatulence), as well as a personal or family history of these diseases. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Clinical features' and "Diagnosis of hyperthyroidism", section on 'Clinical manifestations' and "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults", section on 'Gastrointestinal manifestations'.)
Potassium hydroxide preparation — We usually perform a potassium hydroxide (KOH) preparation in patients who present with clinical findings suggestive of PPP to rule out the possibility of a dermatophyte infection as the cause of the eruption. Alternatively, a fungal culture can be performed. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)
Bacterial culture — The pustules of PPP are sterile. Bacterial cultures are primarily reserved for atypical presentations to rule out infection.
Skin biopsy — Skin biopsies often are not necessary for diagnosis. However, in cases in which the diagnosis is uncertain, biopsies can be helpful for supporting the diagnosis. A 4 mm punch biopsy that includes at least a portion of a pustule and surrounding erythema is our preferred procedure. In challenging cases (eg, prior treatment or atypical clinical features), multiple biopsies may be necessary to identify the histopathologic features of PPP. (See "Skin biopsy techniques", section on 'Punch biopsy'.)
Histopathology — Histologic findings that are consistent with a diagnosis of PPP include [26,69,70]:
●Epidermal changes (parakeratosis, loss of granular layer, psoriasiform epidermal hyperplasia)
●Spongiosis or epidermal vesicle formation (in early lesions)
●Pustules filled with neutrophils and eosinophils in the upper epidermis
●Accumulation of mast cells and eosinophils below pustules in the upper dermis
●Mixed perivascular and diffuse infiltrate in the dermis (lymphocytes, neutrophils, eosinophils, mast cells)
Laboratory studies — Laboratory tests are expected to be normal. If there is clinical suspicion for disorders that may occur at increased frequency in patients with PPP, including thyroid disease, gluten sensitivity, or diabetes, laboratory evaluation for these disorders should be initiated. (See 'Systemic diseases' above.)
DIFFERENTIAL DIAGNOSIS — Several other skin disorders that may present with pustules, erythema, and/or scale on the palms or soles are included in the differential diagnosis of palmoplantar pustulosis (PPP):
●Palmoplantar plaque psoriasis – Palmoplantar plaque psoriasis is plaque psoriasis that primarily involves the palmoplantar area. Patients present with erythematous, scaly plaques on the palms and/or soles (picture 4). Fissures are common. The absence of pustules distinguishes palmoplantar plaque psoriasis from PPP.
●Acute palmoplantar eczema – Acute palmoplantar eczema (dyshidrotic eczema, pompholyx) is a relapsing vesiculobullous palmoplantar disorder that most commonly presents as an acute, intensely pruritic eruption of small vesicles to large bullae on the lateral aspects of the fingers, palms, and/or soles (picture 5A-C). Although pustules are not a primary feature of acute palmoplantar eczema, pustules can develop as a result of secondary infection. The absence of hyperkeratotic and well-defined erythematous lesions that tend to crack in acute palmoplantar eczema facilitates the clinical distinction between PPP and acute palmoplantar eczema. The histologic findings of PPP can be difficult to distinguish from acute palmoplantar eczema with pustules because the disorders share multiple histopathologic features [69]. (See "Acute palmoplantar eczema (dyshidrotic eczema)".)
●Acrodermatitis continua of Hallopeau – Acrodermatitis continua of Hallopeau is a rare, chronic variant of pustular psoriasis characterized by the presence of sterile pustules involving the nails and surrounding skin of the fingers or toes (picture 6A-B). Associated paronychia, onychodystrophy, atrophic skin changes, and osteolysis of the distal phalanges can occur. The term acropustulosis repens has been used to describe a milder presentation [71]. The primary involvement of the digits distinguishes this disorder from PPP. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Acrodermatitis continua of Hallopeau'.)
●Vesicular/bullous tinea pedis or manuum – Vesicular tinea pedis (foot) or manuum (hand) result from dermatophyte infection of the palmar, plantar, or interdigital areas. Affected patients present with vesicles or vesicopustules with associated scale and erythema (picture 7A-B). A potassium hydroxide (KOH) preparation or fungal culture is useful for diagnosing this condition. (See "Dermatophyte (tinea) infections", section on 'Tinea pedis'.)
In rare cases, pemphigus vulgaris can present as a vesicular or vesiculopustular eruption on the palms or soles that may be confused with dyshidrotic eczema or PPP. A patient in whom pemphigus vulgaris manifesting as vesiculopustules on the palms and soles preceded other manifestations of pemphigus has been documented in a case report [72]. A biopsy revealing intraepidermal and suprabasilar acantholytic dyskeratosis and direct immunofluorescence demonstrating intraepidermal deposits of IgG confirm the diagnosis of pemphigus vulgaris. (See "Pathogenesis, clinical manifestations, and diagnosis of pemphigus".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Palmoplantar pustulosis".)
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Palmoplantar pustulosis (PPP) is a pustular skin disorder that usually occurs in adults. Women are more frequently affected than men. Many patients with PPP smoke or have a previous history of smoking. (See 'Epidemiology' above.)
●Pathogenesis – The pathogenesis of PPP is not well understood. Environmental factors (eg, smoking, stress, infection, and certain drugs) may contribute the disease. (See 'Pathogenesis' above.)
●Clinical manifestations – PPP usually presents as recurrent crops of pustules on the palms and/or soles (picture 1A-F). Brown macules representing resolving pustules, erythema, and scale are also often present. Associated symptoms of pruritus, burning sensations, or pain are common. (See 'Clinical manifestations' above.)
●Associated disorders – Extra-palmoplantar findings present in some patients with PPP include psoriasis-like skin lesions (picture 2), subungual pustulation and other nail abnormalities (picture 3), and arthritis. PPP may develop in association with SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome. Additional studies are necessary to clarify the relationship between PPP and thyroid disease, gluten sensitivity, and type 2 diabetes. (See 'Associated disorders' above.)
●Disease course – PPP exhibits a chronic clinical course characterized by exacerbations and partial remissions over the course of several years or decades. The disease can have a significant negative effect on quality of life because of the associated symptoms. (See 'Disease course' above.)
●Diagnosis – The diagnosis of PPP can often be made through clinical evaluation. A potassium hydroxide (KOH) preparation is useful for ruling out a superficial dermatophyte infection as the cause of the symptoms. Biopsy findings can offer support for the diagnosis when then the clinical evaluation is inconclusive. (See 'Diagnosis' above.)
●Differential diagnosis – PPP should be distinguished from other disorders that may present with pustules, erythema, or scale on the hands or feet. Examples include palmoplantar plaque psoriasis, acute palmoplantar eczema (dyshidrotic eczema or pompholyx), acrodermatitis continua of Hallopeau, and vesicular tinea. (See 'Differential diagnosis' above.)
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