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Congenital self-healing reticulohistiocytosis: Concern for a poor prognosis

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Congenital self-healing reticulohistiocytosis: Concern for a poor prognosis
Larissa Larsen MD, Melissa Reyes Merin MD, Thomas Konia MD, April Wang Armstrong MD MPH
Dermatology Online Journal 18 (10): 2

University of California Davis, Sacramento, California


Congenital self-healing reticulohistiocytosis (CSHRH) is a rare type of Langerhans cell histiocytosis with potential for relapse and systemic involvement. Whereas CSHRH was traditionally considered a benign disease, there is an approximately 3 percent risk of mortality and a 10 percent chance of relapse. This article, using an extensive review of cases since Hashimoto and Pritzker first described the condition in 1973, highlights the various presentations of CSHRH and reveals high rates of relapse and systemic involvement in cases that specifically address features of CSHRH occurring within the first year of life. The findings from this review will highlight the importance of considering LCH in the differential diagnosis when evaluating a neonate with congenital skin eruptions. Timely diagnosis of CSHRH and treatment of systemic involvement may decrease the likelihood of adverse outcomes. These patients may require closer follow-up and monitoring than previously recommended, especially in the first year of life when relapses and systemic involvement occur most frequently.


Langerhans cell histiocytosis (LCH) is a rare condition that occurs in 3-5 children per million per year [1]. It is a disorder of the antigen-processing cells known as histiocytes or Langerhans cells. LCH includes a spectrum of disorders that can range from fulminant presentations, including Letterer-Siwe, Hand-Schüller Christian, and eosinophilic granuloma, to those that spontaneously involute without sequelae [2]. The etiology of LCH is unknown, but neoplasia, immune stimulation, and dendritic cell disorders have been implicated in its pathogenesis [3]. Although LCH is usually a sporadic and non-hereditary condition, a limited number of familial cases have been reported [4, 5].

Hashimoto-Pritzker disease is a congenital self-healing form of LCH, also known as congenital self-healing reticulohistiocytosis (CSHRH). Aside from the cutaneous eruption that tends to spontaneously involute over an average of 3 months, the infant is usually otherwise healthy with no evidence of systemic involvement [6]. It is difficult to predict the severity of disease based on initial clinical and histological findings. Therefore, it is important for physicians to rule out more severe congenital forms of LCH and perform regular patient follow-up examinations to prevent future mortality.


This review of 126 CSHRH cases was commenced using and the search terms “congenital reticulohistiocytosis,” “self-healing histiocytosis,” “congenital self-healing reticulohistiocytosis,” and “congenital histiocytosis,” and “self-healing Langerhans histiocytosis.” Further cases were found using the reference section of the located articles. The search was limited to case reports in the English language and infants who presented with an initial diagnosis of CSHRH in the first year of life with no evidence of systemic involvement. A total of 126 infants were reviewed from 59 case reports.

Clinical presentations

Figure 1
Figure 1. A newborn infant with multiple 5 mm to 1.5 cm bluish, compressible, yet slightly firm, non-blanching, vascular papules

According to the 126 infants evaluated in this review, the prevalence in male and female infants is approximately equal; 54 percent and 46 percent, respectively (Table 1). There are a multitude of presentations of CSHRH, but it typically presents as a scattered cutaneous eruption of multiple firm, painless, red, pink, violaceous, or brownish papules and nodules that may develop crusts and vesicles. The vesicles may be pseudovesicular and often develop central ulceration (Table 1). Unusual variants of CSHRH may present as hemorrhagic bullae [4, 7, 8], urticarial plaques with a positive Darier sign [9], “blueberry muffin”-like lesions (Figure 1)[10, 11], or even molluscum-like papules [10-13].

Although CSHRH classically presents with multiple lesions, approximately 20 percent (26/126) of the cases reported in this review showed a solitary lesion (Table 1) [2, 12, 14-22]. The lesions of CSHRH occur most frequently over the face, scalp, extremities and trunk. However, they can also be found on the palms, soles [2, 10, 11, 23-30], groin [6, 8, 17, 19, 27, 28, 31-33], and mucosa [23, 34, 35]. CSHRH is usually present either at birth or develops in the first few months of life, although several cases of late onset self-healing Langerhans histiocytosis have been reported [36]. The lesions usually spontaneously involute, within an average of 3 months (Table 1), but have been reported to take up to 1.5 years [17]. The infants are otherwise healthy with no evidence of systemic involvement, except for occasional hepatosplenomegaly, lymphadenopathy, or mild hematologic abnormalities.


Figure 2Figure 3
Figure 2. Dense dermal infiltration of Langerhans cells within the mid and deep reticular dermis on low power (x100) view

Figure 3. Dense infiltration of histiocytes into the dermis, predominantly Langerhans cells (LCs) with characteristic pale, round, convoluted nuclei and containing abundant amphophilic cytoplasm under high magnification (x400)

Skin biopsy is necessary to make the diagnosis of LCH. CSHRH is characterized by a dense infiltration of histiocytes in the dermis that are predominantly Langerhans cells (LCs) with characteristic, abundant eosinophilic cytoplasm and a lobulated, kidney-shaped nucleus (Figures 2 and 3). LCs display positive staining for CD1a (OKT-6), S-100 protein, langerin protein, HLA-DR, and CD4. Peanut agglutinin, placental alkaline phosphatase, and interferon-gamma-receptor are markers that help distinguish LCH from the LCs of normal skin [4]. Electron microscopy examination shows Birbeck granules and laminated dense bodies within the histocytes [1, 2, 4, 11].


LCH most commonly involves bone and skin, but nearly any organ can be affected [37]. Because of the difficulties in distinguishing CSHRH from the more aggressive forms of LCH, it is essential to perform a thorough workup to rule out systemic involvement in suspected cases of CSHRH. For example, Letterer-Siwe disease, a potentially fatal variant of LCH, also classically occurs within the first year of life but has significant visceral involvement [38].

The Histiocyte Society guidelines for diagnosis and evaluation of LCH includes physical examination, hematologic and coagulation studies, liver function tests, urine osmolality, skeletal radiographic survey, chest radiography, and a bone marrow evaluation if indicated (Table 2). Topical or systemic therapies are generally not required in CSHRH [39].


Studies focused on determining the prognosis of LCH based on histology and clinical presentation have showed varied results. Therefore there are no clear features to determine the presence of skin limited disease or the probability of spontaneous regression. CSHRH may have a better prognosis with skin-limited disease, monolesional disease, necrotic lesions, hypopigmented macules, distal limb lesions, absence of mucous membrane lesions, and absence of lesions in seborrheic areas [2, 40, 41]. Histological findings have also been evaluated for determining prognosis. Findings such as a nodular infiltrate of LCs with a high degree of necrosis, less than 25 percent of LCs with Birbeck granules, dense infiltration of eosinophils, and the presence of Birbeck granules and laminated dense bodies in the same cell have been considered possible clues to a favorable prognosis [2, 40, 42]. Additionally, the presence of E-cadherin may be an indicator of skin-limited disease, but not of the ability of the disease to regress [41, 43]. However, histopathology has not been shown to be a prognostic factor in other studies [41].

Poor prognostic factors for LCH may include multi-organ or bone marrow involvement, age younger than 2 years at diagnosis, and a poor initial response to steroid and/or chemotherapy [44]. Whether or not these specific poor prognostic factors apply to CSHRH has not been determined.

In this review of 126 cases, the most common sequela of CSHRH is post-inflammatory hyper- or hypopigmentation. However, clinical relapses involving the skin, mucosa, bone, thymus, and pituitary have been reported (Table 1) [10, 25, 32, 33, 35, 45-47]. Involuted cutaneous lesions of CSHRH may also leave residual scars, hyperpigmentation, hypopigmentation, milia, and anetoderma, especially in larger lesions [3, 7, 11, 12, 14, 21, 23, 25, 26, 35, 48-55]. There have also been 2 reported cases of diabetes insipidus after initial lesion resolution [17, 46].

Relapse and mortality rate are difficult to assess because the majority of reported cases only followed the patients for a short period of time. Thus, more consistent follow-up is required to determine the actual rate of relapse and mortality. One study reported a relapse rate of 40 percent in patients with exclusive skin involvement [33]. We found a relapse rate of approximately 10 percent (13/126) in the 126 reported cases (Table 1) with about 6 percent (8/126) of the cases mentioning systemic involvement after resolution of skin lesions. All of the reported relapses occurred during the first year of life and about 31 percent (4/13) of the infants with a reported relapse died. With limited long-term follow-up data, the 10 percent relapse rate found in this literature search is likely an underestimation of the actual relapse rate. The total mortality rate in infants initially diagnosed with CSHRH in the literature is approximately 3 percent (4/126), which also likely represents an underestimation. The relatively substantial mortality rate in CSHRH is noteworthy because CSHRH has historically been considered a benign condition. Whether these cases represent truly cutaneous limited presentations is undetermined. However, even with systemic evaluation the reported cases were felt to be benign.

Future directions

CSHRH can present in multiple morphologically distinct forms. It is important to consider LCH when evaluating congenital skin eruptions to arrive at timely, accurate diagnosis and initiate appropriate treatment for systemic involvement. With the relatively high relapse and mortality rate, patients need to be followed closely even after lesion resolution. With all of the cases in this review reporting relapse before the first year we recommend including strict guidelines for CSHRH follow-up in the first 12 months of life that should include scheduled laboratory testing and evaluation. Prospective studies with long-term follow-up and clinical and histologic studies will be valuable to accurately assess prognosis in patients with CSHRH and will help develop appropriate follow-up guidelines to identify relapses early and hopefully prevent mortality.


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