Proctosedyl® and Proctomyxin® are two commonly prescribed hemorrhoid therapies. Their topical application to the perianal region may be complicated by a local allergic contact dermatitis and subsequent autoeczematization reaction. We present three cases of an autoeczematization (ID) reaction to varying topical allergens found in Proctosedyl®/Proctomyxin®. It is our recommendation that physician and patient education, avoidance of allergens (or cross-reactants), and appropriate choice of topical corticosteroid is important in preventing and avoiding flares.

Pediculosis humanus capitus infestations are common and classically present with intense pruritus of the scalp. Although many treatment options are available, lice are becoming more resistant to conventional therapies and severe clinical presentations are bound to become more prevalent. We present a case of treatment-resistant pediculosis capitus resulting in diffuse autoeczematization of the torso and extremities and severe crusting and scaling of the scalp, which we called "crusted lice." This eruption differs from the well-described id reaction known as "pediculid" and represents a more dramatic manifestation of rampant infestation. This paper provides an up-to-date review of treatment options available for pediculosis humanus capitus, including newer medications like the ones that eventually led to resolution of our patient's extreme infestation.

Diaper dermatitis is the most common cutaneous diagnosis in infants. Most cases are associated with the yeast colonisation of Candida or diaper dermatitis candidiasis (DDC). It is an irritating and inflammatory acute dermatitis in the perineal and perianal areas resulting from the occlusion and irritation caused by diapers. Autoeczematization to a distant focus of dermatophyte infection very rarely presents as DDC. We present a 1-month-old boy with lesion on diaper area (gluteal area, perineum, groin and genitalia) and with clusters of pustules and vesicles on a large erythematous base over the dorsal area of both hands.

Id reaction, also known as autoeczematization, is the development of dermatitis that is distant to an initial site of infection or sensitization. Clinical findings typically include an acute, intensely pruritic maculopapular or papulovesicular eruption that most frequently involves the extremities. Histology typically reveals spongiotic dermatitis that often is vesicular, and eosinophils may be present in the infiltrate. Id reactions can result from inflammatory skin conditions such as stasis dermatitis as well as infectious entities including mycobacterial infections. BCG live therapy consists of an attenuated strain of Mycobacterium bovis that is utilized as a first-line treatment of superficial transitional cell carcinomas. We report the case of an id-like reaction in a 90-year-old man who developed an intensely pruritic, scaly, erythematous eruption on all 4 extremities 2 weeks after starting weekly intravesical use of BCG therapy for superficial transitional cell carcinoma. A representative biopsy demonstrated spongiotic dermatitis with overlying scaling and an eosinophilic infiltrate. The eruption resolved after discontinuation of BCG therapy and treatment with topical corticosteroids.

Autoeczematization is characterized by the sudden dissemination of a previously localised form of eczema. While widely described, most cases reported have followed chronic, localized stasis dermatitis. In this study, we describe the clinical scenario of occupational contact dermatitis (OCD) triggering endogenous-like eczema in atopic individuals, who often have not had eczema since childhood, if at all. These cases appear similar to previously described cases of autoeczematization. To show this clinical scenario, a series of 6 patients is presented from the Occupational Dermatology Clinic in Melbourne, Australia. These workers initially developed OCD, usually affecting the hands, which then precipitated a flare of more generalized eczema. This appeared clinically consistent with atopic eczema (AE), and often became recurrent, and sometimes persistent. OCD can precipitate a flare of more generalized eczema, in a pattern consistent with AE, which may then persist. The clinical scenario is similar to that described for autoeczematization. It is possible that the pathophysiology, when clarified, will prove to be similar. Workers' compensation issues may become complicated for these patients, as the relationship between their generalized eczema and their occupational exposures may not be readily apparent. As a result, the work relatedness of their condition may not be recognized.

The pathophysiology and immune mechanisms involved in the clinical syndrome of autoeczematization remain a mystery. In this study of nickel dermatitis without autoeczematization and poison oak dermatitis with autoeczematization, it was noted that the process of autoeczematization was associated with the presence of CD8+ lymphocytes within the epidermis and the expression of HLA-DR antigens on epidermal keratinocytes. It is surmised that since CD8+ clones are induced by poison oak antigen but not by nickel, the inability of nickel to induce CD8+ lymphocytes may explain why uncomplicated nickel dermatitis does not autoeczematize. Since the selective adherence of CD8+ lymphocytes to keratinocytes, probably via the expression of adhesion molecules such as ICAM-1, the generation of antigens on endothelial cells of high endothelial venules involved in lymphocyte trafficking, and the expression of HLA-DR antigens on epidermal keratinocytes are all due to the activity of interferon-8, it is deduced that this lymphokine may play a key role in id eruptions induced by contact allergens.

A patient with classical hypostatic dermatitis-related autoeczematization was found to have an elevated ratio of helper to suppressor T lymphocytes and increased circulating activated T cells in the absence of detectable levels of circulating interferon. Despite the high levels of activated T cells, peripheral blood mononuclear leukocytes did not produce interferon spontaneously in culture. These findings suggest that autoeczematization is a form of cell-mediated autoimmunity and that activated T cells and interferon production may be unrelated in vivo.

Theory behind conditioned hyperirritability (autoeczematization) predicts the lowering of the irritation threshold in the presence of a pre-existing dermatitis. We have attempted to develop an animal model that parallels the syndrome seen in man. Groups of 10 guinea pigs were shaved and depilated; irritation thresholds to benzalkonium chloride and trichloroacetic acid were determined using 1 cm diameter open patches. Reactions were scored 24 h later on the basis of erythema and induration. Animals having as little as 1.56 cm2 of skin acutely inflamed with a known irritant had lowered irritation thresholds to the same irritant on normal skin at remote sites (p less than 0.01). Mild irritation of a much larger surface area produced the same effect (p less than 0.01). More extensive, severe dermatitis did not lower the irritation threshold further. Acute dermatitis induced by a contact allergen (DNCB) lowered the irritation threshold of normal skin to the same level as that obtained with irritants (p less than 0.01). Induction of chronic cutaneous ulcers 3-4 cm in diameter lowered the irritation threshold of normal skin to the same point defined by the acute studies (p less than 0.01). These results indicate that an acute irritant or contact dermatitis, as well as chronic skin ulceration, may alter the reactivity of unaffected normal skin to exhibit a heightened response to irritation. This model appears to differ from that seen in humans, in that a more extensive or chronic dermatitis did not further heighten the susceptibility to irritation.

A total of 113 patients with nummular eruptions of unknown origin were collected over a period of 8 years. This number was reduced to 82 patients by exclusion of known clinical entities which became unmasked during the study. All 82 patients were found to have varicose veins and/or edema of the lower extremities. Autoeczematization may be the common denominator.