Quiz 20: What is your diagnosis?

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Diagnosis: Quiz 20

Quiz 20

Answer:  Suppurative infundibulitis, idiopathic

Criteria for diagnosis clinically: Red papules, each of which is punctuated in its center by a scale-crust, are characteristic of suppurative infundibulitis in the process of involution.

Differential diagnosis clinically:  Insect "bites" are a consideration and biopsy can resolve the dilemma. The absence of purpura militates against leukocytoclastic vasculitis.

Criteria for diagnosis histopathologically: Large collections of neutrophils within contiguous infundibula dilated widely and neutrophils scattered in the interstitium of the upper part of the reticular dermis in company there with a sparse infiltrate of lymphocytes and neutrophils around venules are findings of suppurative infundibulitis.

Differential diagnosis histopathologically: There is none.

Clinicopathologic correlation  The papule came into being by virtue of edema of the papillary dermis in association with an infiltrate of inflammatory cells; the redness is a consequence of venules expanded greatly in the upper part of the dermis, they, in vivo, having been filled with erythrocytes; and the scale-crust is formed of neutrophils overwhelmingly, but also of many cells parakeratotic.

Options for therapy predicated on knowledge of histopathologic findings  A suppurative infundibulitis absent an agent infectious, such as is the situation here, resolves in time. The lesions clinical are well advanced in the process of resolution, they no longer being pustular, but rather crusted largely. In short, no effective therapy will hasten the demise of these lesions.

1) The suppurative infundibulitis shown here is termed, commonly and conventionally, "perforating folliculitis." For one, this is not a folliculitis but an infundibulitis, the epithelium affected being that of infundibular epidermis and not of the hair follicle (which is seated below the infundibulum and from top to bottom consists of an isthmus, a stem, and a bulb). For another, any suppurative infundibulitis in which neutrophils are myriad will cause a breach to form in the wall of infundibular epithelium, it then being "perforating" in the sense that neutrophils which arrived in the infundibulum from small vessels in the vicinity immediate of that funnel-shaped structure are ejected into the dermis through gaps in the epithelium. As a result, many an example of suppurative infundibulitis is "perforating."

2) Every current textbook of dermatopathology categorizes what we deem to be suppurative infundibulitis as "folliculitis" which, conceptually and practically, it is not. For example, in the ninth edition of Lever's Histopathology of the Skin, under the heading "Pathology involving hair follicles" in a section titled "Prominent neutrophils" can be found superficial folliculitis, deep folliculitis, fungal folliculitis, pityrosporum, and viral folliculitis. The section is introduced by the statement that "There is a follicular alteration with an inflammatory infiltrate containing neutrophils, which may result in disruption of the follicle." What is claimed to be follicular and follicle in actuality is infundibular epidermis. In the second edition of Weedon's Skin Pathology, the section on "Folliculitis" begins with the words "Inflammation of the hair follicle (folliculitis)" and goes on to classify the process as follows:  superficial infective folliculitis, superficial and non-infective folliculitis, deep infective folliculitis, and deep non-infective folliculitis. What is said to be folliculitis really is infundibulitis. 

3) Curiously, no matter how extensive is suppuration in infundibular epidermis, the hair follicle subjacent to it is itself devoid of collections of neutrophils, that being the case for suppurative infundibulitides as fulminant as acne conglobata, perifolliculitis abscedens et suffodiens, and hidradenitis suppurativa. Because of expulsion of neutrophils from infundibular epidermis into at least the upper third of the dermis, those polymorphonuclear leukocytes are splayed in a locus between bundles of collagen, a finding indicative highly of suppurative infundibulitis even if the infundibulum affected does not appear in that particular section of tissue.

4) The majority of suppurative infundibulitides are non-infectious, no cause for them being detectable. A small percentage of them are caused by bacteria, such as staphylococci (and, rarely, even by spirochetes, as in the pustular syphilid of secondary syphilis), by dermatophytes in Majocchi's granuloma, and by viruses such as that of herpes. In a case of suppurative infundibulitis brought into being by an agent infectious, the agent itself, such as a specific bacterium, or the effects on the epithelium of products of that agent, such as ones cytopathologic induced by herpesvirus, usually can be observed in sections stained by hematoxylin and eosin, the cause of the infundibulitis thereby being identifiable with assurance. Because bacteria, namely, staphylococci and cornybacteria, are normal inhabitants of infundibula along with Pityrosporum and Demodex, the mere presence of them in a suppurative infundibulitis is not indicting. When bacteria truly are causative, the number of them is increased logarithmically.

5) Suppurative infundibulitis is a distinctive pattern of inflammatory disease in the skin analogous to spongiotic dermatitis and ballooning dermatitis. Just as many conditions manifest themselves histopathologically as spongiotic dermatitis (e.g., allergic contact dermatitis, pityriasis rosea, and Gianotti-Crosti disease) or ballooning dermatitis (e.g., herpes simplex, erythema multiforme, and Mucha-Habermann disease), so, too, it is for suppurative infundibulitis. In most instances, no cause can be discovered for a particular suppurative infundibulitis, but in other circumstances a specific infectious agent can be fingered as etiologic. Moreover, sometimes when no specific cause can be found for a given suppurative infundibulitis, it may turn out that that suppurative phenomenon in an infundibulum expressed clinically as a pustule represents a manifestation of systemic disease, one example of that being Behçet's disease and another Crohn's disease.

6) The small-vessel vasculitis confined to a single venule that houses fibrin in the wall of it (illustrated in the last set of photomicrographs) is an epiphenomenon secondary to the effects of chemicals released from the countless neutrophils. Unlike the situation in authentic primary cutaneous vasculitis, such as leukocytoclastic vasculitis, in which many, if not all, venules in a section of tissue show signs of vasculitis, as a rule only one venule is affected in the epiphenomenon, that being the case here. The changes morphologic in that single venule, to wit, fibrin in the wall of it and neutrophils and nuclear "dust" of neutrophils around and in the wall, are indistinguishable from those of true leukocytoclastic vasculitis.

7) Chemicals released from neutrophils not only are capable of inducing changes vasculitic but, in loci where those innumerable polymorphs are, of altering collagen (it having a blue cast rather than the normal red), and of changing the appearance of elastic fibers (they assuming a red character instead of their normal light blue). Both those modifications are recognizable in some of the photomicrographs.

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