S6C39P33-1: This is a typical pattern seen in vesiculobullous lesions in the setting of porphyria cutanea tarda. The defect in part appears to be intra-epidermal; this may be an artefactual pattern related to the plane of the section; it may be evidence that this lesion represents two generations of vesicles, the superficial, intra-epidermal component being the older lesion, and the sub-epidermal component to the right of the center of the field representing a more recent lesion.

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S6C39P33-2: In this portion of the lesion, the patterns are common ones, as seen in lesions of porphyria; the epidermis is unusually acanthotic. Dermal papillae are elongated and preserved along the floor of the bulla.

S6C39P33-3: The reticular dermis of this lesion of porphyria shows sclerosis; the collagen bundles are coarsened and many are arranged in parallel arrays with the long axes of the collagen bundles parallel to the surface of the skin. There are perivascular and mild interstitial infiltrates of lymphoid cells; the patterns have a sclerodermoid quality.

S6C39P33-4: At higher magnification, the collagen bundles show an alteration in which the bundles are relatively straight; they tend to be in parallel arrays. The vessel shows hyalinization of its wall. Some of the vascular changes may represent duplication of the basal lamina.

S6C39P33-5: This is an example of a scarring alopecia of the scalp in a patient with porphyria. In this field, there is a paucity of follicles. Blue arrows outline fibrous columns; these areas of fibrosis represent the sites in which follicles have undergone atrophy. Over, and to the right of, one of the columns, the epidermis shows effacement of the rete ridges. The papillary dermis is widened and fibrotic; the patterns (i.e., straight interface and effacement of rete ridges) would support the interpretation that a lichenoid reaction may have been involved in the atrophy of the follicular epithelium.

S6C39P33-6: This is another area of the same specimen; there is a paucity of follicles. Areas outlined by blue arrows are interpreted as widened fibrotic perifollicular sheaths; they are the markers for sites in which follicles have undergone atrophy. In one of these areas, lymphocytes form a cluster. To the left of the field, there are patterns compatible with a senescent lichenoid reaction. An old, senescent lesion of lupus erythematosus is a possibility. Pseudopelade might be a favored diagnosis of some observers; but would be a most personal opinion for which the proponent would be hard put to offer a standard definition of what pseudopelade might represent. Some examples of pseudopelade (from my experience in conferences, in which each new “expert” offers his opinion about the nature of pseudopelade) seem to be a form of a lichenoid reaction somewhat similar to the follicular changes in lesions of discoid lupus erythematosus; the lichenoid reaction affects the isthmic portion of the follicle and is followed by perifollicular sclerosis in the same general site; the sclerosis leads to atrophy. Other examples appear to be a sclerosing perifolliculitis affecting the infundibular area of a follicle. Similar patterns of sclerosing perifolliculitis may be seen in lichen spinulosis, or keratosis pilaris.

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