British Journal of Dermatology (1976) 95, 105.

Correspondence

IS ACTINIC (SOLAR) DAMAGE THE PROVOKING CAUSE OF

'POST-INFLAMMATORY ELASTOLYSIS AND CUTIS LAXA (PECL)'?

SIR, on reading the paper by Verhagen & Woerdeman (1975) I noticed an apparent similarity of PECL tocertain reactions occurring in Australia which may be solar-induced and for which I have suggested thename actinic granuloma (CBrien, 1975).

The chief points of similarity between PECL and actinic granuloma are the preference for the sun-exposed areas, the sequence of papules, plaques and rings, and the subsequent local atrophy along with amicroscopic reduction in elastic fibres. Both conditions appear to display clinical and histological evidenceof diffuse actinic elastosis (solar or 'senile' degeneration of the dermis) and indeed this backgroundseems to be prerequisite for the focal lesions.

Admittedly there are some uncertainties, the most significant of which concerns the histologicalpicture of PECL. Thus Verhagen & Woerdeman do not state that their dermal 'degeneration' is actinicelastosis (that is, the alteration of dermal fibres to take the blue stain of haematoxylin). Nor do theyspecifically relate the granulomatous reaction of PECL to a resorption of the elastotic fibres in a zonalmanner as described for actinic granuloma. However, their entire description seems very suggestive ofboth of these basic features.

In an apparently similar case of cutis laxa (affecting a fireman, a possibly significant circumstance)McCarthy, Warin & Read (1965) describe a foreign-body giant cell reaction around fibres which, judgedfrom the description, were probably actinically damaged or elastotic (the elastic fibres showed 'clumping'and 'fragmentation', the collagen was 'irregular and slightly swollen').

Having noted in passing that 'sunlight' might be a factor in PECL, Verhagen & Woerdeman then goon to suggest insect bites as the basis of the focal lesions. They comment that PECL commences aboutthe time the infants 'start to play in grass and vegetation'. However, this is a circtimstance which impliesa greater degree of solar exposure.

Verhagen & Woerdeman do not refer to granuloma multiforme (Leiker, Kok & Spaas, 1964), a diseaseof adult African Negroes which I believe (O'Brien, 1975) is also akin to both PECL and actinic granuloma.

If actinic radiation is indeed the immediate cause of PECL, the extreme susceptibility of the affectedfemale infants requires explanation. For this we need to assume a pronounced genetic defect. In Australiasome observers believe that genetic factors are also important in actinic granuloma and that persons ofCeltic origin are more prone than those of other origin. However, nothing matching the susceptibility ofPECL patients has been described in Australia.

Should further investigation establish that PECL is actinically induced, support will thereby be givento the propositions that persons with black (flight-resistant) skin are not as immune to actinic damage as iscommonly thought and, further, that deeply penetrating infra-red (heat) rays rather than light rays areprobably responsible (O'Brien, 1975).

In summary, it is proposed that PECL, granuloma multiforme and actinic granuloma are related andthat infra-red radiation may be the common provocative external factor. The degree of genetic pre-disposition seems to vary greatly between the three disorders. In future studies, particular attention needsto be given to the antigenic and enzymatic aspects of the elastolysis.

Pathology Laboratory, JOHN P.O'BRIENMedical Centre,66 High Street,Randwick, 2031,Sydney, Australia

105

io6 Correspondence

REFERENCES

LEIKER, D.L.J KOK, S.H. & SPAAS, J .A.J . (1964) Granuloma multiforme. International Journal of Leprosy, 32, 368.MCCARTHY, C.F. , WARIN, R.P. & READ, A.E.A. (1965) Loose skin (Cutis Laxa) associated with systemic abnorm-

alities. Archives of Internal Medicine, 115, 62.O'BRIEN, J.P. (1975) Actinic granuloma. Archives of Dermatology, i i i , 460.VERHAGEN, A.R. & WOERDEMAN, M.J. (i975) Post-inflammatory elastolysis and cutis laxa. British Journal of

Dermatology, 92, 183.

CAUSATION OF PSORIATIC EPITHELIAL HYPERPROLIFERATION

SIR, Shahrad & Marks (1976) recently reported, in psoriatics, significantly elevated labelling indices ofthe interfollicular epidermis and its morphological extension, the upper external root sheath. In thesesame patients they reported normal labelling indices of the matrix and external root sheath (presumablybelow the level of the isthmus). On the basis of these data, they manage to find support for the notion ofdermal causation of psoriatic epithelial hyperproliferation.

It seems to me that their data are more suggestive of the opposite view, namely that psoriasis representsdefect(s) in epidermal differentiation. It is well known, from the work of Hermann Pinkus, that differ-entiation, and in particular keratinization, of epidermis differs from that of hair. The hair productitself and the linings of the inner root sheath keratinize at different levels and in different ways. More-over, the process of keratinization of the external root sheath differs depending on whether the sheath isexamined below, at or above the isthmus. In view of these normally occurring differences in keratiniza-tion, it comes as no surprise that labelling indices differ as well.

Labelling differences between normals and psoriatics are specifically limited to the tissue affected bypsoriasis—which is epidermal epithelium, not hair epithelia. It is suggested that psoriasis involvesdefect(s) in differentiation of epidermal epithelium without involving defect(s) in the quite unrelated anddiverse paths of differentiation seen in hair epithelia. Dermal mechanisms need not be invoked.

Serramonte Medical and DAVID PASLIN

Dental Center,1500 Southgate Avenue,Daly City,California, U.S.A.

REFERENCE

SHAHRAD, P. & MARKS, R. (1976) Hair follicle kinetics in psoriasis. British Journal of Dermatology, 94, 7.

Book Reviews

Practical Dermatology. I.B.SNEDDON and R.E.CHURCH (1976) 3rd edn. London: Edward Arnold.Pp. 226. Price £7.00.

This slim hard-backed introduction to clinical dermatology was an instant success when it first appearedin 1964. The new third edition has been revised but not enlarged and its remains the best of the smallbooks for the undergraduate.

As before, attention is focussed firmly on the clinic and the commonest disorders seen there. Thusonly 4 pages are devoted to the function and structure of skin; a parsimony requiring every word in thischapter to be chosen with care. It is, therefore, a pity to see that this brief account contains several