Leiner’s Disease

Filed under: 2.2 - Leiner's Disease

This is probably a generalized and greatly intensified seborrheic dermati­tis, but has certain features peculiar to itself. It was first described in 1908 by Leiner, a Viennese dermatolo­gist, as follows: “A slight inflamma­tion of the whole cutis, a desquamation of the epidermis, and a seborrhoea of the scalp.”¹ In his first report there were forty-one cases; fifteen of the patients died. It has been said by some that Leiner’s disease is the same as Rittcr’s disease. I am doubtful of this, for it looks nothing like Ritter’s disease (see Figs. 6, 7 and 8). Fur­thermore, Ritter’s disease is a disorder of the newborn infant. Leiner’s dis­ease occurs in young infants (first 3 months) but not in the newborn period (first 3 weeks).

This was at one time a common dis­ease in Europe-it is said to be infre­quent there now. It has never been common in this country. It may be­gin much as seborrheic dermatitis does, with intertrigo, cradle cap, then grad­ual extension, until the whole skin sur­face, except the palms and soles, is in­volved, or it may begin with an acute eruption somewhat resembling measles, then rapid coalescence and scaling of the originally maculopapular lesions. In uncomplicated cases there is little itching, no eosinophilia, no marked general glandular enlargement, and no allergic antibodies to be found in the blood. This applies to the classical type which was originally described by Leiner, and later so carefully studied by Ernst Moro at Heidelberg.² In this country, mixed forms, showing some of the clinical features of both Leiner’s disease and of atopic dermatitis, are not uncommon. (See atopic erythrederma.) I expect that the answer to these mixed forms of a atopic and seborrheic dermatitis is that the process which causes seborrheic derma­titis occurs sometimes in babies who are allergic, sometimes in those who are not. In the first group, the skin appearance suggests both atopic and seborrheic dermatitis; in the second, classical and uncomplicated seborrheic dermatitis.

Diarrhea is common in Leiner’s dis­ease and is often serious. Secondary infection is frequent; nutrition may become poor. There is often a low serum protein with consequent edema, probably caused by loss of nitrogen from the body in the form of scales (keratin). There is evidently some abnormal metabolic process going on which interferes with the normal kera-tini/ation process of the epidermis.

I have seen patients with classical Leiner’s disease (the baby in Pig. 7 was such) who recovered entirely in a few weeks and had no further trouble with the skin. I have seen others who looked in the beginning like those in the first group, but who developed general glandular enlargement, eosino-philia, blue feet, itching, transferable antibodies to egg white and to other food and environmental allergens- who took two years to recover from the dermatitis,   and   who   later   had   hay fever or asthma.

Treatment.-The same diet as for seborrheic dermatitis is recommended, and plenty of it. These babies are poorly, and need food. For local treatment, only mild preparations should be used, such as petrolatum, or petrolatum with the addition of 5 grains of salicylic acid to the ounce.* The scalp is treated the same as in seborrheic dermatitis. These patients can be bathed-indeed it is better to bathe them, and probably better to wash them with pliisoHex than with soap. If they are in a hospital, and con­sequently exposed to all sorts of in­fection, they should be given an anti­biotic. It may be necessary, if they become edematous, to use serum re­placement therapy. Any young pedi­atrician who has passed the Pediatric Board examination knows so much more about this than I do that I would be ashamed to discuss it in detail. I have had no experience with cortisone in Leiner’s disease.

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