Darier's disease ( dyskeratosis follicularis) 
Review 
DARIER'S DISEASE 
(DYSKERATOSIS FOLLICULARIS) 
J. Miljkovič, A. Kansky and B. Korge 
SUMMARY 
The existing data indicate the prevalence of morbus Darier (MD) from 1.0 to 2.8 per 100 000 inhabitants. 
The majority of authors agree that MD is an autosomal dominant disease. The symptoms are not present at 
birth; they usually appear during the first 10 years of life or even later. The major symptoms are brown, greasy 
papules located predominantly in seborrhoic areas, inguinal or perineal flexures and further areas may be 
involved too. Sunlight and poor personal hygiene are substantial triggering factors. There is good evidence that 
the main pathogenic factors are not due to a defect in keratin molecules, but rather to anomalies in the 
structure of the desmosomes. 
KEY WORDS 
dyskeratosis f ollicularis, mb Darier, prevalence, genetics, symptoms, micromorphology, pathogenesis, 
treatment 
INTRODUCTION 
Darier-White disease ( dyskeratosis follicularis, morbus 
Darier, MD) is a relatively rare disease characterized 
by papular skin lesions, predominantly in seborrhoic 
areas. Skin appendages may also be involved. In 
most instances it is inherited. Darier and White 
described it independently in 1889. 
PREVALENCE 
Data on the occurrence of MD were reported from 
certain countries. As they are based on reports from 
clinical departments (mostly dermatologic) they might 
not be correct in a statistical sense; still they 
136 
represent a valuable information. A prevalence of 
1.8/100 000 was reported from central England (1) 
and even 2.8 from northeast England (2), 1.0 from 
Denmark (3), 1.3 from Croatia (4). In Slovenia such 
an investigation is in progress, preliminary data 
show that it will be more than 2.2. Table l. 
GENETICS 
The disease is considered to be determined by an 
autosomal dominant gene with variable penetrance 
(5,6). Burge and Wilkinson mentioned however that 
among their 163 patients in 46 no family history 
could be detected (7). Contrary to this Munro (4) 
acta dennatovenerologica A.P.A. Vol 6, 97, No 4 
Darier's disease ( dyskeratosis follicularis) 
Fig. l . Darier's disease: severe, generalized form. 
reported that in 9 families 66 out of 136 adult 
members (with one affected parent) displayed 
symptoms of MD, thus indicating complete penetrance 
of an autosomal dominant gene. 18 individuals gave 
no family history, but 7 of these were members of 
affected kindred's. New cases whose parents are 
normal probably represent new mutations or non-
paternity rather than incomplete penetrance. 
Efforts are being made by various groups of 
researchers to detect the genetic defect in MD. An 
abnormality in the desmosome-keratin filament 
interaction appears to be responsible for the breakdown 
of cell adhesion, and therefore candidates are genes 
encoding desmosomal and cytoskeletal proteins. 
In 1993 two British groups carried out linkage 
analysis studies (8,9). They excluded linkage of the 
disease to any of the desmosomal genes mapped on 
chromosome 18 as well as to the type II keratins 
clustered at the chromosomal region 12qll-q13 in 
the families investigated. They were however able to 
localize a gene responsible for MD to the chromosome 
12q22-q24. Munro and cow obtained similar results. 
acta dennatovenerologica A.P.A. Vol 6, 97, No 4 
Fig. 2. Darier's disease: face and neck of the same 
patient. 
(10), who used the microsatelite DNA polymorphism 
to examine linkage to the locus of the disease. 
During the following two years further confirmatory 
results have been reported from Britain (11), United 
States and Canada (12,13,14). Table 2. 
CLINICAL SYMPTOMS 
In most cases skin symptoms do not appear at 
birth or soon afterwards, but usually start in childhood, 
in adolescence or even later. Burge and Wilkinson 
(7) mentioned that in 110 out of 163 patients the 
lesions became apparent between the ages of 6 and 
20 years, with a peak between ages of 11 and 15 
years. The disease may start later in life e.g. between 
41 and 50 or 51 and 60 years. Sokol and Kansky 
(3) reported in their 28 cases two peaks of onset: 
the age group 5 to 9 years (21.4%) and 20 to 24 
Fig. 3. Darier's disease: nail dystrophy and sububgual 
hyperkeratoses. 
137 
Darier's disease (dyskeratosis follicularis) 
Table l. Data on the incidence of morbus Darier (dyskeratosis follicularis are available only from a few countries 
Denmark 1.0/100 000 Svendsen LB Acta Derm Ven (Stock) 
Albrechtsen B 1939; 39: 256 
Central England 1.8/100 000 Wilkinson JD et al Br J Dermatol 1977; Suppl 15: 13 
North-East England 2.8/100 000 Munro CS Br J Dermatol 1992; 127: 126 
Croatia 1.3/100 000 Sokol J, Kansky A Acta derm lug 1991; 18: 57 
Slovenia ~ 2.2/100 000 study 
years. Only in one male patient the disease developed 
after the age of 35 years. 
The disease is characterized by firm rather greasy 
keratotic papules of a yellow-brown, dark brown 
color. The predilection sites are seborrhoic areas of 
the trunk and face, the laterni parts of the neck and 
the supraclavicular regions (Fig. 1-5). In certain 
patients the flexures notably the groins, and the 
anogenital region are involved. The papules may 
coalesce to form wart-like, vegetating and often 
malodorous plaques. According to Burge and 
Wilkinson (7) the center of the chest was involved 
in 87%, the back in 85%, the forehead in 84% and 
the supraclavicular fossae in 82% of cases under 
observation. 
On the back of the hands and feet fiat yellow 
papules resembling lesions in akrodermatitis 
verruciformis may be present. The frequency of 
these symptoms is given in Table .... 
On the palms and tips of the fingers punctiform 
keratoses and minute pits are rather frequendy 
observed: in 84% of English and in 53.5 of Croatian 
patients. Similar findings are present on the soles. 
A further observation are the specific dermatoglyphic 
patterns ( discontinued lines ), especially on the tips 
of the fingers and on the palms (15). In contrast to 
such earlier report in a recent study no significant 
quantitative or qualitative differences were found 
between dermatoglyphic features of 11 Jewish patients 
with MD and those of a healthy population (16). 
Nails are frequently involved, characteristic are the 
longitudinal red and/or white lines extending from 
the base of the nail across the lunula to the free 
margin. Both of them may be expressed in the same 
nail. Longitudinal ridging may be expressed as well. 
138 
in progress 
V- shaped notches at the free edge of the nail are 
a pretty constant feature . Painful splits and subungual 
hyperkeratoses are additional symptoms (17). Usually 
only a few nails are affected, but in some patients 
ali the nails can be involved. In the English patients 
the nail involvement was observed in over 90% and 
in Croatian in 71.4%. Toe nails can also be involved. 
Although the typical hyperkeratotic papules are as 
a rule hyperpigmented, depigmented macules or 
even papules may be occasionally observed (18,19). 
Both brown papules and leukoderma showed typical 
histological features in one case (20). 
Lesions of the oral mucosa were obse1ved in 15% 
of patients by Burge and Wilkinson (7) and in 
17.8% in the Croatian patients' (3). They consist of 
fine whitish papular lesions, sometime of cobblestone 
appearance, on the hard palate, tongue, and alveolar 
ridges or on buccal mucosa. Pharynx, larynx, vulva 
and anal mucosa may also be involved. Lately 
affection of the vulva were mentioned again in the 
literature (21). 
Symptoms of obstructive sialadenitis have been 
occasionally reported as a feature of MD. Parotid 
sialograms in 3 patients with MD revealed dilatation's 
with periodic strictures and indentations affecting 
the main ducts (22), thus indicating a probably 
more frequent affection. 
FACTORS 
TRIGGERING SKIN SYMPTOMS 
Sunlight has been mentioned as an exacerbating 
factor in 58% by British and in 89.3% by Croatian 
patients. Heat and sweating as well as dirty working 
conditions or poor personal hygiene have a similar 
acta dermatovenerologica A.P.A. Vol 6, 97, No 4 
Darier's disease ( dyskeratosis follicularis) 
effect. Wool and synthetic fibers may also have a 
deleterious effect on the course of MD. 
Psychic stress was mentioned as impairing the 
condition by 43% of British patients. Only a minority 
of female patients reports premenstrual exacerbations. 
Pregnancy seems to improve the conditions in certain 
women while worsening in others. 
There are two reports on exacerbation of MD by 
lithium carbonate treatment for psychiatric disorders 
(23). In a further case the disease appeared after the 
initiation of lithium carbonate treatment (24). 
INVOLVEMENT OF OTHER ORGANS 
An opinion exists among dermatologists that various 
affections of the central nervous system may coexist 
with MD (3). Burge and Wilkinson reported that 8/ 
163 patients were mentally retarded and 7 had a 
history of epilepsy (7), which is more frequent, 
' 
Fig. 4. Darier's disease. Histopathology: focal acantho-
lytic dyskeratosis 
acta dermatovenerologica A.P.A. Vol 6, 97, No 4 
compared to the incidence in general population. 
A simultaneous occurrence of a major affective 
disorder and MD was reported in 5 mernbers of a 
farnily (25). In an other study linkage between 
rnanic depressive illness and MD was excluded (26). 
All the mentioned observations rnay represent a 
casual association between MD and rnental disorders 
in a certain farnilies. 
Munro (2) believes that the observation of a 
frequent rnental subnorrnality in patients with MD 
in Denmark could indicate that different genes are 
coinvolved in cases observed in that country. 
LIGHT AND ELECTRON MICROSCOPY 
The dominant light-rnicroscopic characteristic of 
MD is acantholytic dyskeratosis of the epiderrnis. 
The appearance of clefts (fissures) above the basal 
layer (lacunae) is a prorninent pathohistologic feature 
Fig. 5. Darier's disease. Histopathology: verruciform 
hyperkeratosis, acantholysis, lacunae 
139 
Darier's disease (dyskeratosis follicularis) 
Table 2. Recent data on the location of the defective gene m patrients with morbus Darier ( dyskeratosis 
follicularis) 
Bashir R et al Hum Mol Genet 1993 
Craddock N et al Hum Mol genet 1993 
Parfitt E et al Hum Mol Genet 1994 
Ikeda S et al J Invest Dermatol 1994 
Kennedy JL et al Amer J Med Genet 1995 
Richard G et al J Invest Dermatol 1994 
Carter SA et al Genomics 1994 
Keratin II gene cluster 
(Fig. 4 and 5). The lacunae may extend throughout 
the prickle celi layer. The basal cells at the floor of 
the lacunae are usually distinctly separated. An up-
ward proliferation of the dermal papillae into lacu-
nae (villi) is often observed (27,28). Inside the 
lacunae there are individual cells as well as small 
groups of cells (acantholytic cells). The intercellular 
spaces between the prickle cells adjacent to lacunae 
are widened and the number of desmosomes is reduced. 
A number of cells display a large, usually dark-
staining nucleus surrounded by clear cytoplasm and a 
glistening ring simulating a membrane (Corps ronds). 
These cells undergo a premature partial keratinization. 
Further upwards, small cells with shrunken, eosinophilic 
cytoplasm, which may contain remnants of the nuclei 
are to be seen (grains). A variable degree of focal 
hyperkeratosis, parakeratosis and/or acanthosis may be 
expressed. Sometimes a hypertrophic, verrucous form 
of MD may be observed (29). 
Although the described histologic features are 
characteristic, they are not specific as certain similar 
observations can be made in a few other acantholytic 
dermatoses e.g. transient or persistent acantholytic 
dermatosis, acantholytic dyskeratotic nevus or chronic 
benign familial pemphigus (Hailey-Hailey). 
Caulfield and Wilgram who have already in 1963 
described the ultrastructural aspects of MD mentioned 
the following observation (30): 
l. In basal cells near to a lacuna the desmosomes at 
140 
12q14-q24.1 D12S78-D12S79 
12q23-q24.1 D12S76 
12q23-q24.l D12S78, D12S79 
12 cM apart 
12q23-q24.l 
5 cM apart 
D12S56-D12S4 
12q23-q24.l D12S84-D12Sl29 
12q23-q24 D12Sl05-D12S129 
12qll-ql3 
the base of a celi facing the basement membrane 
were normal in number and appearance, however on 
ali remaining surfaces there was a decrease in the 
number of desmosomes. 
2. The spaces between adjacent cells were widened. 
3. The tonofilaments were aggregated and rarely 
extended to the attachment plaque. 
4. In basal cells forming the floor of the lacuna the 
changes were more pronounced: there were no 
desmosomes except on the surface opposite the 
basement membrane. The tonofilaments encircled 
the nucleus in thick bands instead of extending in 
thin strands from one celi surface to another. 
5. In prickle cells near lacunae and in corps ronds 
even more intense changes were observed. 
The authors concluded that suprabasal detachment 
and lacunae formation was due to acantholysis, 
which was caused by the fact that tonofilaments 
became separated from desmosomes. In corps ronds 
the individual tonofilaments were normal but aggregated 
around the nucleus in association with large kerato-
hyaline granules to form the dyskeratotic material. 
They defined the dyskeratosis observed as a precocious 
and incomplete keratinization well below the usual 
zone of keratinization. 
Similar observations were made by Biagini et al 
(31) . Man and Haye on the basis of their studies put 
forward the opinion that the acantholytic process 
acta dermatovenerologica A.P.A. Vol 6, 97, No 4 
Darier's disease ( dyskeratosis follicularis) 
Table 4. Morbus Darier (dyskeratosis follicularis). Recent data on pathogenesis 
Setoyama M et al J Dermatol 1991 acantholytic cells 
diffusely in cytoplasm desmoglein I 
(glycoprotein) lost peripheral dotted pattern 
Setoyama M et al J Dermatol Se 1991 plaque component of desmosome desmoplakin I, II 
Burge S et al Br J Dermatol 1995 acantholytic cells 
intracellular distribution 
desmoplakin 
desmoglein 
desmocollin 
Steijlen et al Br J Dermatol extracellular matrix 
component ( dermis) tenascin increased 
Harada M et al J Dermatol diffusely in cytoplasm 
!ost peripheral dotted pattern desmoplakin I,II 
Hashimoto K et a J Dermatol 1995 dissolution attachment plaque desmoplakin 
starts rather m the desmosome and not in the 
tonofilaments (32). 
PATHOGENESIS 
The exact mechanism responsible for the deve-
lopment of skin lesions in MD remains unknown, 
but many interesting new data are available. As 
mentioned already the keratins do not seem to be 
primarily involved, for this reason the investigators 
concentrated their efforts on desmosomes. Table 4. 
It was postulated that desmoglein I, one of the 
major transmembrane glycoproteins of the desmosome 
under normal conditions adheres to the attachment 
plaque inside the celi. Sotoyama et al investigated 
desmoglein I with specific antibodies and mentioned 
that the normally observed dotted or rim-like pattern 
at the celi periphery was !ost already in early acantholysis 
in MD and that the immunoreactive desmoglein protein 
was observed diffusely in the cytoplasm (33). They 
expressed the opinion that primary abnormalities of 
desmosomes may be involved in MD. 
The similar observations were made when investi-
gating the plaque components of the desmosome, the 
desmoplakin I and II (34). The authors concluded 
that primary or secondary abnormalities of desmosomes 
might be involved in the pathogenesis of MD. Burge 
acta dermatovenerologica A.P.A. Vol 6, 97, No 4 
and Garrod studied the distribution of desmoplakin, 
desmoglein and desmocollin, Indicating that acan-
tholysis in MD preceded the abnormal cytoplasmatic 
distribution of desmosomal components (35). 
This observation was confirmed in a recent study 
published by Hashimoto et al (36). In contrast to 
such observations the surface glycoprotein CD 44 
was well preserved even on cell membranes of 
acantholytic cells. They concluded that the dissolution 
of desmosomal attachment plaque is the primary 
event in acantholysis in MD as well as in Hailey-
Hailey and Grover's disease. 
According to a further report the extracellular 
matrix component tenascin is grossly increased in 
MD and in epidermolytic hyperkeratosis (37). 
TREATMENT 
A survey of literature shows that a variety of 
regimens have been applied, but there is no ideal 
method of treatment. First of all attempts should be 
made to eliminate ali the triggering factors and a 
meticulous personal hygiene should be observed. 
Patients with a mild form of the disease require no 
special treatment except for simple emollients. 
Cryotherapy with liquid nitrogen, topical application 
of tretinoin gel, calcipotriol or 5-fluorouracil can be 
141 
Darier's disease ( dyskeratosis follicularis) 
used successfully, when applied to non-irritated skin 
(38,39). Dermabrasion has resulted in some cases in 
longer periods of remission ( 40). 
During periods of irritated skin corticosteroid 
creams and ointments are necessary or even systemic 
application of corticosteroids. One has however to 
bear in mind all the possible side effects. 
Far patients with a severe form of the disease, at 
least in periods of exacerbation, synthetic retinoids 
orally are recommended in doses of 0.5 to 1.0 mg/ 
kg body weight during 2 - 5 weeks. This treatment 
should be followed by a longer period on a 
maintenance dose of 20 to 50 mg etretinate daily 
( 41). The side effects like cheilitis, dryness of 
mucous membranes, hair loss and thinning of the 
skin are usually well tolerated; many patients are 
however refusing reintroduction of such therapy. It 
seems that treatment with cyclosporine was not so 
efficient as it was expected ( 42). 
ACKNOWLEDGEMENT 
The study was supported by the Slovenian Minist,y 
of Science and Technology, Grant No 13-9105. 
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AUTHORS' ADDRESSES 
Jovan Milj~ovič MD, Dpt Dermatology, Maribor Teaching Hospital, Ljubljanska 5, 2000 Maribor, Slovenia 
AlekseJ Kansky MD, PhD, professor of dermatology, Department of Dermatology, University Clinic_al 
Center, Zaloška 2, 1525 Ljubljana, Slovenia 
Bernhard Korge MD, Department of Dermatology, University of Cologne, J. Stelzmannstrasse 9, D-50942 
Cologne, Germany 
acta dennatovenerologica A.P.A. Vol 6, 97, No 4 143