5 December 1970
Fingerprint Changes in Coeliac Disease
T. J. DAVID,* M.B., CH.B.; A. B. AJDUKIEWICZ,t M.B., B.SC., M.R.C.P.; A. E. READt M.D., F.R.C.P.
British MedicalJournal, 1970, 4, 594-596
Summary: Study of the fingerprints of 73 patients with
varying between moderate epidermal ridge atrophy and
actual loss of fingerprint patterns. Of the patients 63 had
these abnormalities, compared with 3 out of 485 controls.
A high degree of correlation existed between ridge atro-
phy and changes in the clinical state of patients with
It is well appreciated that certain diseases affect the condi-
tion and clarity of fingerprints. These include eczema, leprosy,
nigricans (Verbov, 1970), scleroderma (Chatterjee, 1967), and
Darier's disease and skin lesions due to radiation (Cherrill,
1950). Extremes of age also affect the clarity of fingerprints.
During a survey of hospital inpatients unexpected abnormali-
ties were detected in patients with coeliac disease.
Methods and Subjects
Rolled and plain impressions of fingerprints were taken as
directed by the Home Office (1960), after full explanation had
been made to the patients. Ether was used in every case to
obtained by lifting latent impressions from glazed white tiles
as described by the Federal Bureau of Investigation (1963),
using "Bristol black" powder and standard lifting materials.§
were retaken on each visit
department. One to eight sets of fingerprints were obtained
from each patient over a period of two years. All prints were
taken by the same person (T.J.D.).
Patients with Coeliac Disease.-Every patient had been fully
disease. All of them had had a jejunal biopsy which showed
subtotal villous atrophy. The average age of the 73 patients
(25 males and 48 females) studied was 35 years;
under 15 years of age.
Controls.-These consisted of 275 healthy women (hospital
medical staff), 45 healthy men (hospital medical staff),
male inpatients, 85 female inpatients, 5 hospital domestic staff
(not using gloves for washing-up), and 40 patients who had
lost weight (those who had lost 1 to 8 st. (6.4 to 51 kg.) due to
to the outpatient
Of the 73 subjects, 63 had abnormal fingerprints-21 men
(10 on gluten-free diet) and 42 women (31 on gluten-free
diet). Ten patients had normal prints-four males (three on
gluten-free diet) and six females (five on gluten-free diet)-
seven were children. The abnormalities found were as follows:
(1) ridge atrophy, with the appearance of white lines (see
below), and (2) further ridge atrophy, with
ridges and disappearance of white lines.
loss of visible
Avenue, Chicago, Illinois 60640, United States of America.
* House Physician, Department of Medicine,
Bristol BS2 8HW.
Registrar, Department of Medicine,
tProfessor ofMedicine, Universityof Bristol.
theInstitute of Applied Science,
Bristol Royal Infirmary,
In five patients their fingerprints improved when they were
improvement when treated with a gluten-free diet, one of
these having had no clinical improvement either. In two other
patients who relaxed their gluten-free diet their fingerprints
deteriorated (in the reverse of the sequence above); this cor-
responded with a clinical deterioration. The fingerprints of
eight patients deteriorated when they relapsed while still on a
gluten-free diet; in one case these changes occurred 10 days
already on a gluten-free diet showed improvement of their
fingerprints when their clinical condition improved, and in
two of these only after corticosteroids had been given.
Only three controls had the same changes as those found in
the patients with coeliac disease. Of these, two had primary
patients with these two diseases had normal fingerprints. All
the domestic staff had abnormal prints, but the changes were
different from those in patients with coeliac disease, and
consisted of irregular breaks and cracks in the ridges with
white lines but no ridge atrophy.
a gluten-free diet and in two there was no
The changes in coeliac disease (Figs.
(a) Eczema (Fig. 4): Some fingers may be normal and others
affected. In one fingerprint some parts of the pattern may be nor-
mal and other parts completely obscured. The patchiness of the
changes in eczema makes it easily differentiated from ridge atro-
phy, though in a very bad case the fingerprint patterns may be
completely obscured, in which case the disease should be clinically
(b) Trauma: Usually localized to one or two digits, and is com-
monest on the left forefinger (Cherrill, 1954,
cuts leave quite characteristic scars, as do certain occupations such
as carpentry and tailoring (Galton, 1965).
(c) Skin grafts: Individual digits affected only.
(d) Severe mental subnormality: As
nounced ridge atrophy should be self-evident.
(e) Dotted ridges (Fig. 5): Found in Darier's disease; extremely
rare in normal people.
(f) Warts: Easily visible to the naked eye.
(g) Ridge dissociation (Fig. 6): Also wrongly called dysplasia.
Excessively rare and quite distinctive. Thumb most affected of all
fingers in ridge dissociation, whereas little finger worst affected in
patients with coeliac disease.
(h) Early infancy, old age: White lines are normally present. In
old age the skin becomes dry and the ridges appear less distinct.
(i) Denervated hand:
This obscures inked prints and
(k) Ridge aplasia: Complete absence of fingerprints. Very rare,
and found mainly in Japan and the United States of America;
inherited as a Mendelian dominant (Cummins, 1970).
to 3) are distin-
p. 98). Burns and
a cause of occasional
In this preliminary survey 86% of 73 patients with coeliac
disease had ridge atrophy of their fingerprints. If the adults
are taken alone then 95 % have ridge atrophy. The number of
children studied is insufficient to ascertain whether untreated
coeliac disease affects their fingerprints, since 10 of the 12
5 December 1970
Fingerprint Changes in Coeliac Disease-David et al.
not discernible. 2, After one month's treatment with a gluten-free diet. Shows partial ridge atrophy with appearance of white lines. 3, After
gluten-free diet. Ridges almost completely regrown, with almost complete disappearance of white lines. Pattern can now be classified as a whorl with an outer
to 3.-Right little finger of 54-year-old man with coeliac disease.
1, Newly diagnosed, shows ridge atrophy with ridges in the
centre of the pattern
months on a
clinically well. The two untreated children were infants of one
year old, in whom the disease had been recently diagnosed,
and both had abnormal prints. There are not enough controls
in this age group to assess the significance of this. One girl
that when playing "fingerprints"
school two years ago she was the only member of her class
who could not make nice clear prints. Only 3 out of 485 con-
trols had the same changes as the patients with coeliac disease.
To rule out weight loss as a cause of ridge atrophy, we took
cinomatosis, leukaemia, steatorrhoea not due to coeliac disease,
Grohn's disease, ulcerative colitis, thyrotoxicosis, cirrhosis, and
protein-losing enteropathy). Even a patient who had lost 8 st.
(51 kg.) in weight had normal prints recorded at necropsy.
anaemia, and pernicious anaemia all had normal fingerprints.
The improvement in fingerprints after treatment with a glu-
ten-free diet has been started appears rapidly and is easily
detected within a month. Ridge atrophy seemed to precede
clinical deterioration by some weeks in the few patients whose
were taken frequently enough
changes. We cannot explain, however, the finding of normal
fingerprints in three adults with coeliac disease.
Galton (1965) suggested that when the skin becomes thin
the ridges simultaneously subside in height. Though
might account for ridge atrophy in coeliac disease it does not
explain why patients with wasting diseases and thin skin have
to show such
5 December 1970
Fingerprint Changes in Coeliac Disease-David et al.
normal fingerprints., Cummins and Midlo (1961) suggested
that white lines are due to buckling of the skin. An examina-
tion of the fingers with white lines in coeliac patients does not
confirm this, though we have observed two patients with
Marfan's syndrome where buckling of the skin undoubtedly.
did lead to white line formation. Verbov (1970> has stated that
"ridge distortion" may also be seen in dry or atrophic skin
"due to many causes." Though some patients with coeliac
disease do have dry skin this is by no means always the case.
From our findings we think that the white lines in patients
with coeliac disease are merely secondary to ridge atrophy,
and this is supported by the finding that white lines disappear
when ridge atrophy is almost complete and reappear when the
to grow again. Possibly ridge atrophy
manifestation of abnormal cell turnover in the skin, paralleled
by similar changes of the cell turnover in the small bowel
(Croft et al., 1968).
Fingerprinting of patients with coeliac disease may have
two possible uses, subject to further. long-term studies being
made at present: (1) As a diagnostic feature in new cases of
adult coeliac disease, where it is apparently the only wasting
disease where ridge atrophy is seen; (2) as a measure of a full
response to a gluten-free diet. If fingerprint changes correlate
closely with villous atrophy in the gut, then fingerprinting
might also spare patients a repeat small intestinal biopsy. The
changes in coeliac disease need to be carefully distinguished
from other ridge abnormalities, but this has in practice been
found to be fairly simple, provided that the prints are taken
carefully by an experienced operator with the correct mat-
changes with inkless methods (Cherrill, 1954, p. 151), which
are barely adequate for pattern classification let alone for a
study of fingerprint minutiae. The type of paper used is also
ridges -will not be clear enough for close study.
Further long-term studies are being made with quantitative
methods of assessing ridge changes in coeliac disease and
correlating these with changes in the small-bowel villi and
other clinical criteria.
We are grateful to the many doctors who permitted us to study
patients under their care, and to the patients themselves, who
were most helpful.
Requests for reprints should be sent to Dr. T. J. David, Bristol
Royal Infirmary, Bristol BS2 8HW.
It would be quite impossible to detect subtle ridge
if the ink is excessively absorbed then the
Chatterjee, S. K. (1967). Finger, Palm and Sole Prints, 2nd edn., p. 7
Cherrill, F. R. (1950). Nature, 166, 581.
Cherrill, F. R. (1954). The Finger Print System at Scotland Yard. London,
Croft, D. N., Loehry, C. A., and Creamer, B. (1968). Lancet, 2, 68.
Cummins, H. (1967). Finger Print and Identification Magazine, November,
Cummins, H. (1970). Finger Print and Identification Magazine, March, p. 6.
Cummins, H., and Midlo, C. (1961). Finger Prints, Palms and Soles, p. 37.
New York, Dover.
Federal Bureau of Investigation (United States) (1963). The Science of
Fingerprints. Washington, U.S. Government Printing Office.
Galton, Sir F. (1965). Finger Prints, p. 59. New York, Da Capo.
Home Office (1960). Instructions in the Method of Taking Finger and Palm
Prints. London, H.M.S.O.
Verbov, J. (1970). Journal of Investigative Dermatology, 54, 261.
Fibrosing Alveolitis Associated with Renal Tubular Acidosis
A. M. S. MASON,* M.B., M.R.C.P.; M. B. McILLMURRAY,t M.B., B.S.; P. L. GOLDING4, M.B., M.R.C.P.
D. T. D. HUGHES,§ B.M., M.R.C.P.
British MedicalJournal, 1970, 4, 596-599
Summary: The discovery of a case of renal tubular acid-
osis and fibrosing alveolitis led to the investigation of
19 further patients. Abnormal pulmonary function tests
were found in a further four patients with overt renal
tubular acidosis and in four out of eight patients with
"incomplete" renal tubular acidosis. The response to an
ammonium chloride test in seven patients with cryp-
togenic fibrosing alveolitis was normal. Those patients
with a defect of both renal acidification and pulmonary
gas transfer had concurrent autoimmune diseases such as
Sjogren's syndrome and primary biliary cirrhosis. It is
suggested that the renal and pulmonary abnormalities
may be part of a systemic disorder capable of affecting
many organs. Moreover, hyperglobulinaemia and auto-
pathogenesis of these abnormalities.
hyperglobulinaemia (Hobbs and Turner-Warwick, 1967) and
the presence of autoantibodies (Turner-Warwick and Doniach,
1965). Possibly autoimmune processes are concerned in the
pathogenesis of this disorder (Mackay and Ritchie, 1965), and
the concurrence of fibrosing alveolitis with other autoimmune
diseases such as rheumatoid arthritis, Sjogren's syndrome,
Hashimoto's thyroiditis, and active chronic hepatitis has been
reported (Turner-Warwick, 1968; Scadding, 1969).
Renal tubular acidosis similarly may be associated with
autoantibodies (Talal et al., 1968). Diseases recorded as occur-
*Formerly Research Assistant, Southampton General Hospital.
Formerly Senior House Officer, The London Hospital, London E.1.
Senior Medical Registrar, The London Hospital, London E.l.
Senior Lecturer in Medicine, The London Hospital, London E.1.
equests for reprints to Dr. D. T. D. Hughes.
Patients and Methods
The patients selected for investigation were divided into
three groups. Group A consisted of five patients with overt
renal tubular acidosis-one of these (Case 1) is described in