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British Journal of Rheumatology
1996;35:292-294
CASE REPORT
CLUBBING IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION
A. BOONEN, G. SCHREY and Sj. VAN DER LINDEN
Department of Internal Medicine, Division of Rheumatology, University Hospital Maastricht, The Netherlands
SUMMARY
We describe two patients who developed dubbing shortly after HIV seroconversion. None of them had the full syndrome of
hypertropic osteoarthropathy. Other causes of clubbing are unlikely. We suggest that clubbing may belong to the spectrum of
arthropathies associated with HIV infection.
KEY WORDS:
Clubbing, Hypertrophic osteoarthropathy, HIV, AIDS.
Laboratory investigations did not show any abnormalities,
apart from slight but stable elevation of gamma-GT of
121 U/l (normal values 2-50 U/l), ALAT of 120 U/l
(2-50 U/l), ASAT of 79 U/l (5-40 U/l) and LDH of 484 U/l
(200-450 U/l). HBs-Ag was positive and HBe-Ag negative.
The CD4 count was 270 x lO'/l and the HIV-p24-Ag was
positive. A chest X-ray was suspicious for minimally increased interstitial density of both lower lung fields, but
pulmonary investigations, including CO diffusion capacity
and high-resolution CT scanning, were all normal. There
were no radiographic abnormalities of hands, feet or the
distal ends of long bones, and also a technetium bone scan
was unremarkable.
Because of the low CD4 count, treatment with zidovudine
was started in May 1990. Recent follow-up showed that his
clubbing remained unchanged and repeat radiographs still
showed no signs of periostitis of the distal ends of the long
bones.
Case 2, a 39-yr-old male i.v.-drug abuser, tested HIV
positive in 1985. In November 1991, he presented with a
weight loss of 12 kg, nightsweats and painful fingertips. He
was diagnosed as having AIDS-related complex. On clinical
examination, there was pronounced clubbing of all fingers,
but not of the toes. This abnormality had developed over the
past year. There was a negative family history for clubbing.
The patient had smoked 10 cigarettes a day for many years.
Clinical examination showed marked clubbing of fingers, but
was otherwise normal (Fig. 2).
The laboratory tests revealed an ESR of 50 mm, a slight
hypergammaglobulinaemia of 30 g/1 and a haemoglobin of
7.0mmol/l (normal value 8.5-11.0 mmol/1) with normal cell
indices. Serology and polymerase chain reaction (PCR) for
hepatitis C were positive. The CD4 count was 351 x lO'/l and
the HIV-p24-Ag was negative. A chest X-ray was normal, as
were radiographs of hands, feet and the distal ends of long
bones. A technetium bone scan was also normal.
Treatment
with zidovudine and
trimethoprimsulphamethoxazole was started in December 1991 because of
low CD4 count. Later this was changed to didanosine
because zidovudine induced anaemia and leucopenia. The
clubbing did not regress and at recent follow-up no radiological or other signs of HOA had developed.
of the tips of fingers and toes, in which the
angle at the nailbed is lost and the tips expanded, is one
of the best known nail abnormalities associated with
disease. Hippocrates was the first person to describe
this abnormality, but it took until the 19th century
before the association of clubbing with periostosis of
the distal ends of long bones, synovitis of large joints
and occasionally a thick sebaceous skin was established. The Frenchman, Pierre Marie, recognized this
syndrome as being clearly distinctive from acromegaly
and named the entity hypertrophic osteoarthropathy
(HOA)[1,2].
Whether clubbing is a separate disease or an incomplete form of HOA remains unclear. However, as HOA
often starts with isolated clubbing, and because both
conditions can be secondary to the same underlying
disease, certain authors have suggested that clubbing
and HOA are in fact manifestations of the same
disorder. Moreover, the radiological features and the
periungual tissue histopathology are indistinguishable
[3-5].
Secondary clubbing can be seen in a number of
cardiopulmonary and gastrointestinal disorders, as
well as in some infectious diseases. Chronic viral
infections, however, are not yet recognized as an
underlying cause. Here, we report two patients infected
with HFV who presented with clubbing.
CLUBBING
CASE DESCRIPTIONS
Case 1, a 36-yr-old homosexual man, has been HIV
positive since 1985. In that year, he was referred to our clinic
for evalua-tion. At clinical examination, clubbing of fingers
and toes was noted. The patient stated that this had developed only recently. No members of his family had ever shown
clubbing. The patient had smoked 20 cigarettes a day for
many years. Apart from the clubbing, there were no abnormalities on clinical examination (Fig. 1).
Submitted 25 July 1995; revised version accepted 28 September
1995.
Correspondence to: A. Boonen, Department of Internal Medicine,
Division of Rheumatology, University Hospital, P.O. Box 5800,
NL-6202 AZ Maastricht, The Netherlands.
DISCUSSION
As far as we know, after an extensive literature
search, the two cases presented are the first suggesting
© 1996 British Society for Rheumatology
292
BOONEN ET. AL.\ CLUBBING IN HIV INFECTION
293
(a)
(b)
FIG. 1.—The fingers (a) and toes (b) of case 1 demonstrating the clubbing.
an association between clubbing and a chronic
viral infection, in this case a HIV infection. No recognized aetiology of clubbing was found in these two
patients.
It should be noted that four cases of HOA developing in AIDS patients have been reported previously
[6-9]. In three of these four patients, a pneumonia
was diagnosed (a Pneumocystis carinii pneumonia in
two patients and a Gram-positive pneumonia with
Bacteroides melaninogenicus in the third one). The
HOA disappeared after treatment of the pulmonary
infection in these three patients. The fourth report
concerns a 33-yr-old patient with AIDS and HOA.
Interestingly, the clinical and radiological features of
HOA disappeared after starting zidovudine. This
suggests that HOA may be attributed to AIDS.
Because HOA and clubbing most likely represent
different aspects of the same disease, we would like to
suggest that both clubbing and HOA might also be
secondary to HIV infection. The possibility, however,
that the chronic hepatitis B or C infection in the
absence of liver insufficiency would be a contributing
factor cannot be excluded. Whether a possible progression from clubbing to HOA in our patients might
have been delayed by the early start of treatment can
only be speculated upon.
FIG. 2.—Photograph of the hands of case 2 illustrating the clubbing.
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BRITISH JOURNAL OF RHEUMATOLOGY VOL. 35 NO. 3
Infectiologjsts, rheumatologists, as well as other
physicians treating HIV-infected patients, should be
aware of HOA and clubbing in these patients.
Looking with a Hippocratic eye to the fingers (and
toes) of HIV-infected patients may be important. We
also suggest that HIV testing should be considered in
patients presenting with clubbing or HOA of unknown
origin.
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