924

into contact with more superficial layers to initiate keloid formation.5-7 Would it be possible to devise and test a surgical technique that would imitate the "one-way" character of the piercing? Alternatively, might it be possible to identify a keloid-repressing environmental factor affecting the anterior aspect of the ear? If the difference between the front and the back of the earlobe could be elucidated that explain a great deal about keloid scarring.

Organon Teknika) with confirmation by western blot (DuPont de Nemours). 30 patients (81%) were seropositive: HIV seropositive

Diagnoss Tuberculosis (documented) Tuberculosis (presumptive)

Kaposi sarcoma Rheumatic fever

Cardiomyopathy

10/11 (91 %J 18/21 (86 %J 2/2 0/2 0/11

pericardial fluid was a serosanguinous exudate in all the HIV seropositive patients except 1 whereas in all the HIV seronegatives except 1 the fluid was serofibrinous (Fisher’s exact test,

The Department of Emergency Medicine, Texas Tech RAHC EI Paso, EI Paso, Texas 79905, USA

DAVID SLOBODKIN

p = 0-00002). 1. Oluwasanmi JO. Keloids in the African Clin Plastic Surg 1974; 1 (January). 2. Omo Dare P. Genetic studies on keloid. J Nat Med Assoc 1975; 67: 428-32. 3. Shetlar MR, et al. The use of athymic nude mice for the study of human keloid. Proc

Soc Exp Biol Med 1985; 179: 549-52. S, Cram A. Implantation of human keloid into

4. Estrem

athymic mice. Laryngoscope

1987; 97 (October).

immunological aspects of keloid tumor formation. J Surg Oncol 1988; 38: 16-18. 6. Janssen de Limpens AMP, Cormane RH. Studies on the immunologic aspects of keloids and hypertrophic scars. Arch Dermatol Res 1982; 274: 259-66. 7. Smith CJ, Smith JC, Finn MC. The possible role of mast cells (allergy) in the production of keloid and hypertrophic scarring. J Burn Care Rehab 1987; 8: 5. Kazeem AA. The

126-31.

Needlestick

injuries, surgeons, and

Departments of Internal Medicine and Microbiology, Centre Hospitalier de Kigali, Kigali, Rwanda

H. TAELMAN A. KAGAME J. BATUNGWANAYO A. NYIRABAREJA M. ABDEL AZIZ P. BLANCHE J. BOGAERTS

National AIDS Control Program,

P.

HIV risks

SIR,-Dr Leentvaar-Kuijpers and colleagues (March 3, p 546) base their cumulative risk estimate of HIV infection in surgeons on an average transmission risk per percutaneous exposure of 0.005. This figure may well overestimate the seroconversion risk in surgery. The risk of seroconversion after a needlestick is probably related to the type of accident. In a US prospective study of 860 health-care workers who sustained percutaneous exposures to blood from HIV-infected patients1 4 seroconverted. These 4 workers had had deep percutaneous or intramuscular injuries with large hollow needles.",2 Since the study population was not stratified for type of injury, the transmission risk for these needlesticks may have been higher than the average overall, so that the risk of seroconversion after a superficial prick with a solid needle, the sort of injury associated with surgical procedures,’ may be lower. Data from Ho et al4 suggested a substantial difference in infectivity between HIV-1-infected people with and without symptoms. The risk of seroconversion after percutaneous exposure, as calculated from the US data," relates to a population in which 94% of the source patients had symptoms. However, in most surgical practices the proportion of HIV-infected patients who have symptoms will be much smaller. Depending on this proportion, the risk after percutaneous exposure to blood from an "average" HIV-infected patient may be well below 0.005. National Committee on AJDS Control, Polderweg 92, 1093 KP Amsterdam, Netherlands

Tuberculous pericarditis was diagnosed in 32 (86%) patients, on clinical grounds and by response to anti-tuberculosis therapy (21) or through isolation of Mycobacterium tuberculosis (11 [pericardial fluid 1, pleura 5, sputum 4, lymph node 1]). Among the seropositive patients only 11 met World Health Organisation clinical criteria for AIDS. Our findings corroborate those of the Tanzanian study and suggest that pericardial effusion is another extrapulmonary manifestation of HIV-associated tuberculosis, often occurring early in HIV infection. Dual infections with HIV and M tuberculosis is not rare in sub-Saharan Africa and an increase in reports of tuberculous pericarditis can be expected.

FRANK COBELENS

1. Marcus R, CDC Cooperative Needlestick Surveillance Group. Surveillance of health care workers exposed to blood from patients infected with the human immunodeficiency virus. N Engl J Med 1988; 319: 1118-23. 2. McGray E, Cooperative Needlestick Surveillance Group. Occupational nsk of the acquired immunodeficiency syndrome among health care workers. N Engl J Med

1986; 314: 1127-32. ABA, Choudhary AAAA. Risk to surgeons: a survey of accidental injuries during operations. Br J Surg 1988; 75: 314-16. 4. Ho DD, Moudgil T, Alam M. Quantitation of human immunodeficiency virus type 1 in the blood of infected persons. N Engl J Med 1989; 321: 1621-25. 3. Hussain SA, Latif

Pericardial effusion and HIV infection MR,—Ur Uegielski and colleagues m ’I’anzania(Jan 27, p 2U9) found serological evidence of HIV infection in 72% of patients with pericardial effusion. At our department of internal medicine in Kigali, Rwanda, we have had a similar experience. Between August, 1988, and January, 1990, pericardial effusion was diagnosed in 37 patients (28 males; mean age 32, range 15-56). Pericardiocentesis was done in all cases because of tamponade. Patients were screened for HIV antibody by enzyme immunoassay (’Vironostika’,

Kigali

VAN DE

PERRE

Cyclosporin versus methotrexate toxicity in psoriasis SIR,-Dr Powles and colleagues (March 10, p 610) report abnormal liver function tests in patients with psoriasis treated with cyclosporin (Cy) who had previously received methotrexate (MTX), but not in those who had not done so. These abnormalities resulted in higher blood concentrations of Cy in the MTX-treated group. Although we agree with Powles et al that patients with impaired liver function due to MTX may have a higher degree of Cy toxicity, we find their conclusion premature that Cy should be regarded as the first line oral drug for psoriasis (in preference to MTX) in systemic treatment. MTX has been used in psoriasis for over 35 years, whereas Cy has only been prescribed for this disease for about 3-4 years. Although it is well established that MTX may induce liver damage, which in some patients leads to fibrosis and cirrhosis, recent studies have shown that this type of cirrhosis is not aggressive,’ and liver failure due to MTX is very rare. We have noted structural damage in kidney biopsy specimens from patients with psoriasis treated for about a year with low dose Cy (Zachariae H, Kragballe K, Hansen S, Olsen S, unpublished). These patients had normal liver function tests. We did not examine the clinical relevance of these structural changes. We believe, however, that together with other side-effects of the two drugs our findings should be taken into consideration in comparisons of risk/benefit between the drugs. Controversy over which drug should be the first-line oral therapy for severe disabling psoriasis is not best settled in your correspondence columns. Both drugs should only be used for disabling psoriasis, but we emphasise that although we know the risks of long-term MTX-therapy, much is still unknown about Cy treatment in this group of patients. Department of Dermatology, Marselisborg Hospital, University of Aarhus, DK8000 Aarhus, Denmark 1. Zachariae H,

Segaard H. Methotrexate-induced Dermatologica 1987: 175: 178-82.

HUGH ZACHARIAE KNUD KRAGBALLE liver cirrhosis:

a

follow-up.

Cyclosporin versus methotrexate toxicity in psoriasis.

924 into contact with more superficial layers to initiate keloid formation.5-7 Would it be possible to devise and test a surgical technique that woul...
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