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It is known that HIV co-infection with syphilis may accelerate the onset of gummata and neurosyphilis and increase their severity. However, this has only been reported for cardiovascular syphilis in two previous cases.1,2
This case-control study deals with a total of 14 HIV seropositive and 100 HIV 1 and 2 seronegative individuals with syphilis, who were seen in our clinic between June 2000 and May 2001. Of the 14 HIV seropositive individuals, 12 were reactive for VDRL (venereal diseases reference laboratory) and TPHA (Treponema pallidum haemagglutination assay) and two had primary syphilis confirmed by dark field examination forT pallidum. Of the 100 HIV seronegative individuals, 85 had reactive VDRL and TPHA and 15 had primary syphilis confirmed by dark field examination. The prevalence of cardiovascular syphilis in the HIV seropositive and seronegative groups was 14.3% and 2%, respectively (OR 8.2; 95% CI 1.1 to 61.5).
Two HIV seropositive individuals with cardiovascular syphilis had aortic root dilatation while the two HIV seronegative individuals had aortic aneurysm. The HIV seropositive individuals were asymptomatic with regard to cardiac status but one HIV seronegative individual had chest pain and the other was asymptomatic. None in the HIV seronegative group had aortic root dilatation (p<0.01). There was a theoretical possibility that aortic root dilatation could be a manifestation of HIV or opportunistic infections involving the heart. A parallel study done on cardiovascular involvement in HIV seropositive individuals from the same institute during the same time interval had revealed that none of the 61 non-syphilitic HIV seropositive individuals had aortic root dilatation, compared with 2 out of 14 with syphilis (p<0.01; paper in preparation).
The mean duration of diagnosing cardiovascular syphilis from the time of acquiring syphilis was 40 months (27 and 53) in the HIV seropositive group and 102 months (84 and 120) in the HIV seronegative group. The mean age of the HIV seropositive individuals who had cardiovascular syphilis was 31.5 years (29 and 34) and that of HIV seronegative individuals was 45.5 years (44 and 47).
The shorter duration for diagnosing cardio vascular syphilis from the time of acquiring syphilis for the HIV seropositive group (40 months) compared with the HIV seronegative group (102 months) (p<0.003) could be explained by the fact that HIV hastens the progression to late syphilis,3 which might be due to an alteration to the immune system. It could also be possible that HIV infected individuals seek medical attention because of opportunistic infections, which might have led to the earlier diagnosis of cardiac lesions because the two individuals with aortic root dilatation were asymptomatic with regard to cardiac status. The difference in the clinical manifestation of cardiovascular syphilis between these two groups could not be explained at this point of time.
MM designed the study, collected the data, interpreted the results, and analysed the results and statistics; SKG contributed to collecting data, interpretation of results and laboratory collaboration.
We thank M Muthu, retired Director and Professor of Anatomy, for his valuable guidance. We also thank D Muthukumar, cardiologist, Institute of Cardiology, Madras Medical College, Chennai, for his active participation and guidance in performing and interpreting ECHO and ECG.
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