798
The KS lesions remained untreated until the patient presented in 1985 complaining of an increase in their size and number. He declined radiotherapy and was treated with topical dinitrochlorobenzene. This was poorly tolerated and he was switched to 3-monthly courses of cryotherapy. He was last seen in October, 1988, when he was well. His KS lesions persisted unchanged and he refused further investigations. Professor Beral and her colleagues (Jan 10, p 123) suggest that KS in patients with AIDS may be caused by an as yet unidentified infectious agent, transmitted mainly by sexual contact. They also suggest that the incidence of KS is higher among adults with heterosexually acquired HIV from Haiti, the Caribbean, Central America, and Africa than in those from the United States. Our patient gave a history of homosexual contact in Haiti and the Caribbean in 1964, 1974, and 1978. In contrast to the patient described by Friedman-Kien et al, he was untreated for 18 years with no demonstrable adverse effects, suggesting that immediate treatment post diagnosis in this group of patients may not always be
fatigue, and a maculopapular eruption on her face and thorax. Her temperature was not recorded. All signs disappeared within a few days. She thought that this episode could have been a primary HIV infection, and on Sept 12 she was tested for HIV-1 antibody and was found negative by ELISA. Tests for HIV-1 antigen (Abbott), for IgM to viral capsid antigen Epstein-Barr virus (Biolab immunofluorescence assay), and for IgM to cytomegalovirus (Behring ELISA) were negative. On Nov 25 ELISAs for HIV-1 antibody (Abbott and Wellcome) were positive, but a western-blot for HIV-1 antibodies (Dupont) was positive for p24 only. A western blot for antibody to HIV-2 revealed the specific serological profile of HIV-2 infection. An analysis of sequential sera by radioimmunopredpitation assay is shown in the figure. One year after the probable exposure, the patient is clinically well, she has some non-painful cervical and axillary lymph nodes and two molluscum contagiosum lesions. Her immunological status is normal, with a total lymphocyte count of 2100/Itl and a CD4/CD8
mandatory.
Although the HIV status of the sexual partner is not known, it is likely that HIV-2 was transmitted at this sexual intercourse. patient had never been to Africa, nor had she had any blood transfusions, and it was her first sexual intercourse. The clinical manifestations were non-specific, and similar to those described for
We feel that this unusual case further illustrates the likely role of an infectious agent in the pathogenesis of KS, possibly even predating HIV infection. Department of Clinical Immunology, Royal Perth Hospital, Perth, Western Australia
Symptomatic
HIV-2
V. S. KITCHEN M. A. H. FRENCH R. L. DAWKINS
primary infection
SIR,-HIV-2-associated AIDS has been reported in West Africa, and the United States1-3 but the pathogenesis seems to differ from that of HIV-1, the very long asymptomatic stage being
ratio of 1 ’4. very The
HIV-1 infection. The incubation time was three weeks. It that HIV-2, like HIV-1, can induce a non-specific acute phase syndrome. HIV-2 infection should be looked for in individuals ii risk groups who present with such clinical features. A sensitive assay for HIV-2 antigen might prove useful for early acute
seems
diagnosis. JEAN-MARC BESNIER
Europe, the
striking characteristic.4,s
To our knowledge, HIV-2 primary infection has not yet been described. We report such a case. A 19-year-old white woman had her first sexual relationship, including anal intercourse, on Aug 17, 1988, with an African man, whose age, nationality, and HIV status are not known. Three weeks later she felt ill with painful cervical lymph nodes, shivering, intense most
FRANCIS BARIN ARMELLE BAILLOU FRANÇOIS LIARD PATRICK CHOUTET ALAIN GOUDEAU
Medicine Service A and Virology Laboratory, CHU Bretonneau, Tours, France
F, Rey MA, Katlama C, et al. Lymphadenopathy associated virus 2 m AIDS and AIDS-related complex: clinical and virological features in four patients Lancet 1987; i: 128-32. 2. Clavel F, Mansinho K, Chamaret S, et al. Human immunodeficiency virus type 2 infection associated with AIDS in Africa. N Engl J Med 1987; 316: 1180-85. 3. Ayanian JZ, Maguire JJ, Marlink RG, Essex M, Kanki PJ. HIV-2 infection in the United-States. N Engl J Med 1989; 320: 1422-23. 4. Dufoort G, Courouce AM, Ancelle-Park R, Bletry O. No clinical signs 14 years after HIV-2 transmission via blood transfusion. Lancet 1988; ii: 510. 5. Ancelle R, Bletry O, Baglin AC, Brun-Vezinet F, Rey MA, Godeau P. Long incubation penod for HIV-2 infection. Lancet 1987; 2: 510. 1. Brun-Vezinet
Prevention of pain
during injection of propofol
Radioimmunoprecipitation assays on sequential sera. 35S-cysteine labelled HIV-2T, purified viral preparation was used; procedure has been described 6 HIV-1 positive control. Lane 1 Lane 2 = H IV-2 positive control. Lane 3= H IV-negative control. Lanes 4-8: sequential sera from patient collected at days 26 (acute phase sample) 69, 84, 118, and 150 post-infection, respectively. =
SIR,-Propofol injections are often painful when given through small peripheral veins, the frequency of pain being up to 50%. One suggestion is that lignocaine should be administered before the injection or premixed with propofol. 1-3 Anaphylactoid reactions have been reported after lignocaine4 and propofol,’--8 and in the event of a reaction after propofol premixed with lignocaine, the manufacturers of propofol could deny responsibility on the ground that the formulation of their drug had been altered. Their data sheet states that propofol "should not be mixed prior to administration with other therapeutic agents or infusion fluids". One answer is to inject propofol through larger veins.9 However, if smaller veins are to be used, it would seem advisable not to mix propofol and lignocaine but to give lignocaine beforehand. No previous study has looked at the effect of varying the interval between the two injections. Observations were made on five randomly selected groups of 20 unpremedicated patients scheduled for minor gynaecological surgery. A tourniquet was applied to the proximal part of the forearm and a 23 G cannula was placed in a vein in the dorsum of the hand. In the control group the tourniquet was released and propofol (2 mg/kg) was injected over 30 s. In the other groups 2 ml 1%
The KS lesions remained untreated until the patient presented in 1985 complaining of an increase in their size and number. He declined radiotherapy and was treated with topical dinitrochlorobenzene. This was poorly tolerated and he was switched to 3-monthly courses of cryotherapy. He was last seen in October, 1988, when he was well. His KS lesions persisted unchanged and he refused further investigations. Professor Beral and her colleagues (Jan 10, p 123) suggest that KS in patients with AIDS may be caused by an as yet unidentified infectious agent, transmitted mainly by sexual contact. They also suggest that the incidence of KS is higher among adults with heterosexually acquired HIV from Haiti, the Caribbean, Central America, and Africa than in those from the United States. Our patient gave a history of homosexual contact in Haiti and the Caribbean in 1964, 1974, and 1978. In contrast to the patient described by Friedman-Kien et al, he was untreated for 18 years with no demonstrable adverse effects, suggesting that immediate treatment post diagnosis in this group of patients may not always be
fatigue, and a maculopapular eruption on her face and thorax. Her temperature was not recorded. All signs disappeared within a few days. She thought that this episode could have been a primary HIV infection, and on Sept 12 she was tested for HIV-1 antibody and was found negative by ELISA. Tests for HIV-1 antigen (Abbott), for IgM to viral capsid antigen Epstein-Barr virus (Biolab immunofluorescence assay), and for IgM to cytomegalovirus (Behring ELISA) were negative. On Nov 25 ELISAs for HIV-1 antibody (Abbott and Wellcome) were positive, but a western-blot for HIV-1 antibodies (Dupont) was positive for p24 only. A western blot for antibody to HIV-2 revealed the specific serological profile of HIV-2 infection. An analysis of sequential sera by radioimmunopredpitation assay is shown in the figure. One year after the probable exposure, the patient is clinically well, she has some non-painful cervical and axillary lymph nodes and two molluscum contagiosum lesions. Her immunological status is normal, with a total lymphocyte count of 2100/Itl and a CD4/CD8
mandatory.
Although the HIV status of the sexual partner is not known, it is likely that HIV-2 was transmitted at this sexual intercourse. patient had never been to Africa, nor had she had any blood transfusions, and it was her first sexual intercourse. The clinical manifestations were non-specific, and similar to those described for
We feel that this unusual case further illustrates the likely role of an infectious agent in the pathogenesis of KS, possibly even predating HIV infection. Department of Clinical Immunology, Royal Perth Hospital, Perth, Western Australia
Symptomatic
HIV-2
V. S. KITCHEN M. A. H. FRENCH R. L. DAWKINS
primary infection
SIR,-HIV-2-associated AIDS has been reported in West Africa, and the United States1-3 but the pathogenesis seems to differ from that of HIV-1, the very long asymptomatic stage being
ratio of 1 ’4. very The
HIV-1 infection. The incubation time was three weeks. It that HIV-2, like HIV-1, can induce a non-specific acute phase syndrome. HIV-2 infection should be looked for in individuals ii risk groups who present with such clinical features. A sensitive assay for HIV-2 antigen might prove useful for early acute
seems
diagnosis. JEAN-MARC BESNIER
Europe, the
striking characteristic.4,s
To our knowledge, HIV-2 primary infection has not yet been described. We report such a case. A 19-year-old white woman had her first sexual relationship, including anal intercourse, on Aug 17, 1988, with an African man, whose age, nationality, and HIV status are not known. Three weeks later she felt ill with painful cervical lymph nodes, shivering, intense most
FRANCIS BARIN ARMELLE BAILLOU FRANÇOIS LIARD PATRICK CHOUTET ALAIN GOUDEAU
Medicine Service A and Virology Laboratory, CHU Bretonneau, Tours, France
F, Rey MA, Katlama C, et al. Lymphadenopathy associated virus 2 m AIDS and AIDS-related complex: clinical and virological features in four patients Lancet 1987; i: 128-32. 2. Clavel F, Mansinho K, Chamaret S, et al. Human immunodeficiency virus type 2 infection associated with AIDS in Africa. N Engl J Med 1987; 316: 1180-85. 3. Ayanian JZ, Maguire JJ, Marlink RG, Essex M, Kanki PJ. HIV-2 infection in the United-States. N Engl J Med 1989; 320: 1422-23. 4. Dufoort G, Courouce AM, Ancelle-Park R, Bletry O. No clinical signs 14 years after HIV-2 transmission via blood transfusion. Lancet 1988; ii: 510. 5. Ancelle R, Bletry O, Baglin AC, Brun-Vezinet F, Rey MA, Godeau P. Long incubation penod for HIV-2 infection. Lancet 1987; 2: 510. 1. Brun-Vezinet
Prevention of pain
during injection of propofol
Radioimmunoprecipitation assays on sequential sera. 35S-cysteine labelled HIV-2T, purified viral preparation was used; procedure has been described 6 HIV-1 positive control. Lane 1 Lane 2 = H IV-2 positive control. Lane 3= H IV-negative control. Lanes 4-8: sequential sera from patient collected at days 26 (acute phase sample) 69, 84, 118, and 150 post-infection, respectively. =
SIR,-Propofol injections are often painful when given through small peripheral veins, the frequency of pain being up to 50%. One suggestion is that lignocaine should be administered before the injection or premixed with propofol. 1-3 Anaphylactoid reactions have been reported after lignocaine4 and propofol,’--8 and in the event of a reaction after propofol premixed with lignocaine, the manufacturers of propofol could deny responsibility on the ground that the formulation of their drug had been altered. Their data sheet states that propofol "should not be mixed prior to administration with other therapeutic agents or infusion fluids". One answer is to inject propofol through larger veins.9 However, if smaller veins are to be used, it would seem advisable not to mix propofol and lignocaine but to give lignocaine beforehand. No previous study has looked at the effect of varying the interval between the two injections. Observations were made on five randomly selected groups of 20 unpremedicated patients scheduled for minor gynaecological surgery. A tourniquet was applied to the proximal part of the forearm and a 23 G cannula was placed in a vein in the dorsum of the hand. In the control group the tourniquet was released and propofol (2 mg/kg) was injected over 30 s. In the other groups 2 ml 1%
