Clinical anti laboraloru sluOies I
I I
I
II
Psoriasis and human immunodeficiency virus infection Marian L. Obuch, MD, Toby A. Maurer, MD, Brad Becker, MD, and Timothy G. Berger, M D San Francisco, California
Background." Psoriasis associated with human immunodeficiency virus (HIV) infection has been reported to be severe and perhaps associated with decreased survival. Objective: Our purpose was to document the natural history, response to therapy, and effect of psoriasis and its treatment on survival in HIV-infected patients with psoriasis. Methods: This was an observational cohort study of 50 persons with psoriasis and HIV infection followed up during a 2-year period. Results: In one third of the patients the psoriasis appeared before 1978, the year when HIV seroconversion began in San Francisco (group I). In two thirds psoriasis developed after 1978 (group II). Group I had a lower mean age of onset (19 vs 36 years) and more commonly had a family history of psoriasis. Palmoplantar and inverse psoriasis were more common in group II. Severe psoriasis occurred in one fourth of this group (12 of 50 patients). The median survival in this group after diagnosis of acquired immunodeficiency syndrome (AIDS) was 19 months, which is comparable to the median survival for all AIDS patients diagnosed in San Francisco between 1984 and 1990. Conclusion: Psoriasis in the setting of HIV disease may be mild, moderate, or severe. Standard therapies and zidovudine are effective in management. Survival does not seem to be adversely affected by the presence of psoriasis or its therapy. (J AM ACAD DERMATOL 1992;27:667-73.) Psoriasis, often severe, has been reported in patients infected with the human immunodeficiency virus ( H I V ) , 13 and it has been suggested that it implies a poor prognosis. 2 The number of reported HIV-infected patients with psoriasis is limited and follow-up has in general been less than 1 year. W e report our experience with 50 HIV-infected psoriasis patients seen in 2 years in one university-based hospital system. M E T H O D S AND STUDY DESIGN Fifty persons (49 men, 1 woman) with psoriasis and HIV infection were identified and their medical records reviewed. These patients were enrolled in an observational longitudinal cohort study during a 2-year period (19881990). Patients were seen in the outpatient Dermatology and HIV Clinics of San Francisco General Hospital, the University of California, San Francisco Medical Center, and the San Francisco Veterans Administration Medical
From the Department of Dermatology,San FranciscoGeneral Hospital and Universityof California, San Francisco. Acceptedfor publication April 21, 1992. Reprints not available. 16/1/38764
Center. Approximately 2000 HIV-infected patients were seen in these hospitals during this period. Exclusion criteria included anyone refusing to participate, anyone younger than 18 years of age, and anyone with significant cognitive impairment. The diagnosis of psoriasis was made clinically by one of the authors (T. B.) in all but three participants: two had atypical lesions for which biopsy findings indicated guttate psoriasis; and one had a previous history of psoriasis that had been documented by skin biopsy findings. Histologic confirmation was not required in the rest of the group. Classification of the stage of HIV infection followed the Centers for Disease Control (CDC) guidelines. 4 Patients were classified as having HIV infection-asymptomatic, HIV infection-symptomatic (previously called acquired immunodefieiency syndrome [AIDS]-related complex), or AIDS. Psoriasis is not a CDC-defined, HIV-associated sign. Patients receiving zidovudine (AZT) were questioned about any changes in their psoriasis while taking the drug. The skin examination recorded all psoriatic lesions, including their morphology, extent, and severity. Representative photographs were taken. Mild psoriasis was defined as involving less than 10% of the body surface, moderate psoriasis as involving between 10% and 50%, and severe psoriasis as involving more than 50%. Joint abnormalities were sought. 667
668
Journal of the American Academy of Dermatology
Obuch et aL
20 I
Psoriasis [N = 49) HIV (N = 310, Hap B)
15 Q_
o 10
i
IL IIII
5
0
I
1960 62
64
66
,,I ,,, 68 1970 72
74
76
78 1980 82
84
86
88 1990
YEAR OF DIAGNOSIS
Fig. 1. Year of onset of psoriasis and its association with seroconversion in San Francisco. Note large number of new psoriasis cases occurring after seroconversion to HIV by about 5 years. Total helper T-cell (CD4) counts were available in 32 participants (64%). (CD4 counts were not routinely available in our institution during the course of this study.) Throat cultures for group A r-hemolytic streptococci were obtained in all participants with a guttate flare (n = 10). In those patients with a previous history of guttate psoriasis, the medical record was reviewed for throat culture results. A complete drug history was obtained to look specifically for medications known to worsen psoriasis. Patients were followed up at weekly to 3-month intervals, depending on the severity of psoriasis, for a maximum of 18 months or until death. Vital status and subsequent diagnoses were ascertained through prospective follow-up until January 1991 by reviewing material from medical records and from the AIDS surveillance system in San Francisco. Five participants (10%) were lost to follow-up. Values comparing descriptive results in group 1 and group 2 participants were analyzed with the chi-square and odds ratio tests. Median survival and the cumulative probability of survival at 1 and 2 years after the diagnosis of AIDS were calculated with the KaplanMeier product limit method.5 The p values for testing differences in survival curves between this cohort and persons diagnosed with AIDS in San Francisco were two-sided values from the Mantel-Haenszel chi-square test. s An adjusted X2 was calculated to compensate for a possible 5% prevalence rate of psoriasis in the San Francisco cohort. The p values for testing differences in survival curves between group 1 atad group 2 were from the Gehan-Wilcoxon test. 7 RESULTS Thirty-five participants (70%) in the study acquired HIV infection through male homosexual contact. Eleven participants (22%) had two risk
factors: intravenous drug use and homosexual contact. Intravenous drug use was the HIV risk factor in three participants (6%). The ethnic diversity and age distribution of study participants reflect a representative cross-section of HIV-infected persons in San Francisco with 74% whites, 16% Hispanics, 6% blacks, and 4% of mixed ethnicity, s To investigate the relation between HIV infection and psoriasis, we divided the cohort into two groups on the basis of the date of onset of their psoriasis. HIV seropositivity was rare to nonexistent in San Francisco before 1978 and the time of HIV sero= conversion was between 1978 and 1984; 1982 was the peak year for acquiring HIV infection. This was based on data derived from a cohort of homosexual men in whom serially banked blood was collected for several years as part of a large hepatitis B vaccine trial. 9 In approximately one third (15 of 49) of our cohort psoriasis developed before 1978 (group I) and they were presumed to be HIV seronegative when their psoriasis appeared. In approximately two thirds (34 of 49) psoriasis developed after 1978 (group II), either coinciding with or after the period of peak HIV seroconversion in San Francisco. In this group, the onset of psoriasis is represented by a curve that mirrors the curve of HIV seroconversion in San Francisco, displaced by 5 years (Fig. 1). At study entry 9 of 15 group I patients (60%) had AIDS, 3 of 15 (20%) had symptomatic HIV disease, and 3 of 15 (20%) were without symptoms. Group II had a similar distribution; 29 of 34 (82%) had AIDS, 4 of 34 (12%) had symptomatic HIV disease, and 2 of 34 (6%) were asymptomatic. Of the 34 patients whose psoriasis began after
Volume 27 Number 5, Part 1 November 1992
Psoriasis and H I V
669
Table I. Pattern of psoriasis* GroupII (n = 34)
Total (n = 49)
GroupI (n = 15)
Ty~
No.
%
No.
%
No.
Vulgaris Inverse Guttate Palmoplantar Erythroderrnic Pustular]"
38 18 14 12 7 4
78 37 29 24 14 8
25 14 8 11 4 4
71 41 29 29 12 12
13
87
4
27 40
6
[
%
1
7
3 0
20 0
*Values of p > 0.05. Not statistically significant by chi-square test. tlncludes palmoplantar pustulosis.
presumed infection with HIV (group II), there was a wide variety of HIV disease activity at the time of onset of psoriasis: 15% were asymptomatic, 35% had symptomatic HIV infection, 24% had AIDS, and 26% did not remember whether they were symptomatic at the time of the onset of their psoriasis (but they did not have AIDS). The mean age of psoriasis onset differed significantly between group I and group II (p < 0.001). In patients in whom psoriasis developed before they became HIV infected (group I), the mean age of onset was 19 years (range 10 to 30 years), whereas the mean age of onset in subjects in whom psoriasis developed after HIV infection (group II) was 36 years (range 23 to 58 years). A family history of psoriasis was significantly more common in group I than in group II (40% vs 9%, p < 0.01). The overall prevalence of seborrheic dermatitis was 69% and did not differ between group I and group II. More than one morphologic pattern of psoriasis was commonly observed either concurrently or sequentially in both groups. Table I outlines the various patterns. The most common pattern in both groups was psoriasis vulgaris. An inverse pattern with prominent plaques in the scalp, axillae, and groin (Fig. 2) was more common when HIV infection preceded the onset of psoriasis (group II) (odds ratio [OR] 1.9, confidence interval [CI] .[0.6 to 6.5]). Palmoplantar involvement was also more common in this group (OR, 4.73; CI, 0.76 to 29.28) (Fig. 3). Guttate psoriasis was observed in both groups. In those patients from whom throat cultures for group A/3-hemolytic streptococci had been obtained during guttate flares, two of two group I patients had positive cultures, whereas only three of eight group II patients had a positive culture. In both group I patients guttate lesions cleared with antibiotic therapy, whereas guttate psoriasis in group II
patients was refractory to antibiotic therapy. These numbers are too small for statistical comparison. Erythrodermic psoriasis was seen in both groups and was not significantly different in either group (OR, 0.52; CI, 0.12 to 2.47). Localized or generalized pustular psoriasis was observed in four group II patients but not in group I patients. The severity of psoriasis was documented over time. The relation between psoriasis severity and stage of HIV disease is shown in Table II. Patients in all stages of disease had all grades of psoriasis severity, except that no patients with asymptomatic HIV infection had severe psoriasis. Severe psoriasis developed in approximately one-fourth of this cohort (12 of 50 patients). Twenty percent of group I patients (3 of 15) had severe psoriasis at some time, compared with 27% of group II patients (9 of 34). Analysis of the relation between severity of psoriasis and CD4 count was possible to a limited extent because only 32 of 50 patients had T-cell panels (Table III). Six of 22 participants (27%) with severe psoriasis had CD4 counts less than 200, compared with 1 of 10 participants (10%) who had CD4 counts more than 200. This trend did not reach statistical validity (OR, 2.49; CI, 0.35 to 17.4; p = 0.526). In addition, severity of psoriasis was not associated with survival (OR, 0.995; CI, 0.269 to 3.67; p = 0.742) (Table IV). In one patient in group I (7%) arthritis developed compared with six (18%) in group II (OR, 2.2; CI, 0.335 to 14.5;p = 0.569). Nopatients in group I met the criteria for Reiter's syndrome, although two patients in group II did. Many patients (31 of 50) were receiving AZT at the time of enrollment. They were asked to evaluate in retrospect the change in severity of their psoriasis after AZT therapy had been started. A significant proportion ( 12 of 31 patients) could either not recall
670
Obuch et aI.
Journal of the American Academy of Dermatology
Fig. 2. Typical inverse psoriasis. or had other treatments initiated for their psoriasis at the same time A Z T was begun; this precluded evaluation of the effect of AZT. Improvement of psoriasis was noted by 11 patients (35% of the whole group or 58% of those who could recall); of these, only two described marked improvement. Some of these patients had psoriatic flares when the A Z T dose was decreased or discontinued. The improvement with A Z T therapy was not preferentially reported in group II versus group I patients: 8 of 14 versus 3 of 5 or approximately 60% of those who could recall. Our data collection methods did not allow us to evaluate the relation between AZT dose and response. Patients with mild to moderate psoriasis were treated mainly with topical steroids, tars, and anthralin. Of the 37 patients with mild to moderate psoriasis, 15 patients received UVB therapy, three of whom also received PUVA. Nine of 13 patients with severe psoriasis were treated with UVB therapy, three of whom also received PUVA. Some patients with severe psoriasis were also treated, with etretinate (7 of 13) and methotrexate (2 of 13). There was no association noted between the presence of Kaposi's sarcoma (KS) and light therapy in this cohort. Seven of the patients with KS had received UVB or PUVA and nine had not. Only one patient receiving UVB therapy had progression of his KS. The cumulative probability of survival at 1 year after AIDS diagnosis was comparable in both groups: 55.5% for group I and 61.5~ for group II
Fig. 3. Severe plantar psoriasis(A) before AZT therapy, and (B) after 3 weeks of treatment with AZT.
(Table V). In this cohort, median survival for those diagnosed with AIDS between 1984 and 1990 was 19 months (range 1 to 62 months) with 1-year cumulative survival at 65.5% and 2-year cumulative survival at 35.5%. Survival was comparable to the cumulative survival for AIDS patients diagnosed in San Francisco between 1984 and 1990 where 1-year survival was 57.5% and 2-year survival was 22% (Table V).* Stratifying by year of diagnosis of AIDS and comparing median months of survival and cumulative survival to San Francisco AIDS patients, there was no statistical difference between survival curves for the years 1987, 1988, and 1989 (data not shown). Adjusting for a 5% prevalence rate of psoriasis in the San Francisco AIDS population, there still was no statistical difference between the survival curve of the study cohort and the San Francisco AIDS patients (data not shown). *Letup G, Hirozawa AM, Aranata MR. Survival of AIDS patients in San Francisco by year of diagnosis ( 1981-1990). VII International Conference on AIDS. Florence, June 18, 1991.
Volume 27 N u m b e r 5, Part 1 November 1992
Psoriasis and H I V
671
Table II. Severity of psoriasis at worst Group I and Group 11 n = 49 (%)
Mild
t
,
Asymptomatic Symptomatic AIDS
5 (10) 6 (12) 38 (78)
,
Moderate
Severe
4 (8) 2 (4) 12 (24)
-3 (6) 10 (20)
,=
1 (2) 1 (2) 16 (33)
Mild,
I I
I
II
Psoriasis and human immunodeficiency virus infection Marian L. Obuch, MD, Toby A. Maurer, MD, Brad Becker, MD, and Timothy G. Berger, M D San Francisco, California
Background." Psoriasis associated with human immunodeficiency virus (HIV) infection has been reported to be severe and perhaps associated with decreased survival. Objective: Our purpose was to document the natural history, response to therapy, and effect of psoriasis and its treatment on survival in HIV-infected patients with psoriasis. Methods: This was an observational cohort study of 50 persons with psoriasis and HIV infection followed up during a 2-year period. Results: In one third of the patients the psoriasis appeared before 1978, the year when HIV seroconversion began in San Francisco (group I). In two thirds psoriasis developed after 1978 (group II). Group I had a lower mean age of onset (19 vs 36 years) and more commonly had a family history of psoriasis. Palmoplantar and inverse psoriasis were more common in group II. Severe psoriasis occurred in one fourth of this group (12 of 50 patients). The median survival in this group after diagnosis of acquired immunodeficiency syndrome (AIDS) was 19 months, which is comparable to the median survival for all AIDS patients diagnosed in San Francisco between 1984 and 1990. Conclusion: Psoriasis in the setting of HIV disease may be mild, moderate, or severe. Standard therapies and zidovudine are effective in management. Survival does not seem to be adversely affected by the presence of psoriasis or its therapy. (J AM ACAD DERMATOL 1992;27:667-73.) Psoriasis, often severe, has been reported in patients infected with the human immunodeficiency virus ( H I V ) , 13 and it has been suggested that it implies a poor prognosis. 2 The number of reported HIV-infected patients with psoriasis is limited and follow-up has in general been less than 1 year. W e report our experience with 50 HIV-infected psoriasis patients seen in 2 years in one university-based hospital system. M E T H O D S AND STUDY DESIGN Fifty persons (49 men, 1 woman) with psoriasis and HIV infection were identified and their medical records reviewed. These patients were enrolled in an observational longitudinal cohort study during a 2-year period (19881990). Patients were seen in the outpatient Dermatology and HIV Clinics of San Francisco General Hospital, the University of California, San Francisco Medical Center, and the San Francisco Veterans Administration Medical
From the Department of Dermatology,San FranciscoGeneral Hospital and Universityof California, San Francisco. Acceptedfor publication April 21, 1992. Reprints not available. 16/1/38764
Center. Approximately 2000 HIV-infected patients were seen in these hospitals during this period. Exclusion criteria included anyone refusing to participate, anyone younger than 18 years of age, and anyone with significant cognitive impairment. The diagnosis of psoriasis was made clinically by one of the authors (T. B.) in all but three participants: two had atypical lesions for which biopsy findings indicated guttate psoriasis; and one had a previous history of psoriasis that had been documented by skin biopsy findings. Histologic confirmation was not required in the rest of the group. Classification of the stage of HIV infection followed the Centers for Disease Control (CDC) guidelines. 4 Patients were classified as having HIV infection-asymptomatic, HIV infection-symptomatic (previously called acquired immunodefieiency syndrome [AIDS]-related complex), or AIDS. Psoriasis is not a CDC-defined, HIV-associated sign. Patients receiving zidovudine (AZT) were questioned about any changes in their psoriasis while taking the drug. The skin examination recorded all psoriatic lesions, including their morphology, extent, and severity. Representative photographs were taken. Mild psoriasis was defined as involving less than 10% of the body surface, moderate psoriasis as involving between 10% and 50%, and severe psoriasis as involving more than 50%. Joint abnormalities were sought. 667
668
Journal of the American Academy of Dermatology
Obuch et aL
20 I
Psoriasis [N = 49) HIV (N = 310, Hap B)
15 Q_
o 10
i
IL IIII
5
0
I
1960 62
64
66
,,I ,,, 68 1970 72
74
76
78 1980 82
84
86
88 1990
YEAR OF DIAGNOSIS
Fig. 1. Year of onset of psoriasis and its association with seroconversion in San Francisco. Note large number of new psoriasis cases occurring after seroconversion to HIV by about 5 years. Total helper T-cell (CD4) counts were available in 32 participants (64%). (CD4 counts were not routinely available in our institution during the course of this study.) Throat cultures for group A r-hemolytic streptococci were obtained in all participants with a guttate flare (n = 10). In those patients with a previous history of guttate psoriasis, the medical record was reviewed for throat culture results. A complete drug history was obtained to look specifically for medications known to worsen psoriasis. Patients were followed up at weekly to 3-month intervals, depending on the severity of psoriasis, for a maximum of 18 months or until death. Vital status and subsequent diagnoses were ascertained through prospective follow-up until January 1991 by reviewing material from medical records and from the AIDS surveillance system in San Francisco. Five participants (10%) were lost to follow-up. Values comparing descriptive results in group 1 and group 2 participants were analyzed with the chi-square and odds ratio tests. Median survival and the cumulative probability of survival at 1 and 2 years after the diagnosis of AIDS were calculated with the KaplanMeier product limit method.5 The p values for testing differences in survival curves between this cohort and persons diagnosed with AIDS in San Francisco were two-sided values from the Mantel-Haenszel chi-square test. s An adjusted X2 was calculated to compensate for a possible 5% prevalence rate of psoriasis in the San Francisco cohort. The p values for testing differences in survival curves between group 1 atad group 2 were from the Gehan-Wilcoxon test. 7 RESULTS Thirty-five participants (70%) in the study acquired HIV infection through male homosexual contact. Eleven participants (22%) had two risk
factors: intravenous drug use and homosexual contact. Intravenous drug use was the HIV risk factor in three participants (6%). The ethnic diversity and age distribution of study participants reflect a representative cross-section of HIV-infected persons in San Francisco with 74% whites, 16% Hispanics, 6% blacks, and 4% of mixed ethnicity, s To investigate the relation between HIV infection and psoriasis, we divided the cohort into two groups on the basis of the date of onset of their psoriasis. HIV seropositivity was rare to nonexistent in San Francisco before 1978 and the time of HIV sero= conversion was between 1978 and 1984; 1982 was the peak year for acquiring HIV infection. This was based on data derived from a cohort of homosexual men in whom serially banked blood was collected for several years as part of a large hepatitis B vaccine trial. 9 In approximately one third (15 of 49) of our cohort psoriasis developed before 1978 (group I) and they were presumed to be HIV seronegative when their psoriasis appeared. In approximately two thirds (34 of 49) psoriasis developed after 1978 (group II), either coinciding with or after the period of peak HIV seroconversion in San Francisco. In this group, the onset of psoriasis is represented by a curve that mirrors the curve of HIV seroconversion in San Francisco, displaced by 5 years (Fig. 1). At study entry 9 of 15 group I patients (60%) had AIDS, 3 of 15 (20%) had symptomatic HIV disease, and 3 of 15 (20%) were without symptoms. Group II had a similar distribution; 29 of 34 (82%) had AIDS, 4 of 34 (12%) had symptomatic HIV disease, and 2 of 34 (6%) were asymptomatic. Of the 34 patients whose psoriasis began after
Volume 27 Number 5, Part 1 November 1992
Psoriasis and H I V
669
Table I. Pattern of psoriasis* GroupII (n = 34)
Total (n = 49)
GroupI (n = 15)
Ty~
No.
%
No.
%
No.
Vulgaris Inverse Guttate Palmoplantar Erythroderrnic Pustular]"
38 18 14 12 7 4
78 37 29 24 14 8
25 14 8 11 4 4
71 41 29 29 12 12
13
87
4
27 40
6
[
%
1
7
3 0
20 0
*Values of p > 0.05. Not statistically significant by chi-square test. tlncludes palmoplantar pustulosis.
presumed infection with HIV (group II), there was a wide variety of HIV disease activity at the time of onset of psoriasis: 15% were asymptomatic, 35% had symptomatic HIV infection, 24% had AIDS, and 26% did not remember whether they were symptomatic at the time of the onset of their psoriasis (but they did not have AIDS). The mean age of psoriasis onset differed significantly between group I and group II (p < 0.001). In patients in whom psoriasis developed before they became HIV infected (group I), the mean age of onset was 19 years (range 10 to 30 years), whereas the mean age of onset in subjects in whom psoriasis developed after HIV infection (group II) was 36 years (range 23 to 58 years). A family history of psoriasis was significantly more common in group I than in group II (40% vs 9%, p < 0.01). The overall prevalence of seborrheic dermatitis was 69% and did not differ between group I and group II. More than one morphologic pattern of psoriasis was commonly observed either concurrently or sequentially in both groups. Table I outlines the various patterns. The most common pattern in both groups was psoriasis vulgaris. An inverse pattern with prominent plaques in the scalp, axillae, and groin (Fig. 2) was more common when HIV infection preceded the onset of psoriasis (group II) (odds ratio [OR] 1.9, confidence interval [CI] .[0.6 to 6.5]). Palmoplantar involvement was also more common in this group (OR, 4.73; CI, 0.76 to 29.28) (Fig. 3). Guttate psoriasis was observed in both groups. In those patients from whom throat cultures for group A/3-hemolytic streptococci had been obtained during guttate flares, two of two group I patients had positive cultures, whereas only three of eight group II patients had a positive culture. In both group I patients guttate lesions cleared with antibiotic therapy, whereas guttate psoriasis in group II
patients was refractory to antibiotic therapy. These numbers are too small for statistical comparison. Erythrodermic psoriasis was seen in both groups and was not significantly different in either group (OR, 0.52; CI, 0.12 to 2.47). Localized or generalized pustular psoriasis was observed in four group II patients but not in group I patients. The severity of psoriasis was documented over time. The relation between psoriasis severity and stage of HIV disease is shown in Table II. Patients in all stages of disease had all grades of psoriasis severity, except that no patients with asymptomatic HIV infection had severe psoriasis. Severe psoriasis developed in approximately one-fourth of this cohort (12 of 50 patients). Twenty percent of group I patients (3 of 15) had severe psoriasis at some time, compared with 27% of group II patients (9 of 34). Analysis of the relation between severity of psoriasis and CD4 count was possible to a limited extent because only 32 of 50 patients had T-cell panels (Table III). Six of 22 participants (27%) with severe psoriasis had CD4 counts less than 200, compared with 1 of 10 participants (10%) who had CD4 counts more than 200. This trend did not reach statistical validity (OR, 2.49; CI, 0.35 to 17.4; p = 0.526). In addition, severity of psoriasis was not associated with survival (OR, 0.995; CI, 0.269 to 3.67; p = 0.742) (Table IV). In one patient in group I (7%) arthritis developed compared with six (18%) in group II (OR, 2.2; CI, 0.335 to 14.5;p = 0.569). Nopatients in group I met the criteria for Reiter's syndrome, although two patients in group II did. Many patients (31 of 50) were receiving AZT at the time of enrollment. They were asked to evaluate in retrospect the change in severity of their psoriasis after AZT therapy had been started. A significant proportion ( 12 of 31 patients) could either not recall
670
Obuch et aI.
Journal of the American Academy of Dermatology
Fig. 2. Typical inverse psoriasis. or had other treatments initiated for their psoriasis at the same time A Z T was begun; this precluded evaluation of the effect of AZT. Improvement of psoriasis was noted by 11 patients (35% of the whole group or 58% of those who could recall); of these, only two described marked improvement. Some of these patients had psoriatic flares when the A Z T dose was decreased or discontinued. The improvement with A Z T therapy was not preferentially reported in group II versus group I patients: 8 of 14 versus 3 of 5 or approximately 60% of those who could recall. Our data collection methods did not allow us to evaluate the relation between AZT dose and response. Patients with mild to moderate psoriasis were treated mainly with topical steroids, tars, and anthralin. Of the 37 patients with mild to moderate psoriasis, 15 patients received UVB therapy, three of whom also received PUVA. Nine of 13 patients with severe psoriasis were treated with UVB therapy, three of whom also received PUVA. Some patients with severe psoriasis were also treated, with etretinate (7 of 13) and methotrexate (2 of 13). There was no association noted between the presence of Kaposi's sarcoma (KS) and light therapy in this cohort. Seven of the patients with KS had received UVB or PUVA and nine had not. Only one patient receiving UVB therapy had progression of his KS. The cumulative probability of survival at 1 year after AIDS diagnosis was comparable in both groups: 55.5% for group I and 61.5~ for group II
Fig. 3. Severe plantar psoriasis(A) before AZT therapy, and (B) after 3 weeks of treatment with AZT.
(Table V). In this cohort, median survival for those diagnosed with AIDS between 1984 and 1990 was 19 months (range 1 to 62 months) with 1-year cumulative survival at 65.5% and 2-year cumulative survival at 35.5%. Survival was comparable to the cumulative survival for AIDS patients diagnosed in San Francisco between 1984 and 1990 where 1-year survival was 57.5% and 2-year survival was 22% (Table V).* Stratifying by year of diagnosis of AIDS and comparing median months of survival and cumulative survival to San Francisco AIDS patients, there was no statistical difference between survival curves for the years 1987, 1988, and 1989 (data not shown). Adjusting for a 5% prevalence rate of psoriasis in the San Francisco AIDS population, there still was no statistical difference between the survival curve of the study cohort and the San Francisco AIDS patients (data not shown). *Letup G, Hirozawa AM, Aranata MR. Survival of AIDS patients in San Francisco by year of diagnosis ( 1981-1990). VII International Conference on AIDS. Florence, June 18, 1991.
Volume 27 N u m b e r 5, Part 1 November 1992
Psoriasis and H I V
671
Table II. Severity of psoriasis at worst Group I and Group 11 n = 49 (%)
Mild
t
,
Asymptomatic Symptomatic AIDS
5 (10) 6 (12) 38 (78)
,
Moderate
Severe
4 (8) 2 (4) 12 (24)
-3 (6) 10 (20)
,=
1 (2) 1 (2) 16 (33)
Mild,
