Social and psychosocial effects on atopic eczema symptom severity - a scoping review of observational studies published from 1989 to 2019.

Social and psychosocial factors are thought to have an effect on the course of atopic eczema. The aim of this scoping review was to search for and summarize observational studies that investigated the effects of (psycho-)social factors on symptoms in atopic eczema and to identify research gaps. We searched PubMed and PsycINFO for literature published between 1 January 1989 and 31 December 2019 using a systematic search strategy. We included observational studies that analysed the effect of (psycho-)social factors on symptom severity in atopic eczema patients. Reviews and non-observational studies, articles with research on animals, and articles with languages other than English or German were excluded. We identified 17 observational studies that met the inclusion criteria. Several studies found significant results for an exacerbating effect of stress on atopic eczema severity. Although coping and social support does not seem to moderate the effect of stress, coping strategies might mediate the impact that stress has on symptoms. Depression is associated with atopic eczema severity. The effect of depression as a consequence of atopic eczema severity is stronger than the effect as an exacerbating factor. Illness identity, anger, frustration and psychosomatic states have been found to affect atopic eczema symptoms. For attachment security, anxiety and social status, contradictory results were found. Statistically non-significant results were reported for personality, being in a partnership, satisfaction with the partnership, childhood experiences and body consciousness. Only the association between psychosocial stress and atopic eczema symptom severity seems robust. To date, other (psycho-)social factors, especially protective and health-promoting factors, were analysed only in a few studies, mostly with low sample sizes and cross-sectional design. Biopsychosocial interactions between stress, protective factors and the course of atopic eczema as well as the psycho-neuroimmunological mechanisms underlying those interactions are considered fields for future research contributions.

Brain HMPAO-SPECT and ocular microangiopathic syndrome in HIV-1-infected patients.

OBJECTIVE: The pathogenesis of neurologic and neuropsychologic dysfunction in HIV-1 infection is unclear. The purpose of the study was to determine an association between cerebral perfusion and HIV-1-related ocular microangiopathic syndrome. METHODS: We studied 28 HIV-1-infected patients, seven of whom presented with asymptomatic HIV infection, nine with lymphadenopathy syndrome or AIDS-related complex, and 12 with AIDS. Cerebral perfusion was semi-quantitatively measured by single photon emission computed tomography of the brain using technetium-99 hexamethyl-propylenamine oxime (HMPAO-SPECT). The conjunctival manifestation of HIV-1-related microangiopathic syndrome was measured by a rating scale determining blood-flow sludging and, retinal cotton-wool spots were counted. CD4 count, neopterin, beta 2-microglobulin (beta 2M), haemoglobin, and age were determined as putative confounding variables. RESULTS: Mean conjunctival sludge in patients with normal HMPAO-SPECT findings was 1.3 +/- 0.5 (mean +/- s.e.m.); no cotton-wool spots were present. In patients with slightly impaired HMPAO-SPECT, it was 2.1 +/- 0.6 and mean cotton-wool spot count was 1.1 +/- 0.4. In patients with severely impaired HMPAO-SPECT, mean conjunctival sludge was 4.5 +/- 0.3 and mean cotton-wool spot count was 4.9 +/- 1.1 HMPAO-SPECT findings were closely associated with conjunctival sludge (r = 0.72; P < 0.001) and number of cotton-wool spots (r = 0.78; P < 0.001), whereas only a slight association with staging of HIV disease was found (P = 0.052). Analysis of covariance controlling for CD4 count neopterin, beta 2M, age, and haemoglobin demonstrated a significant difference between the three HMPAO-SPECT groups for both the number of cotton-wool spots (P < 0.001) and the conjunctival sludge rating (P < 0.001). CONCLUSION: There was a close association between severity of HIV-1-related ocular microangiopathic syndrome and severity of cerebral hypoperfusion. Microvascular alterations might contribute to the pathogenesis of neurological and neuropsychological symptoms in patients with HIV-1 disease. Furthermore, the conjunctival sludge rating and the number of cotton-wool spots might be appropriate indicators for severity of microvascular changes of the central nervous system [corrected].

HIV-related ocular microangiopathic syndrome and color contrast sensitivity.

PURPOSE: Color vision deficits in patients with acquired immunodeficiency syndrome (AIDS) or human immunodeficiency virus (HIV) disease were reported, and a retinal pathogenic mechanism was proposed. The purpose of this study was to evaluate the association of color vision deficits with HIV-related retinal microangiopathy. METHODS: A computer graphics system was used to measure protan, deutan, and tritan color contrast sensitivity (CCS) thresholds in 60 HIV-infected patients. Retinal microangiopathy was measured by counting the number of cotton-wool spots, and conjunctival blood-flow sludging was determined. Additional predictors were CD4+ count, age, time on aerosolized pentamidine, time on zidovudine, and Walter Reed staging. The relative influence of each predictor was calculated by stepwise multiple regression analysis (inclusion criterion; incremental P value = < 0.05) using data for the right eyes (RE). The results were validated by using data for the left eyes (LE) and both eyes (BE). RESULTS: The only included predictors in multiple regression analyses for the RE were number of cotton-wool spots (tritan: R = .70; deutan: R = .46; and protan: R = .58; P < .0001 for all axes) and age (tritan: increment of R [Ri] = .05, P = .002; deutan: Ri = .10, P = .004; and protan: Ri = .05, P = .002). The predictors time on zidovudine (Ri = .05, P = .002) and Walter Reed staging (Ri = .03, P = .01) were additionally included in multiple regression analysis for tritan LE. The results for deutan LE were comparable to those for the RE. In the analysis for protan LE, the only included predictor was number of cotton-wool spots. In the analyses for BE, no further predictors were included. The predictors Walter Reed staging and CD4+ count showed a significant association with all three criteria in univariate analysis. Additionally, tritan CCS was significantly associated with conjunctival blood-flow sludging. CONCLUSION: CCS deficits in patients with HIV disease are primarily associated with the number of cotton-wool spots. Results of this study are in accordance with the hypothesis that CCS deficits are in a relevant part caused by neuroretinal damage secondary to HIV-related microangiopathy.

Impairment of colour contrast sensitivity and neuroretinal dysfunction in patients with symptomatic HIV infection or AIDS.

Ophthalmic and neurological complications are frequent findings in patients with AIDS. Little is known about neuroretinal dysfunction in patients with HIV infection. The purpose of this study was to measure and evaluate colour vision in patients with HIV infection or AIDS. Colour contrast sensitivity tests were performed on 75 patients (150 eyes) in different stages of HIV infection. A highly sensitive computer graphics system was used to measure tritan, deutan, and protan colour contrast thresholds. Patients were classified into three clinical groups: (a) asymptomatic HIV infection, (b) lymphadenopathy syndrome or AIDS-related complex, and (c) AIDS. Overall, tritan (p < 0.0001), deutan (p = 0.003), and protan (p = 0.009) colour contrast sensitivities were significantly impaired in patients with HIV infection compared with normal controls. Colour thresholds in patients with asymptomatic HIV infection (mean tritan threshold: 4.33; deutan: 4.41; protan: 3.97) were not impaired compared with normal controls. Colour vision was slightly impaired in patients with lymphadenopathy syndrome or AIDS-related complex (tritan: 6.25 (p < 0.0001); deutan: 4.99 (p = 0.02); protan: 4.45 (p = 0.05)). In patients with AIDS the impairment was even more marked (tritan: 7.66 (p < 0.0001); deutan: 5.15 (p < 0.0009); protan: 4.63 (p = 0.004)). Analysis of covariance controlling for age demonstrated a close association between impairment of tritan colour contrast sensitivity and progression of HIV disease (p < 0.0001). Following Köllner's rule, our study suggests that neuroretinal dysfunction occurs in patients with symptomatic HIV infection or AIDS. This is emphasised by the finding that the relative impairment in tritan vision compared with deutan/protan vision might reflect the difference in the number of cones or receptive fields. Measurement of tritan colour contrast sensitivity appears to be an appropriate and easily applicable method to detect early neuroretinal dysfunction in patients with HIV disease.

Influence of selective management on the prognosis and the risk of rupture of abdominal aortic aneurysms.

A total of 199 patients with abdominal aortic aneurysms were followed up to investigate the influence of selective management on the prognosis and the risk rupture of abdominal aortic aneurysms. Decisions to operate or to continue watchful waiting with treatment of risk factors for expansion were based on aneurysm size, expansion rate, aneurysm-related symptoms, and individual operative risk. Rupture occurred in eight cases. All aneurysms were larger than 5 cm, and six were larger than 6 cm in diameter at the last measurement before rupture. The resulting overall 5-year cumulative rate of rupture was 7.3% (Kaplan Meier). The 134 patients who underwent more than one ultrasound examination were observed for an average of 4.0 years (536 patient-years). The expansion rate was significantly correlated with the initial diameter and the diastolic blood pressure (best subset multiple regression analysis: r = 0.403; P < 0.001). A correlation with the systolic blood pressure was found only in univariate analysis (r = 0.236; P = 0.011). Amplitude of blood pressure, serum cholesterol level, low-density and high-density lipoproteins, ratio of low- to high-density lipoproteins age, and the extent of smoking habits were not correlated with the expansion rate. Our conclusion is that larger diameter and higher diastolic blood pressure are important risk factors for expansion of abdominal aortic aneurysms. Selective management of abdominal aortic aneurysms based on aneurysmal size, expansion rate, and patient characteristics may result in a low rate of rupture.