The \"make worse\" meaning is far more common in published prose than the \"rouse to anger\" meaning. Such is not the case, however, with aggravation and aggravating. Aggravation is used in the \"irritation, provocation\" sense somewhat more than in its earlier senses; aggravating has practically no use other than to express annoyance.
Background: Clinical findings indicated that a fraction of coronavirus disease 2019 (COVID-19) patients diagnosed as mild early may progress to severe cases. However, it is difficult to distinguish these patients in the early stage. The present study aimed to describe the clinical characteristics of these patients, analyze related factors, and explore predictive markers of the disease aggravation.
Methods: Clinical and laboratory data of nonsevere adult COVID-19 patients in Changsha, China, were collected and analyzed on admission. A logistic regression model was adopted to analyze the association between the disease aggravation and related factors. The receiver operating characteristic curve (ROC) was utilized to analyze the prognostic ability of C-reactive protein (CRP).
Results: About 7.7% (16/209) of nonsevere adult COVID-19 patients progressed to severe cases after admission. Compared with nonsevere patients, the aggravated patients had much higher levels of CRP (median [range], 43.8 [12.3-101.9] mg/L vs 12.1 [0.1-91.4] mg/L; P = .000). A regression analysis showed that CRP was significantly associated with aggravation of nonsevere COVID-19 patients, with an area under the curve of 0.844 (95% confidence interval, 0.761-0.926) and an optimal threshold value of 26.9 mg/L.
The possibility that so-called anti-epileptic drugs (AEDs) may aggravate epilepsy must always be borne in mind by the clinician. Many reports of such aggravation of seizures have been published. Most such reports are anecdotal and speculative, and suggest that many such reactions are idiosyncratic. However, for some there is a sufficient body of evidence to suggest that some AEDs used in certain epilepsies may consistently cause worsening of seizures. Seizure aggravation may include increase in the frequency or severity of existing seizures, emergence of new types of seizure, or the occurrence of status epilepticus. The pathophysiology of seizure aggravation is poorly understood including non-specific effects such as those associated with sedation, drug-induced encephalopathy, and paradoxical or inverse pharmacodynamic effects. For some epilepsies the choice of AEDs may be inappropriate, and although the mechanism of seizure aggravation is not clear, its occurrence may be fairly predictable. This is best documented for the use of carbamazepine in idiopathic generalized and myoclonic epilepsies. Most other AEDs have been reported occasionally to cause seizure aggravation. The lowest risk of seizure aggravation appears to be with valproate. Risk factors for worsening of seizures are epileptic encephalopathy, polytherapy, high frequency of seizures, and cognitive impairment. Advances in pharmacogenomics may in the future enable such adverse effects to be predicted for individual patients. Meanwhile, a systematic approach to reporting AED-induced seizure aggravation should be developed.
Results. Analysis of the Aggravation in Parenting Scale showed that 26% of foreign-born parents with foreign-born children were highly aggravated, followed by 22% of foreign-born parents with US-born children and 11% of US-born parents. Multivariable analyses indicated that all minority parents experienced high parenting aggravation compared with non-Hispanic White US-born parents; the odds of reporting parenting aggravation were 5 times higher for Hispanic foreign-born parents. All foreign-born parents, regardless of race/ethnicity, reported significantly elevated parenting aggravation. Parents of adolescents, children with special health care needs, and nontraditional and lower-income households were also more likely to report high parenting aggravation.
Table 3 shows the multivariable analysis of predictors of high and low parenting aggravation, where immigrant family type and race/ethnicity were included as a 12-category joint variable. In the model for high aggravation, foreign-born Hispanic parents of both foreign-born and US-born children were 5 times more likely to be highly aggravated than US-born, non-Hispanic White parents of US-born children (the reference group). In Hispanic households with a US-born child in which 1 parent or both parents were foreign born, parents had 3 and 2 times greater odds of high aggravation, respectively, than did the reference group. In households with 1 or 2 non-Hispanic White foreign-born parents, the parents had 50% greater odds of high aggravation than their US-born counterparts. All non-Hispanic Black parents, both foreign born and US born, had 70% greater odds of high aggravation than the reference group. Among all other ethnic groups, in households in which 1 or both parents were foreign born, the odds of high aggravation were 2.4 greater than in the reference group if there was a foreign-born child and 2.1 times greater if there was a US-born child.
late 15c., \"an increasing in gravity or seriousness,\" from French aggravation, from Late Latin aggravationem (nominative aggravatio), noun of action from past-participle stem of Latin aggravare \"make heavier,\" figuratively \"to embarrass further, increase in oppressiveness,\" from ad \"to\" (see ad-) + gravare \"weigh down,\" from gravis \"heavy\" (from PIE root *gwere- (1) \"heavy\"). The sense of \"irritation\" is from 1610s.
One type of aggravation for disability purposes is defined in the United States Code (USC) in this manner: \"A preexisting injury or disease will be considered to have been aggravated by active military, naval, or air service, where there is an increase in disability during such service, unless there is a specific finding that the increase in disability is due to the natural progress of the disease.\" (38 USC 1153). This kind of aggravation, known as aggravation of a preexisting condition, is present when there is permanent increase in the severity of a condition during or as a result of military service and the increase is not due to the condition's natural progression.
Another type of aggravation is present when there is permanent increase in the severity of a nonservice-connected condition due to an already service-connected condition, and the increase is not due to the condition's natural progression. This is known as aggravation of a nonservice-connected condition by a service-connected condition, or secondary (Allen) aggravation.
Epidemiologic studies have highlighted the association of environmental factors with the development and progression of autoimmune and chronic inflammatory diseases. Among the environmental factors, smoking has been associated with increased susceptibility and poor prognosis in rheumatoid arthritis (RA). However, the immune and molecular mechanism of smoking-induced arthritis aggravation remains unclear. The transcription factor aryl hydrocarbon receptor (AHR) regulates the generation of Th17 cells, CD4 T cells linked the development of autoimmune diseases. AHR is activated by organic compounds including polycyclic aromatic hydrocarbons (PAHs), which are environmental pollutants that are also present in cigarette smoke. In this study, we investigated the role of AHR activation in the aggravation of experiment arthritis induced by exposure to cigarette smoke.
Mice were exposed to cigarette smoke during the developmental phase of antigen-induced arthritis and collagen-induced arthritis to evaluate the effects of smoking on disease development. Aggravation of articular inflammation was assessed by measuring neutrophil migration to the joints, increase in articular hyperalgesia and changes in the frequencies of Th17 cells. In vitro studies were performed to evaluate the direct effects of cigarette smoke and PAH on Th17 differentiation. We also used mice genetically deficient for AHR (Ahr KO) and IL-17Ra (Il17ra KO) to determine the in vivo mechanism of smoking-induced arthritis aggravation.
We found that smoking induces arthritis aggravation and increase in the frequencies of Th17 cells. The absence of IL-17 signaling (Il17ra KO) conferred protection to smoking-induced arthritis aggravation. Moreover, in vitro experiments showed that cigarette smoke can directly increase Th17 differentiation of T cells by inducing AHR activation. Indeed, Ahr KO mice were protected from cigarette smoke-induced arthritis aggravation and did not display increase in TH17 frequencies, suggesting that AHR activation is an important mechanism for cigarette smoke effects on arthritis. Finally, we demonstrate that PAHs are also able to induce arthritis aggravation.
Our data demonstrate that the disease-exacerbating effects of cigarette smoking are AHR dependent and environmental pollutants with AHR agonist activity can induce arthritis aggravation by directly enhancing Th17 cell development.
To understand how smoking modulates the immune response and disease aggravation, we developed a murine model of cigarette smoke exposure during antigen-induced articular disease development. Using this model, we identified that smoking-induced arthritis aggravation is dependent on AHR activation in T cells, Th17 expansion, and interleukin 17 receptor A (IL-17RA) signaling, showing a strong link between this pollutant receptor and arthritis progression. Our results suggest that AHR activation in Th17 cells might be a convergent mechanism by which different environmental pollutants aggravate autoimmune diseases.
We then investigated whether PAH present in cigarette smoke could modulate Th17 differentiation and exacerbate arthritis. As a PAH prototype we used benzo[b]fluoranthen (BFA), which is found in high concentrations in cigarette smoke  and exhibits a potent AHR agonist activity (Fig. 3d). BFA induced an increase in Th17 differentiation in vitro to a similar level as that induced by the AhR endogenous agonist, FICZ, or CSEM (Fig. 3e and f). In vivo, BFA and FICZ also induced arthritis aggravation and an increase of the frequency of Th17 in the draining lymph nodes of AIA mice (Fig. 3g). 59ce067264