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ACE inhibitor-mediated angioedema.
Montinaro, V, Cicardi, M
International immunopharmacology. 2020;:106081
Abstract
Angioedema (AE) occurring during ACE inhibitor therapy (ACEi-AE) is a rare complication involving between 0.1 and 0.7% of treated patients. AE can also complicate other therapeutic regimens that block the renin-angiotensin aldosterone system. Other drugs, such as immune suppressors, some type of antidiabetics or calcium antagonists, can increase the likelihood of ACEi-AE when associated to ACEi. There is a clear ethnic predisposition, since African-Americans or Hispanics show a higher prevalence of this condition compared to Caucasians. At least in African-Americans the genetic predisposition accounts for a general higher prevalence of AE, independently from the cause. People that experience ACEi-AE may have some recurrence when they are switched to an angiotensin-receptor blocker (ARB); however, epidemiological studies on large cohorts have shown that angiotensin receptor blockers (ARB) do not increase the likelihood of AE compared to other antihypertensives. Clinical manifestations consist of edema of face, lips, tongue, uvula and upper airways, requiring intubation or tracheotomy in severe cases. Attacks last for 48-72 h and require hospital admission in most cases. Intestinal involvement with sub-occlusive symptoms has also been reported. The pathogenesis of ACEi-AE depends mainly on a reduced catabolism and accumulation of bradykinin, which is normally metabolized by ACE. Genetic studies have shown that some single nucleotide polymorphisms at genes encoding relevant molecules for bradykinin metabolism and action may be involved in ACEi-AE, giving a basis for the ethnic predisposition. Treatment of ACEi-AE is still a matter of debate. Corticosteroids and antihistamines do not show efficacy. Some therapeutic attempts have shown some efficacy for fresh frozen plasma or C1 inhibitor concentrate infusion. Interventional studies with the specific bradykinin receptor antagonist icatibant have shown conflicting results; there might be a different ethnic predisposition to icatibant efficacy which has been proven in caucasian but not in black patients.
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Impact of radon and combinatory radon/carbon dioxide spa on pain and hypertension: Results from the explorative RAD-ON01 study.
Rühle, PF, Klein, G, Rung, T, Tiep Phan, H, Fournier, C, Fietkau, R, Gaipl, US, Frey, B
Modern rheumatology. 2019;(1):165-172
Abstract
OBJECTIVES Therapies with low doses of radon have beneficial effects on patients suffering from chronic painful degenerative and inflammatory diseases. We already showed that this is accompanied by systemic immune modulations. We here focus on pain-reducing effects of very low doses of radon by adding carbon dioxide water and its impact on heart rate variability (HRV), blood pressure and free radicals. METHODS 97 of 103 patients receiving radon spa (1.200 Bq/l at 34 °C or 600 Bq/l, 1 g/l CO2 at 34 °C) were monitored before and at three different time points after therapy. Individual pain perception was analyzed and the capability to process radicals. At each time point, the hypertensive patients (n = 46) were examined over 24 h for blood pressure and HRV. RESULTS Long-term pain reduction was observed in the majority of patients. A modulation of superoxide dismutase was identified, presumably representing a priming effect for lowering radiation stress. Further, lowering of blood pressure, especially in those patients who additionally received carbon dioxide, was seen. Radon did in particular impact on HRV implying lasting relaxation effects. CONCLUSION Radon/carbon dioxide spa efficiently reduces pain. In particular, patients simultaneously suffering from painful and cardiovascular diseases should be treated by combination of radon and CO2.
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Hypertension linked to allostatic load: from psychosocial stress to inflammation and mitochondrial dysfunction.
Mocayar Marón, FJ, Ferder, L, Saraví, FD, Manucha, W
Stress (Amsterdam, Netherlands). 2019;(2):169-181
Abstract
Although a large number of available treatments and strategies, the prevalence of cardiovascular diseases continues to grow worldwide. Emerging evidence supports the notion of counteracting stress as a critical component of a comprehensive therapeutic strategy for cardiovascular disease. Indeed, an unhealthy lifestyle is a burden to biological variables such as plasma glucose, lipid profile, and blood pressure control. Recent findings identify allostatic load as a new paradigm for an integrated understanding of the importance of psychosocial stress and its impact on the development and maintenance of cardiovascular disease. Allostasis complement homeostasis and integrates behavioral and physiological mechanisms by which genes, early experiences, environment, lifestyle, diet, sleep, and physical exercise can modulate and adapt biological responses at the cellular level. For example, variability is a physiological characteristic of blood pressure necessary for survival and the allostatic load in hypertension can contribute to its related cardiovascular morbidity and mortality. Therefore, the current review will focus on the mechanisms that link hypertension to allostatic load, which includes psychosocial stress, inflammation, and mitochondrial dysfunction. We will describe and discuss new insights on neuroendocrine-immune effects linked to allostatic load and its impact on the cellular and molecular responses; the links between allostatic load, inflammation, and endothelial dysfunction; the epidemiological evidence supporting the pathophysiological origins of hypertension; and the biological embedding of allostatic load and hypertension with an emphasis on mitochondrial dysfunction.
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[Development of therapeutic vaccine for life style-related diseases].
Nakagami, H
Nihon yakurigaku zasshi. Folia pharmacologica Japonica. 2019;(5):270-274
Abstract
In the 18th century, Edward Jenner proposed the vaccine for smallpox as a first vaccine therapy based on the legend that a vaccinia prevents the infection with smallpox. Recently, the therapeutic target of vaccine will expand from infectious diseases to various diseases, such as amyloid β or tau vaccine for Alzheimer's disease. We are now going to develop a therapeutic vaccine to lifestyle-related diseases (i.e. high blood pressure), and aim to realize a novel therapy which will be injected once or twice per year from a daily medication. For this purpose, the appropriate choice of an antigen, carrier and adjuvants should be required to activate hormonal immunity by the vaccine, leading to efficient antibody production without toxicity, because the therapeutic target of our vaccine is an endogenous protein (i.e. hormone). The clinical advantage of this therapeutic vaccine is to improve the medical adherence and drug management because the multiple drug users are increased in particular old patients, so called polypharmacy. If the vaccine will take place of a part of medicine in future, it may give us a novel therapeutic option with several social benefits.
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Renal effects of cytokines in hypertension.
Wen, Y, Crowley, SD
Current opinion in nephrology and hypertension. 2018;(2):70-76
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Abstract
PURPOSE OF REVIEW Inflammatory cytokines contribute to the pathogenesis of hypertension through effects on renal blood flow and sodium handling. This review will update recent advances that explore the renal actions of immune cells and cytokines in the pathogenesis of hypertension. RECENT FINDINGS Populations of cells from both the innate and adaptive immune systems contribute to hypertension by modulating functions of the vasculature and epithelial cells in the kidney. Macrophages and T lymphocytes can directly regulate the hypertensive response and consequent target organ damage. Dendritic cells and B lymphocytes can alter blood pressure (BP) indirectly by facilitating T-cell activation. Proinflammatory cytokines, including tumor necrosis factor-α, interleukin 17, interleukin 1, and interferon-γ augment BP and/or renal injury when produced by T helper 1 cells, T helper 17 cells, and macrophages. In contrast, interleukin 10 improves vascular and renal functions in preclinical hypertension studies. The effects of transforming growth factor-β are complex because of its profibrotic and immunosuppressive functions that also depend on the localization and concentration of this pleiotropic cytokine. SUMMARY Preclinical studies point to a key role for cytokines in hypertension via their actions in the kidney. Consistent with this notion, anti-inflammatory therapies can attenuate BP elevation in human patients with rheumatologic disease. Conversely, impaired natriuresis may further polarize both T lymphocytes and macrophages toward a proinflammatory state, in a pathogenic, feed-forward loop of immune activation and BP elevation. Understanding the precise renal actions of cytokines in hypertension will be necessary to inhibit cytokine-dependent hypertensive responses while preserving systemic immunity and tumor surveillance.