Fatal Asthma Research Articles

The significance of CD163-expressing macrophages in asthma

BackgroundCD163 is one of the scavenger receptors that are specifically expressed on macrophages and are well known to be upregulated by various inflammatory responses, including chronic obstructive pulmonary disease in airway diseases. ObjectiveTo evaluate the CD163 expression in the lungs of patients with fatal asthma and investigated whether CD163 contributes to the pathogenesis in asthma. MethodsThe CD163 expressions in the lungs of patients with fatal asthma (n = 9) and in those of nonasthma control subjects (n = 8) were tested by immunohistochemistry. In mouse models of asthma, airway hyperresponsiveness (AHR) and the numbers of airway inflammatory cells in the bronchoalveolar lavage fluid (BALF) were analyzed in the CD163-deficient mice and the control wild-type mice. ResultsThe numbers of CD163-positive macrophages in the lung tissues were significantly increased in the all 6 patients with fatal asthma than in the control subjects. In mouse models of asthma, AHR and the numbers of infiltrating leukocytes, such as eosinophils, lymphocytes, neutrophils, and macrophages, in the BALF were significantly decreased in the CD163-deficient mice when compared with control wild-type mice. The concentrations of interferon γ and interleukin 5 in the BALF were significantly decreased in the CD163-deficient mice when compared with those in the control wild-type mice. ConclusionCD163 may play important roles in airway inflammation and AHR in asthma.

Characteristics of inner-city children with life-threatening asthma

BackgroundIntensive care unit (ICU) admission is a risk factor for fatal asthma. Little is known about risk factors for pediatric ICU admissions for asthma. ObjectiveTo examine characteristics of underserved minority children with prior ICU admissions for asthma. MethodsBaseline survey data, salivary cotinine levels, and allergen specific IgE serologic test results were obtained from children with uncontrolled asthma enrolled in a randomized clinical trial of a behavioral education environmental control intervention. Characteristics of children with and without prior ICU admission were compared using χ2 and t tests. Logistic regression assessed significance of higher odds of prior ICU admission comparing factor-level categories. ResultsPatients included 222 primarily African American (93.7%), male (56%), Medicaid-insured (92.8%) children with a mean (SD) age of 6.4 (2.7) years with uncontrolled asthma. Most (57.9%) had detectable cotinine levels, 82.6% were sensitized to more than 1 environmental allergen, and 27.9% had prior ICU admissions. Prior ICU patients were more likely to be very poor (<$10,000 per year) and sensitized to more than 1 allergen tested (most importantly mouse) (P < .05). Allergen sensitization in the groups did not differ for cockroach, cat, dog, Alternaria, Aspergillus, dust mite, grass, or tree. Although more ICU patients received combination controller therapy, they also overused albuterol. Only 27.4% of ICU patients received specialty care in the previous 2 years, which was not significantly different from non-ICU patients. ConclusionChildren with high mortality risk, including history of ICU admission, were twice as likely to live in extreme poverty, have atopy (particularly mouse allergen), use combination controller therapy, and overuse albuterol. Trial RegistrationClinicalTrials.gov Identifier: NCT01981564.

Fatal asthma: an audit of 30 million patient-years of health plan membership from 2007 to 2015

Fatal asthma: an audit of 30 million patient-years of health plan membership from 2007 to 2015

Fatal and near-fatal thunderstorm asthma epidemic in a desert country.

BACKGROUND:Reports of thunderstorm asthma in the Middle East are few. This study is the first to report on cases of near-fatal and fatal thunderstorm asthma in Kuwait on December 1, 2016.METHODS:We conducted a chart review and interview with adult patients admitted to Mubarak Al-Kabir Hospital with near-fatal asthma, defined as an exacerbation requiring intubation and mechanical ventilation or hypercapnia with a PaCO2≥6 kPa. Information, including patient age, gender, occupation, asthma history, medication usage, and clinical outcome, was collected. For fatal asthma cases, patients' data were collected from the Forensic Department at the Kuwait Ministry of Interior.RESULTS:A total of 17 patients were admitted with near-fatal asthma. Fifteen patients (93.8%) had a prior history of asthma, with an average duration of 9 years. Five patients (33.3%) reported receiving a corticosteroid inhaler from their physician. Fifteen patients (93.8%) reported relying on a short-acting β2-agonist alone to manage their asthma. Eleven patients (68.8%) reported being outdoors during the storm. Eleven patients were diagnosed with fatal asthma.CONCLUSION:The study is the first to report on a thunderstorm-associated asthma epidemic in Kuwait and emphasizes the potential dangers associated with this entity.

Autopsy and Imaging Studies of Mucus in Asthma. Lessons Learned about Disease Mechanisms and the Role of Mucus in Airflow Obstruction.

Autopsy studies in fatal asthma have clearly documented the central role of airway plugging with pathologic mucus in the pathophysiology of death from asthma, but the role of mucus plugs in chronic severe asthma has been less well understood. Recently, multidetector computerized tomography imaging of the lungs has emerged as a valuable method to visualize mucus plugs in asthma. These multidetector computerized tomography data have revealed mucus plugs as a common occurrence in severe forms of asthma. In addition, an image-based mucus plug scoring system shows that mucus plugs are strongly associated with measures of airflow obstruction and with biomarkers of type 2 cytokine and eosinophilic inflammation. These data provide a rationale for treating airflow obstruction in severe asthma with mucolytics, and they also raise the possibility that treatments that target type 2 inflammation may decrease mucus plugs in asthma.

Monocytes accumulate in the airways of children with fatal asthma.

Activated T helper type 2 (Th2) cells are believed to play a pivotal role in allergic airway inflammation, but which cells attract and activate Th2 cells locally have not been fully determined. Recently, it was shown in an experimental human model of allergic rhinitis (AR) that activated monocytes rapidly accumulate in the nasal mucosa after local allergen challenge, where they promote recruitment of Th2 cells and eosinophils. To investigate whether monocytes are recruited to the lungs in paediatric asthma. Tissue samples obtained from children and adolescents with fatal asthma attack (n = 12), age-matched non-atopic controls (n = 9) and allergen-challenged AR patients (n = 8) were subjected to in situ immunostaining. Monocytes, identified as CD68+S100A8/A9+ cells, were significantly increased in the lower airway mucosa and in the alveoli of fatal asthma patients compared with control individuals. Interestingly, cellular aggregates containing CD68+S100A8/A9+ monocytes obstructing the lumen of bronchioles were found in asthmatics (8 out of 12) but not in controls. Analysing tissue specimens from challenged AR patients, we confirmed that co-staining with CD68 and S100A8/A9 was a valid method to identify recently recruited monocytes. We also showed that the vast majority of accumulating monocytes both in the lungs and in the nasal mucosa expressed matrix metalloproteinase 10, suggesting that this protein may be involved in their migration within the tissue. Monocytes accumulated in the lungs of children and adolescents with fatal asthma attack. This finding strongly suggests that monocytes are directly involved in the immunopathology of asthma and that these pro-inflammatory cells are potential targets for therapy.

Fatal Asthma: An Audit of 30 Million Patient-Years of Health Plan Membership from 2007 to 2015

Without accurate data on deaths directly caused by asthma, prevention will be difficult. To determine how often asthma could be confirmed as a proximal cause of death in a large well-defined population with active health plan membership and no acute barriers to medical care. All deaths occurring in active Kaiser Permanente Southern California health plan members between 2007 and 2015 were identified. Asthma-coded deaths were manually audited for cause. Health care and asthma medication use in the 6 months before death were determined. There were 248 (0.80 per 100,000 patient-years) unaudited asthma-coded deaths. There were only 63 (26.5%) (0.20 per 100,000 patient-years) asthma-confirmed deaths. Individuals with asthma-confirmed deaths were younger, less likely to have ever smoked, and had fewer emergency visits in the 6 months before death compared with those with asthma excluded. Individuals with asthma-confirmed deaths used preventative inhalers at very low rates. We unexpectedly found that ever inclusion in the 2016 National Committee for Quality Assurance health effectiveness data and information set (HEDIS) for persistent asthma was associated with a higher risk of all-cause early death. Individuals with asthma-confirmed deaths were also unlikely to be in the HEDIS asthma dataset in the year they died, thus not targeted for outreach. Audit-confirmed fatal asthma is more likely to occur in younger, nonsmoking, individuals, using very low rates of preventive inhalers. This will be a very difficult group to prospectively identify and manage effectively. Further research into the reasons for early death after HEDIS asthma dataset inclusion is warranted.

Unraveling a Clinical Paradox: Why Does Bronchial Thermoplasty Work in Asthma?

Bronchial thermoplasty is a relatively new but seemingly effective treatment in subjects with asthma who do not respond to conventional therapy. Although the favored mechanism is ablation of the airway smooth muscle layer, because bronchial thermoplasty treats only a small number of central airways, there is ongoing debate regarding its precise method of action. Our aim in the present study was to elucidate the underlying method of action behind bronchial thermoplasty. We employed a combination of extensive human lung specimens and novel computational methods. Whole left lungs were acquired from the Prairie Provinces Fatal Asthma Study. Subjects were classified as control (n = 31), nonfatal asthma (n = 32), or fatal asthma (n = 25). Simulated lungs for each group were constructed stochastically, and flow distributions and functional indicators (e.g., resistance) were quantified both before and after a 75% reduction in airway smooth muscle in the "thermoplasty-treated" airways. Bronchial thermoplasty triggered global redistribution of clustered flow patterns wherein structural changes to the treated central airways led to a reopening cascade in the small airways and significant improvement in lung function via reduced spatial heterogeneity of flow patterns. This mechanism accounted for progressively greater efficacy of thermoplasty with both severity of asthma and degree of muscle activation, broadly consistent with existing clinical findings. We report a probable mechanism of action for bronchial thermoplasty: alteration of lung-wide flow patterns in response to structural alteration of the treated central airways. This insight could lead to improved therapy via patient-specific, tailored versions of the treatment-as well as to implications for more conventional asthma therapies.

Obesity increases airway smooth muscle responses to contractile agonists.

The asthma-obesity syndrome represents a major public health concern that disproportionately contributes to asthma severity and induces insensitivity to therapy. To date, no study has shown an intrinsic difference between human airway smooth muscle (HASM) cells derived from nonobese subjects and those derived from obese subjects. The objective of this study was to address whether there is a greater response to agonist-induced calcium mobilization, phosphorylation of myosin light chain (MLC), and greater shortening in HASM cells derived from obese subjects. HASM cells derived from nonobese and obese subjects were age and sex matched. Phosphorylation of MLC was measured after having been stimulated by carbachol. Carbachol- or histamine-induced mobilization of calcium and cell shortening were assessed in HASM cells derived from nonobese and obese donors. Agonist-induced MLC phosphorylation, mobilization of calcium, and cell shortening were greater in obese compared with non-obese-derived HASM cells. The MLC response was comparable in HASM cells derived from obese nonasthma and nonobese fatal asthma subjects. HASM cells derived from obese female subjects were more responsive to carbachol than HASM cells derived from obese male subjects. Insulin pretreatment had little effect on these responses. Our results show an increase in agonist-induced calcium mobilization associated with an increase in MLC phosphorylation and an increase in ASM cell shortening in favor of agonist-induced hyperresponsiveness in HASM cells derived from obese subjects. Our studies suggest that obesity induces a retained phenotype of hyperresponsiveness in cultured human airway smooth muscle cells.

Airway smooth muscle proliferation and inflammation in asthma.

In asthma, it is unclear if the airway smooth muscle cells proliferate more or are increased at the onset of asthma and remain stable. This study aimed to compare smooth muscle cell proliferation in individuals with and without asthma and correlate proliferation rates with cell size and number and with granulocytic airway inflammation. Postmortem airway sections were labeled with proliferating cell nuclear antigen (PCNA) and percent positive muscle cells calculated. On the same sections, smooth muscle cell size and number and the number of eosinophils and neutrophils were estimated and compared in cases of nonfatal ( n = 15) and fatal ( n = 15) asthma and control subjects ( n = 15). The %PCNA+ muscle cells was not significantly different in fatal (29.4 ± 7.7%, mean ± SD), nonfatal asthma (28.6 ± 8.3%), or control subjects (24.6 ± 6.7%) and not related to mean muscle cell size ( r = 0.09), number ( r = 0.36), thickness of the muscle layer ( r = 0.05), or eosinophil numbers ( r = 0.04) in the asthma cases. These data support the hypothesis that in asthma the increased thickness of the smooth muscle layer may be present before or at the onset of asthma and independent of concurrent granulocytic inflammation or exacerbation. NEW & NOTEWORTHY There is debate regarding the origins of the increased airway smooth muscle in asthma. It may be independent of inflammation or arise as a proliferative response to inflammation. The present study found no increase in the proportion of proliferating smooth muscle cells in asthma and no relation of proliferation to numbers of airway smooth muscle cells or inflammation. These results support a stable increase in smooth muscle in asthma that is independent of airway inflammation.

Primary pneumomediastinum in a young woman with near fatal asthma. Diagnosis by ultrasound: a case report

We present the case of a female patient presenting with severe asthma crisis with evolution to severe respiratory failure due to primary pneumomediastinum The early diagnosis of this pathology was made through the use of ultrasound where we discard pneumotorax as the etiology of decompensation The diagnosis was subsequently corroborated by Thorax Computed Tomography CT as gold standard

The Detroit Young Adult Asthma Project: Proposal for a Multicomponent Technology Intervention for African American Emerging Adults With Asthma.

BackgroundRacial and ethnic minority youth have poorer asthma status than white youth, even after controlling for socioeconomic variables. Proper use of asthma controller medications is critical in reducing asthma mortality and morbidity. The clinical consequences of poor asthma management include increased illness complications, excessive functional morbidity, and fatal asthma attacks. There are significant limitations in research on interventions to improve asthma management in racial minority populations, particularly minority adolescents and young adults, although illness management tends to deteriorate after adolescence during emerging adulthood, the unique developmental period beyond adolescence but before adulthood.ObjectiveThe objective of the pilot study was to test the feasibility, acceptability, and signals of efficacy of an intervention targeting adherence to controller medication in African American youth (ages 18-29) with asthma. All elements of the protocol were piloted in a National Heart, Lung, and Blood Institute (NHLBI)–funded pilot study (1R34HL107664 MacDonell). Results suggested feasibility and acceptability of the protocol as well as proof of concept. We are now ready to test the intervention in a larger randomized clinical trial.MethodsThe proposed study will include 192 African American emerging adults with moderate to severe persistent asthma and low controller medication adherence recruited from clinic, emergency department, and community settings. Half of the sample will be randomized to receive a multicomponent technology-based intervention targeting adherence to daily controller medication. The multicomponent technology-based intervention consists of 2 components: (1) 2 sessions of computer-delivered motivational interviewing targeting medication adherence and (2) individualized text messaging focused on medication adherence between the sessions. Text messages will be individualized based on ecological momentary assessment. The remaining participants will complete a series of computer-delivered asthma education modules matched for length, location, and method of delivery of the intervention session. Control participants will also receive text messages between intervention sessions. Message content will be the same for all control participants and contain general facts about asthma (not tailored).ResultsIt is hypothesized that youth randomized to multicomponent technology-based intervention will show improvements in medication adherence (primary outcome) and asthma control (secondary outcome) compared with comparison condition at all postintervention follow-ups (3, 6, 9, and 12 months). The proposed study was funded by NHLBI from September 1, 2016 through August 31, 2021.ConclusionsThis project will test a brief, technology-based intervention specifically targeting adherence to asthma controller medications in an under-researched population, African American emerging adults. If successful, our multicomponent technology-based intervention aimed at improving adherence to asthma medications has the potential to improve quality of life of minority emerging adults with asthma at relatively low cost. It could eventually be integrated into clinical settings and practice to reach a large number of emerging adults with asthma.Trial RegistrationClinicalTrials.gov NCT03121157; https://clinicaltrials.gov/ct2/show/NCT03121157 (Archived by WebCite at http://www.webcitation.org/6wq4yWHPv)

Very low asthma death incidence among Finnish children from 1999 to 2015.

The most recent reports concerning asthma fatalities in Finnish children are from 1998. Since that time, asthma care has improved and asthma-related hospitalizations have decreased. Yet, it is unknown whether pediatric asthma deaths have similarly decreased. To investigate the epidemiology of asthma deaths in the Finnish pediatric population from 1999 onward and to describe the details of fatal asthma exacerbations. We obtained copies of the death certificates from Statistics Finland of all Finnish children aged 0-19 years who died from asthma between 1999 and 2015. After analyzing the death certificates, the medical records of those with possible asthma death were evaluated in detail to confirm the diagnosis. Incidence rates (IR) of asthma deaths were estimated per 1 000 000 person-years by dividing the number of asthma deaths by the total number of person-years. Between 1999-2015, there were 6845 deaths among 0-19 year-old children, of which 21 were possible asthma deaths. Based on patient records and pathological findings, we identified four convincing asthma deaths: aged 7 months, 1 year, 2.5 years, and 19 years. None had known allergies or regularly used inhaled corticosteroids. No pre-school or school-aged children died from asthma in Finland between 1999 and 2015. The cumulative incidence of pediatric asthma deaths was 0.19 per million person-years. Four Finnish children died from asthma between 1999 and 2015. This corresponds to a total incidence of 0.19 per million person-years. No pre-school or school-aged children died from asthma in Finland during the study period.

Downregulation of Guanylate Cyclase Enzyme in Human Asthma model to Investigate NO‐sGc‐ cGMP as a Therapeutic Pathway in Asthma

Asthma is characterized by airway smooth muscle hypersensitivity. Common treatments include β‐adrenergic agonist therapy, such as budesonide, to induce airway smooth muscle relaxation via increased cAMP. However, 70% of patients develop resistance to such therapies. Nitric oxide is a locally produced smooth muscle relaxant that operates via stimulation of soluble guanylate cyclase (sGc) to increase cGMP production. In this study, the NO‐sGc‐cGMP pathway was investigated as an alternate pharmacologic pathway for asthma therapy. Previous studies have found that asthma patients are insensitive to NO signaling and have used sGc drugs to directly stimulate the enzyme. The objective of this study was to examine the expression of the two sGc subunits, α and β, within smooth muscle cells isolated from asthma patients in order to understand how NO‐sGC‐cGMP signaling may be disrupted. Further, we examined how budesonide treatment altered sGc expression. RNA sequencing data showed increased mRNA for both sGc subunits in asthmatic patients and that budesonide downregulated the gene expression of both subunits. We hypothesized that this increased gene expression was in part due to a lack of cGMP signaling due to decreased protein levels that is further impaired with steroids such as budesonide. To examine sGc, we measured the protein levels of both the α and β subunits of sGC by western blot in cultured smooth muscle cells. Fatal asthma and non‐asthma donor derived primary airway smooth muscle cells were cultured with and 24 hours of budesonide treatment. Statistical analysis of western blotting was performed by ANOVA. Densitometry of sGC western blots indicated a 2‐fold downregulation of the α (p&lt;0.0001) and 1.5 fold downregulation of the β (p&lt;0.05) subunits in asthmatic compared to normal patients. No significant changes were observed with normal or asthmatic patients with budesonide treatment (p&gt;0.05), indicating no effect of steroids on the NO‐sGc‐cGMP pathway. A downregulation of sGc protein levels in asthmatic patients would lower cGMP production, which could explain the lack of NO responsiveness in these patients and would contribute to increased airway constriction in fatal asthma. These results indicate the NO‐sGc‐cGMP pathway as a potential new therapeutic pathway in asthma, and future work will examine cGMP levels.Support or Funding InformationSupported by R25ES020721 and ASPET SURF Intern ProgramThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Pulmonary interstitial emphysema in fatal asthma: case report and histopathological review

BackgroundMortality related to asthma has decreased worldwide since the introduction of inhaled corticosteroid therapy in the past decades. However, there are still some asthma fatalities identified mainly in populations with less access to regular treatment. Pulmonary interstitial emphysema due to alveolar rupture has been rarely described as a complication of an acute severe asthma attack, and its identification in pathological analysis can be difficult. Previous studies reported the association of pulmonary interstitial emphysema and bronchial ductal gland ectasia in asthma.Case presentationWe present the case of a 42-year- old man that died due to a fatal asthma attack. Postmortem computed tomography revealed the unusual finding of acute Pulmonary Interstitial Emphysema, confirmed by pathological analysis. We reviewed 28 cases of fatal asthma tissue and identified the presence of pulmonary interstitial emphysema in 10% of the cases.ConclusionsPostmortem computed tomography is a useful complimentary diagnostic tool for autopsies. Pulmonary Interstitial Emphysema in acute exacerbations of asthma seems to be more frequent than reported. Alveolar hyperdistension and bronchial duct gland ectasia causing tissue rupture are possible mechanisms involved in the formation of Pulmonary Interstitial Emphysema. The clinical impact of Pulmonary Interstitial Emphysema in asthma is unknown.

Lung Recovery and Survival After Extracorporeal Membrane Oxygenation for Near Fatal Pediatric Asthma

Lung Recovery and Survival After Extracorporeal Membrane Oxygenation for Near Fatal Pediatric Asthma

Myofibroblasts are increased in the lung parenchyma in asthma.

BackgroundIncreased airway smooth muscle is observed in large and small airways in asthma. Semi-quantitative estimates suggest that cells containing alpha smooth muscle actin (α-SMA) are also increased in the lung parenchyma. This study quantified and characterized α-SMA positive cells (α-SMA+) in the lung parenchyma of non-asthmatic and asthmatic individuals.MethodsPost-mortem sections of peripheral lung from cases of fatal asthma (FA), persons with asthma dying of non-respiratory causes (NFA) and non-asthma control subjects (NAC) were stained for α-SMA, quantified using point-counting and normalised to alveolar basement membrane length and interstitial area.Resultsα-SMA+ fractional area was increased in alveolar parenchyma in both FA (14.7 ± 2.8% of tissue area) and NFA (13.0 ± 1.2%), compared with NAC (7.4 ± 2.4%), p < 0.05 The difference was greater in upper lobes compared with lower lobes (p < 0.01) in both asthma groups. Similar changes were observed in alveolar ducts and alveolar walls. The electron microscopic features of the α-SMA+ cells were characteristic of myofibroblasts.ConclusionsWe conclude that in asthma there is a marked increase in α-SMA+ myofibroblasts in the lung parenchyma. The physiologic consequences of this increase are unknown.

Should oral steroids be routinely supplied to prevent asthmatic relapse?

In 2014, the National review of Asthma Deaths recognised the significant burden of associated morbidity, amongst avoidable factors and recent contact with healthcareprofessionals that commonly occur prior to a fatal asthma exacerbation. It also recognised delayed and undersupply of preventer medications, particularly oral steroids, that are linked to relapsing into a repeat exacerbation. Oral steroids are not without significant systemic side effects and carry their own risks which must be balanced against the risk of relapse. This literature review seeks to establish if oral steroids should be routinely supplied to prevent asthmatic relapse. Exacerbations induced by viruses, allergies and medications are commonly known to contribute towards deterioration and these high risk patients have been found to gain the most benefit from a 7-10 day course of oral steroids. This is recommended as an effective, cheap and safe option with minimal side effects for higher risk patients. Paramedics should consider supplying, or obtaining a supply of oral steroids for high risk asthmatics following an acute exacerbation of asthma when the patient does not require, or refuses, further assessment or observation in an accident and emergency department.

MUC5AC and a Glycosylated Variant of MUC5B Alter Mucin Composition in Children With Acute Asthma

BackgroundDiffuse airway mucus obstruction is an important feature of severe and fatal asthma. MUC5AC and MUC5B are the principal gel-forming mucins found in airway mucus. The mucin composition of airway mucus likely affects its functional properties.MethodsWe quantified the principal airway mucins MUC5AC and MUC5B in the sputum of age-matched children with acute and stable asthma and healthy control subjects by using Western blotting.ResultsSputum samples from 38 children (13 with acute asthma, 15 with stable asthma, 10 control subjects) were obtained. Sputum MUC5AC concentrations were 7.6 μg/mL in control subjects, 22.4 μg/mL in those with stable asthma (P = .17), and 44.7 μg/mL in those with acute asthma (P < .05). MUC5B concentrations showed less variation, with 238.5, 208.4 and 165.9 μg/mL in control subjects, those with stable asthma, and those with acute asthma, respectively. The greater MUC5AC concentration in those with acute asthma resulted in a significantly altered MUC5B:MUC5AC ratio between control subjects and those with acute asthma (P < .05). Significant differences in MUC5B glycoforms were present between the groups, with the low-charge-only glycoform being found uniquely in those with acute asthma.ConclusionsIncreased MUC5AC and the presence of a low-charge-only MUC5B glycoform significantly altered mucin composition in children with acute asthma. These changes may be important contributory factors to the airway mucus obstruction observed during acute asthma.

Mediators of Inflammation in Asthma: A Forensic Perspective.

In the clinical setting, the role of systemic inflammation in patients with asthma has attracted increased attention, and some authors showed that increased IL-6 and high-sensitivity C-reactive protein characterized a group of asthmatic patients. In the realm of forensic pathology, a postmortem diagnosis of asthmatic death can be extremely challenging. The aim of this study was to determine the postmortem serum levels of C-reactive protein, IL-6, and tumor necrosis factor α in a series of severe acute bronchial asthma deaths that underwent medicolegal investigations. A total of 35 autopsy cases were retrospectively selected and included deaths in asthmatic subjects (related and unrelated to severe acute bronchial asthma, in situations characterized or not by systemic inflammation) as well as deaths in nonasthmatic individuals (in situations characterized or not by systemic inflammation). Our findings suggest that IL-6 is selectively increased in the systemic circulation of individuals with asthma, irrespective of whether the cause of death depends on a fatal asthma attack, compared with other biomarkers. Accordingly, postmortem serum IL-6 values in cases of death during severe acute bronchial asthma can be measured and considered of diagnostic relevance to estimate the magnitude of the systemic inflammation responses characterizing the disease.