scholarly journals COVID-19 assessment in family practice—A clinical decision rule based on self-rated symptoms and contact history

2021 ◽  
Vol 31 (1) ◽  
Author(s):  
Antonius Schneider ◽  
Katharina Rauscher ◽  
Christina Kellerer ◽  
Klaus Linde ◽  
Frederike Kneissl ◽  
...  

AbstractThe study aimed to evaluate the diagnostic accuracy of contact history and clinical symptoms and to develop decision rules for ruling-in and ruling-out SARS-CoV-2 infection in family practice. We performed a prospective diagnostic study. Consecutive inclusion of patients coming for COVID-PCR testing to 19 general practices. Contact history and self-reported symptoms served as index test. PCR testing of nasopharyngeal swabs served as reference standard. Complete data were available from 1141 patients, 605 (53.0%) female, average age 42.2 years, 182 (16.0%) COVID-PCR positive. Multivariable logistic regression showed highest odds ratios (ORs) for “contact with infected person” (OR 9.22, 95% CI 5.61–15.41), anosmia/ageusia (8.79, 4.89–15.95), fever (4.25, 2.56–7.09), and “sudden disease onset” (2.52, 1.55–4.14). Patients with “contact with infected person” or “anosmia/ageusia” with or without self-reported “fever” had a high probability of COVID infection up to 84.8%. Negative response to the four items “contact with infected person, anosmia/ageusia, fever, sudden disease onset” showed a negative predictive value (NPV) of 0.98 (95% CI 0.96–0.99). This was present in 446 (39.1%) patients. NPV of “completely asymptomatic,” “no contact,” “no risk area” was 1.0 (0.96–1.0). This was present in 84 (7.4%) patients. To conclude, the combination of four key items allowed exclusion of SARS-CoV-2 infection with high certainty. With the goal of 100% exclusion of SARS-CoV-2 infection to prevent the spread of SARS-CoV-2 to the population level, COVID-PCR testing could be saved only for patients with negative response in all items. The decision rule might also help for ruling-in SARS-CoV-2 infection in terms of rapid assessment of infection risk.

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e045420
Author(s):  
Christina Kellerer ◽  
Alexander Hapfelmeier ◽  
Rudolf A Jörres ◽  
Konrad Schultz ◽  
Benjamin Brunn ◽  
...  

IntroductionThe measurement of fractional exhaled nitric oxide (FeNO) is promising for diagnosing asthma and might substitute for bronchial provocation (BP) tests. To evaluate the diagnostic accuracy of FeNO within a confirmatory study, the following hypotheses will be tested: (1) A FeNO cut-off >50 ppb (parts per billion) is suitable for diagnosing asthma (sensitivity 35%, specificity 95%); (2) If the clinical symptoms ‘allergic rhinitis’ and ‘wheezing’ are present, asthma can be diagnosed at FeNO >33 ppb with a positive predictive value (PPV) >70% and (3) A FeNO >33 ppb can predict responsiveness to inhaled corticosteroid (ICS) with a PPV >70%.Methods and analysisA prospective diagnostic study will be conducted in three practices of pneumologists in Germany. 300 patients suspected of suffering from asthma will be included. As an index test, patients perform FeNO measurement with the device NIOX VERO. As reference a test, patients are examined with whole bodyplethysmography and BP, if necessary. After 3 months, patients with an asthma diagnosis will be examined again to verify the diagnosis and evaluate ICS responsiveness. Patients who did not receive an asthma diagnosis at the initial examination will be phoned after 3 months and asked about persistent respiratory symptoms to exclude false negative findings. As a primary target, sensitivity and specificity of FeNO >50 ppb will be determined. As a secondary target the PPV for asthma at FeNO >33 ppb, when the symptoms ‘allergic rhinitis’ and ‘wheezing’ are present, will be calculated. Regarding ICS responsiveness, the PPV of FeNO >33 ppb will be determined.Ethics and disseminationThe study was approved by the Ethical Committee of the Technical University of Munich (Reference number 122/20 S). The major results will be published in peer-reviewed academic journals and disseminated through conferences.Trial registration numberDRKS00021125.


2021 ◽  
Vol 8 ◽  
Author(s):  
Liena E. O. Elsayed ◽  
Isra Zuhair Eltazi ◽  
Ammar E. Ahmed ◽  
Giovanni Stevanin

Hereditary spastic paraplegias (HSP) are a heterogeneous group of motor neurodegenerative disorders that have the core clinical presentation of pyramidal syndrome which starts typically in the lower limbs. They can present as pure or complex forms with all classical modes of monogenic inheritance reported. To date, there are more than 100 loci/88 spastic paraplegia genes (SPG) involved in the pathogenesis of HSP. New patterns of inheritance are being increasingly identified in this era of huge advances in genetic and functional studies. A wide range of clinical symptoms and signs are now reported to complicate HSP with increasing overall complexity of the clinical presentations considered as HSP. This is especially true with the emergence of multiple HSP phenotypes that are situated in the borderline zone with other neurogenetic disorders. The genetic diagnostic approaches and the utilized techniques leave a diagnostic gap of 25% in the best studies. In this review, we summarize the known types of HSP with special focus on those in which spasticity is the principal clinical phenotype (“SPGn” designation). We discuss their modes of inheritance, clinical phenotypes, underlying genetics, and molecular pathways, providing some observations about therapeutic opportunities gained from animal models and functional studies. This review may pave the way for more analytic approaches that take into consideration the overall picture of HSP. It will shed light on subtle associations that can explain the occurrence of the disease and allow a better understanding of its observed variations. This should help in the identification of future biomarkers, predictors of disease onset and progression, and treatments for both better functional outcomes and quality of life.


2020 ◽  
Vol 8 (12) ◽  
pp. 842-846
Author(s):  
Yehouenou Tessi T. Romeo ◽  
◽  
Asaad El Bakkari ◽  
Adeyemi A. Boris ◽  
Khadija Ben El Hosni ◽  
...  

Mucocele of the appendix is a descriptive term for mucinous distension of the appendiceal lumen (vermiform appendix) regardless of the underlying pathology. It refers to the progressive retrograde dilatation of the vermiform appendix with concomitant intraluminal accumulation of the mucoid substance. It is an uncommon pathology that occurs in both sexes. it especially poses the problem of differential diagnosis in particular in women because of the location of clinical symptoms in the right iliac fossa. The incidence is estimated between 0.2 % and 0.4 % of the appendectomied specimens.The estimated incidence is approximately 1/1 000 000/year. The disease onset is usually after the age of 40 years and more frequently affects females.The means of medical imaging are mainly ultrasound and scanner. On CT typical mucocele appears as a cecal-based, rounded and well-defined mass, thin-walled, with fine parietal calcifications CT density is variable, from fluid to tissue. A stercolith is sometimes visible at the base of the appendix. The wall of the mucocele may be thickened, irregular, taking the contrast there may be peri-appendicular inflammation, which may be inflammatory or tumor, without specificity.The treatment of unbroken appendicular mucocele is surgical, preferably by laparotomy than laparoscopy. The appendectomy is performed, without breaking the appendix, with complete resection of the meso-appendix, and sampling for cytology of the peritoneal fluid.


2021 ◽  
Author(s):  
Flavia Camponovo ◽  
Tamsin E Lee ◽  
Jonathan Russell ◽  
Lydia Burgert ◽  
Jaline Gerardin ◽  
...  

Background: Malaria blood-stage infection length and intensity are important drivers of disease and transmission; however, the underlying mechanisms of parasite growth and the host's immune response during infection remain largely unknown. Over the last 30 years, several mechanistic mathematical models of malaria parasite within-host dynamics have been published and used in malaria transmission models. Methods: We identified mechanistic within-host models of parasite dynamics through a review of published literature. For a subset of these, we reproduced model code and compared descriptive statistics between the models using fitted data. Through simulation and model analysis, we compare and discuss key features of the models, including assumptions on growth, immune response components, variant switching mechanisms, and inter-individual variability. Results: The assessed within-host malaria models generally replicate infection dynamics in malaria-na&iumlve individuals. However, there are substantial differences between the model dynamics after disease onset, and models do not always reproduce late infection parasitemia data used for calibration of the within host infections. Models have attempted to capture the considerable variability in parasite dynamics between individuals by including stochastic parasite multiplication rates; variant switching dynamics leading to immune escape; variable effects of the host immune responses; or via probabilistic events. For models that capture realistic length of infections, model representations of innate immunity explain early peaks in infection density that cause clinical symptoms, and model representations of antibody immune responses control the length of infection. Models differed in their assumptions concerning variant switching dynamics, reflecting uncertainty in the underlying mechanisms of variant switching revealed by recent clinical data during early infection. Overall, given the scarce availability of the biological evidence there is limited support for complex models. Conclusions: Our study suggests that much of the inter-individual variability observed in clinical malaria infections has traditionally been attributed in models to random variability, rather than mechanistic disease dynamics. Thus, we propose that newly developed models should assume simple immune dynamics that minimally capture mechanistic understandings and avoid over-parameterisation and large stochasticity which inaccurately represent unknown disease mechanisms.


2019 ◽  
Vol 179 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Hanneke E. M. van der Hoek-Snieders ◽  
Antonius J. M. L. van den Heuvel ◽  
Harmieke van Os-Medendorp ◽  
Digna M. A. Kamalski

AbstractThis systematic review aims to determine the diagnostic accuracy of fetal MRI for detecting cleft palate in fetuses at risk for orofacial clefts. Pubmed, Embase, and CINAHL were searched systematically. A diagnostic study was included if it performed MRI (index test) and postnatal examination (reference test) in fetuses at risk for orofacial clefts. Methodological quality was assessed using the QUADAS-2. A meta-analysis was performed with a random-effects model, calculating the pooled sensitivity, specificity, and area under the curve. The search resulted in eight studies (334 fetuses) to be included: four prospective and four retrospective studies. The applicability concern was low. There was, however, a risk of selection and information bias. All studies showed that MRI well predicted the chance of cleft palate. The sensitivity results were homogeneous, but heterogeneity was assumed regarding the specificity estimate (Cochrane’s Q test: p = 0.00). The pooled sensitivity was 0.97 (95% CI 0.93–0.99); the pooled specificity was 0.94 (0.89–0.97). The area under the curve was 0.98 (95% CI 0.98–0.99).Conclusion: This meta-analysis shows that MRI has an excellent sensitivity and good to excellent specificity for diagnosing cleft palate in fetuses at risk for orofacial clefts. Future research should assess applicability for clinical care.What is Known:• Using ultrasound for prenatal detection of cleft palate leads to misdiagnosis frequently.• MRI could potentially improve the prenatal detection rate of cleft palate.What is New:• Eight studies describe the diagnostic accuracy of MRI for detecting cleft palate.• Combined results show excellent sensitivity and good to excellent specificity.


2019 ◽  
Vol 56 (5) ◽  
pp. 1389-1394 ◽  
Author(s):  
M Areso Apesteguía ◽  
J B Areso Portell ◽  
N Halaihel Kassab ◽  
M J Gracia Salinas

Abstract This study records the clinical findings in nine hunting dogs showing systemic illness associated with trombiculids and identifies the mite species involved. In fall, coinciding with the seasonality of mites, all dogs were infested with mites and had been in the risk area (Sierra Cebollera Natural Park, La Rioja, Spain) a few hours before the onset of symptoms. The symptoms included vomiting, anorexia, weakness and lethargy, diarrhea, and even stupor. The clinical picture was fast-acting and potentially fatal. The infestations varied from low to severe. Molecular analysis of mites that fed on the dogs confirmed that they were larvae of Neotrombicula inopinata (Oudemans, Acari, Trombiculidae). This is the first time that N. inopinata has been identified as feeding on dogs and implicated in canine systemic illness associated with trombiculids. In contrast to other chiggers, N. inopinata does not seem to cause dermatitis. Likewise, the clinical and epidemiological similarity between the clinical symptoms we describe herein and the occurrence of seasonal canine illness (SCI) led us to suspect that this illness may be caused by infestation with these mites. The condition could be the consequence of severe infestation from large numbers of feeding mites, especially N. inopinata. Whether or not the cases were due to a severe allergic host response to salivary proteins or the result of the transmission of a new or emerging trombiculid-borne pathogen is not known.


2019 ◽  
Vol 20 (7) ◽  
pp. 1664 ◽  
Author(s):  
Anita Gołaszewska ◽  
Wojciech Bik ◽  
Tomasz Motyl ◽  
Arkadiusz Orzechowski

The average life span steadily grows in humans and in animals kept as pets or left in sanctuaries making the issue of elderly-associated cognitive impairment a hot-spot for scientists. Alzheimer’s disease (AD) is the most prevalent cause of progressive mental deterioration in aging humans, and there is a growing body of evidence that similar disorders (Alzheimer’s-like diseases, ALD) are observed in animals, more than ever found in senescent individuals. This review reveals up to date knowledge in pathogenesis, hallmarks, diagnostic approaches and modalities in AD faced up with ALD related to different animal species. If found at necropsy, there are striking similarities between senile plaques (SP) and neurofibrillary tangles (NFT) in human and animal brains. Also, the set of clinical symptoms in ALD resembles that observed in AD. At molecular and microscopic levels, the human and animal brain histopathology in AD and ALD shows a great resemblance. AD is fatal, and the etiology is still unknown, although the myriad of efforts and techniques were employed in order to decipher the molecular mechanisms of disease onset and its progression. Nowadays, according to an increasing number of cases reported in animals, apparently, biochemistry of AD and ALD has a lot in common. Described observations point to the importance of extensive in vivo models and extensive pre-clinical studies on aging animals as a suitable model for AD disease.


Biostatistics ◽  
2018 ◽  
Vol 21 (1) ◽  
pp. 122-138
Author(s):  
Xiang Li ◽  
Donglin Zeng ◽  
Karen Marder ◽  
Yuanjia Wang

Summary Potential disease-modifying therapies for neurodegenerative disorders need to be introduced prior to the symptomatic stage in order to be effective. However, current diagnosis of neurological disorders mostly rely on measurements of clinical symptoms and thus only identify symptomatic subjects in their late disease course. Thus, it is of interest to select and integrate biomarkers that may reflect early disease-related pathological changes for earlier diagnosis and recruiting pre-sypmtomatic subjects in a prevention clinical trial. Two sources of biological information are relevant to the construction of biomarker signatures for time to disease onset that is subject to right censoring. First, biomarkers’ effects on disease onset may vary with a subject’s baseline disease stage indicated by a particular marker. Second, biomarkers may be connected through networks, and their effects on disease may be informed by this network structure. To leverage these information, we propose a varying-coefficient hazards model to induce double smoothness over the dimension of the disease stage and over the space of network-structured biomarkers. The distinctive feature of the model is a non-parametric effect that captures non-linear change according to the disease stage and similarity among the effects of linked biomarkers. For estimation and feature selection, we use kernel smoothing of a regularized local partial likelihood and derive an efficient algorithm. Numeric simulations demonstrate significant improvements over existing methods in performance and computational efficiency. Finally, the methods are applied to our motivating study, a recently completed study of Huntington’s disease (HD), where structural brain imaging measures are used to inform age-at-onset of HD and assist clinical trial design. The analysis offers new insights on the structural network signatures for premanifest HD subjects.


2022 ◽  
Vol 8 ◽  
Author(s):  
Zhenkui Hu ◽  
Xing Huang ◽  
Jianguo Zhang ◽  
Shixiang Fu ◽  
Daoyin Ding ◽  
...  

Background: As delta variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) prevailed in the current coronavirus disease 2019 (COVID-19) pandemic, its clinical characteristics with the difference from those of wild-type strains have been little studied.Methods: We reported one cohort of 341 wild-type patients with COVID-19 admitted at Wuhan, China in 2020 and the other cohort of 336 delta variant patients with COVID-19 admitted at Yangzhou, China in 2021, with comparisons of their demographic information, medical history, clinical manifestation, and hematological data. Furthermore, within the delta variant cohort, patients with none, partial, and full vaccination were also compared to assess vaccine effectiveness.Findings: For a total of 677 patients with COVID-19 included in this study, their median age was 53.0 years [interquartile range (IQR): 38.0–66.0] and 46.8% were men. No difference was found in age, gender, and percentage of patients with the leading comorbidity between wild-type and delta variant cohorts, but delta variant cohort showed a lessened time interval between disease onset to hospitalization, a reduced portion of patients with smoking history, and a lowered frequency of clinical symptoms. For hematological parameters, most values demonstrated significant differences between wild-type and delta variant cohorts, while full vaccination rather than partial vaccination alleviated the disease condition. This reflected the viremic effect of delta variant when vaccination succeeds or fails to protect.Interpretation: Delta variant of SARS-CoV-2 may cause severe disease profiles, but timely diagnosis and full vaccination could protect patients with COVID-19 from worsened disease progression.


2020 ◽  
Author(s):  
Shaohua Tang ◽  
Rui Sun ◽  
Qi Xiao ◽  
Tingting Mao ◽  
Weigang Ge ◽  
...  

AbstractLittle is known regarding why a subset of COVID-19 patients exhibited prolonged positivity of SARS-CoV-2 infection. Here, we studied the sera proteomic dynamics in 37 COVID-19 patients over nine weeks, quantifying 2700 proteins with high quality. Remarkably, we found that during the first three weeks since disease onset, while clinical symptoms and outcome were indistinguishable, patients with prolonged disease course displayed characteristic immunological responses including enhanced Natural Killer cell-mediated innate immunity and regulatory T cell-mediated immunosuppression. We further showed that it is possible to predict the length of disease course using machine learning based on blood protein levels during the first three weeks. Validation in an independent cohort achieved an accuracy of 82%. In summary, this study presents a rich serum proteomic resource to understand host responses in COVID-19 patients and identifies characteristic Treg-mediated immunosuppression in patients with prolonged disease course, nominating new therapeutic target and diagnosis strategy.


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