Subclinical Hypercortisolism: An Important, Unrecognized Dysfunction.
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ABSTRACT:
SUBMITTER: Pizzorno L
PROVIDER: S-EPMC9380834 | biostudies-literature | 2022 Jul
REPOSITORIES: biostudies-literature
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Subclinical Hypercortisolism: An Important, Unrecognized Dysfunction.
Pizzorno Lara L Pizzorno Joseph J
Integrative medicine (Encinitas, Calif.) 20220701 3
While Cushing syndrome is rare, but well-recognized, subclinical hypercortisolism (defined as excessive cortisol secretion without the classic manifestations of Cushing syndrome) is significantly more common. Subclinical hypercortisolism contributes to several chronic diseases, such as diabetes, osteoporosis, sarcopenia and hypertension. The incidence increases with age and correlates with body load of environmental toxins such as bisphenol A (BPA). This editorial discusses prevalence, contribut ...[more]
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Project description:BackgroundCoronavirus Disease-2019 (COVID-19) is associated with cardiovascular injury, but left ventricular (LV) function is largely preserved. We aimed to evaluate for subclinical LV dysfunction in patients with COVID-19 through myocardial strain analysis.MethodsWe performed a single-center retrospective cohort study of all patients hospitalized with COVID-19 who underwent echocardiography. Traditional echocardiographic and global longitudinal strain (GLS) values were compared with prior and subsequent echocardiograms.ResultsAmong 96 patients hospitalized with COVID-19 with complete echocardiograms, 67 (70%) had adequate image quality for strain analysis. The cohort was predominantly male (63%) and 18% had prevalent cardiovascular disease (CVD). Echocardiograms were largely normal with median [IQR] LV ejection fraction (EF) 62% [56%, 68%]. However, median GLS was abnormal in 91% (-13.5% [-15.0%, -10.8%]). When stratified by CVD, both groups had abnormal GLS, but presence of CVD was associated with worse median GLS (-11.6% [-13.4%, -7.2%] vs -13.9% [-15.0%, -11.3%], p = 0.03). There was no difference in EF or GLS when stratified by symptoms or need for intensive care. Compared to pre-COVID-19 echocardiograms, EF was unchanged, but median GLS was significantly worse (-15% [-16%, -14%] vs -12% [-14%, -10%], p = 0.003). Serial echocardiograms showed no significant changes in GLS or EF overall, however patients who died had stable or worsening GLS, while those who survived to discharge home showed improved GLS.ConclusionsPatients with COVID-19 had evidence of subclinical cardiac dysfunction manifested by reduced GLS despite preserved EF. These findings were observed regardless of history of CVD, presence of COVID-19 symptoms, or severity of illness.
| S-EPMC7988446 | biostudies-literature
Project description:Reduced exercise capacity is well documented in end-stage chronic kidney disease (CKD), preceded by changes in cardiac morphology in CKD stage 3. However, it is unknown whether subclinical cardiopulmonary dysfunction occurs in CKD stage 3 independently of heart failure.Prospective observational cross-sectional study of exercise capacity assessed by cardiopulmonary exercise testing in 993 preoperative patients. Primary outcome was peak oxygen consumption (VO2peak). Anaerobic threshold (AT), oxygen pulse and exercise-evoked measures of autonomic function were analysed, controlling for CKD stage 3, age, gender, diabetes mellitus and hypertension.CKD stage 3 was present in 93/993 (9.97%) patients. Diabetes mellitus (RR 2.49 (95% CI 1.59 to 3.89); p<0.001), and hypertension (RR 3.20 (95% CI 2.04 to 5.03); p<0.001)) were more common in CKD stage 3. Cardiac failure (RR 0.83 (95% CI 0.30 to 2.24); p=0.70) and ischaemic heart disease (RR 1.40 (95% CI 0.97 to 2.02); p=0.09) were not more common in CKD stage 3. Patients with CKD stage 3 had lower predicted VO2peak (mean difference: 6% (95% CI 1% to 11%); p=0.02), lower peak heart rate (mean difference:9 bpm (95% CI 3 to 14); p=0.03)), lower AT (mean difference: 1.1 mL/min/kg (95% CI 0.4 to 1.7); p<0.001) and impaired heart rate recovery (mean difference: 4 bpm (95% CI 1 to 7); p<0.001)).Subclinical cardiopulmonary dysfunction in CKD stage 3 is common. This study suggests that maladaptive cardiovascular/autonomic dysfunction may be established in CKD stage 3, preceding pathophysiology reported in end-stage CKD.
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Project description:BackgroundSocioeconomic deprivation is associated with higher cardiovascular morbidity and mortality. Whether deprivation status should be incorporated in more cardiovascular risk estimation scores remains unclear. This study evaluates how socioeconomic deprivation status affects the performance of 3 primary prevention cardiovascular risk scores.MethodsThe Generation Scotland Scottish Family Health Study was used to evaluate the performance of 3 cardiovascular risk scores with (ASSIGN [Assessing cardiovascular risk using SIGN (Scottish Intercollegiate Guidelines Network) guidelines to ASSIGN preventive treatment]) and without (SCORE2 [Systematic Coronary Risk Evaluation 2 algorithm], Pooled Cohort Equations) socioeconomic deprivation as a covariate in the risk prediction model. Deprivation was defined by Scottish Index of Multiple Deprivation score. The predicted 10-year risk was evaluated against the observed event rate for the cardiovascular outcome of each risk score. The comparison was made across 3 groups defined by the deprivation index score consisting of group 1 defined as most deprived, group 3 defined as least deprived, and group 2, which consisted of individuals in the middle deprivation categories.ResultsThe study population consisted of 15 506 individuals (60.0% female, median age of 51). Across the population, 1808 (12%) individuals were assigned to group 1 (most deprived), 8119 (52%) to group 2, and 4708 (30%) to group 3 (least deprived), and 871 (6%) individuals had a missing deprivation score. Risk scores based on models that did not include deprivation status significantly under predicted risk in the most deprived (6.43% observed versus 4.63% predicted for SCORE2 [P=0.001] and 6.69% observed versus 4.66% predicted for Pooled Cohort Equations [P<0.001]). Both risk scores also significantly overpredicted the risk in the least deprived group (3.97% observed versus 4.72% predicted for SCORE2 [P=0.007] and 4.22% observed versus 4.85% predicted for Pooled Cohort Equations [P=0.028]). In contrast, no significant difference was demonstrated in the observed versus predicted risk when using the ASSIGN risk score, which included socioeconomic deprivation status in the risk model.ConclusionsSocioeconomic status is a largely unrecognized risk factor in primary prevention of cardiovascular disease. Risk scores that exclude socioeconomic deprivation as a covariate under- and overestimate the risk in the most and least deprived individuals, respectively. This study highlights the importance of incorporating socioeconomic deprivation status in risk estimation systems to ultimately reduce inequalities in health care provision for cardiovascular disease.
| S-EPMC9287096 | biostudies-literature
Project description:ImportanceClinical hyperthyroidism accelerates bone resorption without compensatory bone formation, reducing bone density and increasing the risk of fracture. The association between subclinical hyperthyroidism and fracture risk is less clear.ObjectiveTo investigate the association of endogenous subclinical thyroid dysfunction and fracture risk, independent of clinical confounders.Design, setting, and participantsThis cohort study included 10 946 participants from the Atherosclerosis Risk in Communities Study, an ongoing prospective cohort study of community-dwelling individuals conducted from 1987-1989 through December 31, 2019, in Washington County, Maryland; Forsyth County, North Carolina; Jackson, Mississippi; and the suburbs of Minneapolis, Minnesota. Participants were not taking thyroid medications and had no history of fractures.ExposuresThyrotropin and free thyroxine levels were measured at visit 2 (1990-1992). Subclinical hyperthyroidism was defined as a thyrotropin level lower than 0.56 mIU/L, subclinical hypothyroidism as a thyrotropin level higher than 5.1 mIU/L, and euthyroidism as a thyrotropin level of 0.56 to 5.1 mIU/L, with normal free thyroxine levels from 0.85 to 1.4 ng/dL.Main outcomes and measuresIncident fracture was ascertained using hospitalization discharge codes through 2019 and linkage to inpatient and outpatient Medicare claims through 2018.ResultsOf 10 946 participants (54.3% women; mean [SD] age, 57 [5.7] years), 93.0% had euthyroidism, 2.6% had subclinical hyperthyroidism, and 4.4% had subclinical hypothyroidism. During a median follow-up of 21 years (IQR, 13.0-27.3 years), there were 3556 incident fractures (167.1 per 10 000 person-years). The adjusted hazard ratios of fracture were 1.34 (95% CI, 1.09-1.65) for those with subclinical hyperthyroidism and 0.90 (95% CI, 0.77-1.05) for those with subclinical hypothyroidism compared with individuals with euthyroidism. Among those with normal free thyroxine levels, thyrotropin levels in the lower-than-normal range were significantly associated with higher fracture-related hospitalization risk; fracture risk was greater among individuals with thyrotropin concentrations below 0.56 mIU/L.Conclusions and relevanceThis community-based cohort study suggests that subclinical hyperthyroidism was an independent risk factor associated with fracture. The increased risk for fracture among individuals with a thyrotropin level lower than 0.56 mIU/L highlights a potential role for more aggressive screening and monitoring of patients with subclinical hyperthyroidism to prevent bone mineral disease.
| S-EPMC9644261 | biostudies-literature
Project description:BackgroundThe effect of subclinical thyroid dysfunction on vascular atherosclerosis remains uncertain. The objective of this study was to elucidate the association between sustained subclinical thyroid dysfunction and carotid plaques, which are an early surrogate marker of systemic atherosclerosis.MethodsThe study included 21,342 adults with consistent thyroid hormonal status on serial thyroid function tests (TFTs) and carotid artery duplex ultrasonography at a health screening center between 2007 and 2014. The effect of subclinical thyroid dysfunction on baseline carotid plaques and newly developed carotid plaques during 5-year follow-up was determined by logistic regression analyses and GEE (Generalized Estimating Equations), respectively.ResultsCarotid plaques were more common in the subclinical hypothyroidism (55.6%) than the euthyroidism (47.8%) at baseline. However, in multivariable analysis, thyroid status was not a significant risk for the carotid plaques at baseline. Instead, traditional cardiovascular risk factors, such as age (P <0.001), systolic blood pressure (P = 0.023), fasting blood glucose (P = 0.030), and creatinine (P = 0.012) were associated with baseline carotid plaques in subclinical hypothyroidism. In longitudinal analyses of subjects who were followed up for more than 5 years, there was no significant difference in the cumulative incidence of new carotid plaques according to time between subjects with subclinical hypothyroidism and those with euthyroidism (P = 0.392).ConclusionsSustained subclinical thyroid dysfunction did not affect the baseline or development of carotid plaques in healthy individuals.
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Project description:Background: Several studies conducted in America or Europe have described major cardiac remodeling and diastolic dysfunction in patients with sickle cell disease (SCD). We aimed at assessing cardiac involvement in SCD in sub-Saharan Africa where SCD is the most prevalent. Methods: In Cameroon, Mali and Senegal, SCD patients and healthy controls of the CADRE study underwent transthoracic echocardiography if aged ≥10 years. The comparison of clinical and echocardiographic features between patients and controls, and the associations between echocardiographic features and the vascular complications of SCD were assessed. Results: 612 SCD patients (483 SS or Sβ0, 99 SC, and 19 Sβ+) and 149 controls were included. The prevalence of dyspnea and congestive heart failure was low and did not differ significantly between patients and controls. While left ventricular ejection fraction did not differ between controls and patients, left and right cardiac chambers were homogeneously more dilated and hypertrophic in patients compared to controls and systemic vascular resistances were lower (p < 0.001 for all comparisons). Three hundred and forty nine SCD patients had extra-cardiac organ damages (stroke, leg ulcer, priapism, microalbuminuria or osteonecrosis). Increased left ventricular mass index, cardiac dilatation, cardiac output, and decreased systemic vascular resistances were associated with a history of at least one SCD-related organ damage after adjustment for confounders. Conclusions: Cardiac dilatation, cardiac output, left ventricular hypertrophy, and systemic vascular resistance are associated with extracardiac SCD complications in patients from sub-Saharan Africa despite a low prevalence of clinical heart failure. The prognostic value of cardiac subclinical involvement in SCD patients deserves further studies.
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Project description:ObjectiveProteasome-associated autoinflammatory syndrome (PRAAS) is caused by mutations affecting components of the proteasome and activation of the type I interferon (IFN) pathway. This study was undertaken to investigate the pathogenic mechanisms of a newly recognized type of PRAAS caused by PSMD12 haploinsufficiency.MethodsWhole-exome sequencing was performed in members of a family with skin rash, congenital uveitis, and developmental delay. We performed functional studies to assess proteasome dysfunction and inflammatory signatures in patients, and single-cell RNA sequencing to further explore the spectrum of immune cell activation.ResultsA novel truncated variant in PSMD12 (c.865C>T, p.Arg289*) was identified in 2 family members. The impairment of proteasome function was found in peripheral blood mononuclear cells (PBMCs), as well as in PSMD12-knockdown HEK 293T cell lines. Moreover, we defined the inflammatory signatures in patient PBMCs and found elevated IFN signals, especially in monocytes, by single-cell RNA sequencing.ConclusionThese findings indicate that PSMD12 haploinsufficiency causes a set of inflammation signatures in addition to neurodevelopmental disorders. Our work expands the genotype and phenotype spectrum of PRAAS and suggests a bridge between the almost exclusively inflammatory phenotypes in the majority of PRAAS patients and the almost exclusively neurodevelopmental phenotypes in the previously reported Stankiewicz-Isidor syndrome.
| S-EPMC9321778 | biostudies-literature
Project description:BackgroundMyocardial injury (MI) can be detected during the acute phase of Coronavirus disease 19 (COVID-19) and is associated with a dismal prognosis. Recent imaging studies described the persistence of cardiac abnormalities after the recovery. The aim of the study was to investigate the spectrum of cardiac abnormalities at mid-term follow-up in patients recovered from COVID-19 using clinical assessment, laboratory tests, and imaging evaluation with comprehensive echocardiography.MethodsThis is an observational, cross-sectional study assessing an unselected cohort of consecutive patients recovered from COVID-19. MI was defined by elevated plasma levels of high sensitive troponin T (hsTnT). At the follow-up, a complete examination including echocardiography was performed.ResultsThe 123 patients included were divided into two groups according to the presence of MI during hospitalization: group A (without MI) and group B (with MI). After a median of 85 days, group B patients were more frequently symptomatic for dyspnea and had significantly higher values of hsTnT and N-Terminal prohormone of Brain Natriuretic Peptide (NT-proBNP), compared to Group A. No differences between the two groups in left nor right ventricle dimension and ejection fraction were found. However, in group B a significant reduction of mean left ventricle global longitudinal strain was observed (-15.7±.7 vs -18.1± .3 in group A, p < 0.001), together with higher frequency of impaired diastolic function and higher values of pulmonary pressure.ConclusionsIn patients recovered from COVID-19, echocardiography with speckle-tracking analysis may be an useful imaging tool to identify subclinical myocardial dysfunction and potentially guide management strategies.
| S-EPMC8652678 | biostudies-literature
Project description:ImportanceAssociations between subclinical thyroid dysfunction and fractures are unclear and clinical trials are lacking.ObjectiveTo assess the association of subclinical thyroid dysfunction with hip, nonspine, spine, or any fractures.Data sources and study selectionThe databases of MEDLINE and EMBASE (inception to March 26, 2015) were searched without language restrictions for prospective cohort studies with thyroid function data and subsequent fractures.Data extractionIndividual participant data were obtained from 13 prospective cohorts in the United States, Europe, Australia, and Japan. Levels of thyroid function were defined as euthyroidism (thyroid-stimulating hormone [TSH], 0.45-4.49 mIU/L), subclinical hyperthyroidism (TSH <0.45 mIU/L), and subclinical hypothyroidism (TSH ≥4.50-19.99 mIU/L) with normal thyroxine concentrations.Main outcome and measuresThe primary outcome was hip fracture. Any fractures, nonspine fractures, and clinical spine fractures were secondary outcomes.ResultsAmong 70,298 participants, 4092 (5.8%) had subclinical hypothyroidism and 2219 (3.2%) had subclinical hyperthyroidism. During 762,401 person-years of follow-up, hip fracture occurred in 2975 participants (4.6%; 12 studies), any fracture in 2528 participants (9.0%; 8 studies), nonspine fracture in 2018 participants (8.4%; 8 studies), and spine fracture in 296 participants (1.3%; 6 studies). In age- and sex-adjusted analyses, the hazard ratio (HR) for subclinical hyperthyroidism vs euthyroidism was 1.36 for hip fracture (95% CI, 1.13-1.64; 146 events in 2082 participants vs 2534 in 56,471); for any fracture, HR was 1.28 (95% CI, 1.06-1.53; 121 events in 888 participants vs 2203 in 25,901); for nonspine fracture, HR was 1.16 (95% CI, 0.95-1.41; 107 events in 946 participants vs 1745 in 21,722); and for spine fracture, HR was 1.51 (95% CI, 0.93-2.45; 17 events in 732 participants vs 255 in 20,328). Lower TSH was associated with higher fracture rates: for TSH of less than 0.10 mIU/L, HR was 1.61 for hip fracture (95% CI, 1.21-2.15; 47 events in 510 participants); for any fracture, HR was 1.98 (95% CI, 1.41-2.78; 44 events in 212 participants); for nonspine fracture, HR was 1.61 (95% CI, 0.96-2.71; 32 events in 185 participants); and for spine fracture, HR was 3.57 (95% CI, 1.88-6.78; 8 events in 162 participants). Risks were similar after adjustment for other fracture risk factors. Endogenous subclinical hyperthyroidism (excluding thyroid medication users) was associated with HRs of 1.52 (95% CI, 1.19-1.93) for hip fracture, 1.42 (95% CI, 1.16-1.74) for any fracture, and 1.74 (95% CI, 1.01-2.99) for spine fracture. No association was found between subclinical hypothyroidism and fracture risk.Conclusions and relevanceSubclinical hyperthyroidism was associated with an increased risk of hip and other fractures, particularly among those with TSH levels of less than 0.10 mIU/L and those with endogenous subclinical hyperthyroidism. Further study is needed to determine whether treating subclinical hyperthyroidism can prevent fractures.
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Project description:The relationship between subclinical thyroid dysfunction and uric acid was not well established. This study aimed to determine if subclinical thyroid dysfunction is associated with hyperuricemia risk and to evaluate the levels of uric acid in patients with different forms of subclinical thyroid dysfunction. A systematic search was conducted in 4 databases to obtain relevant studies on subclinical thyroid dysfunction (subclinical hyperthyroidism and subclinical hypothyroidism) and uric acid. The standardized mean difference (SMD) or odds ratio (OR) and 95% confidence interval (95% CI) were used for evaluation, and the sensitivity analysis was conducted. Publication bias was estimated by funnel plot, Egger's test, and Begg's test. A total of 73 studies were included in this meta-analysis. The results demonstrated that serum levels of uric acid in patients with subclinical hypothyroidism were significantly higher than those of controls and patients with subclinical hyperthyroidism. Patients with subclinical thyroid dysfunction had a higher prevalence of hyperuricemia compared with normal clinical thyroid function. Subclinical thyroid dysfunction was associated with the prevalence of hyperuricemia. Different types of subclinical thyroid dysfunction had varied effects on serum levels of uric acid.
| S-EPMC8687809 | biostudies-literature