Infective dermatitis (ID) is a chronic, relapsing dermatitis associated with human T-lymphotrophic virus (HTLV)-1 which was initially described in Jamaican children. Although most cases have been ...reported in Jamaica, ID may be seen in other HTLV-1 endemic areas, such as Brazil, Japan, sub-Saharan Africa, and Trinidad and Tobago. Since HTLV-1 infection has been implicated in the development of adult T-cell leukemia/lymphoma, an aggressive hematologic malignancy, and HTLV-1-associated myelopathy/tropical spastic paraparesis, a neurodegenerative disease, ID may serve as an early clinical marker for either condition. Although HTLV-1-associated infective dermatitis is considered by most to be rare, it has been increasingly diagnosed over the past 20 years; some suggest ID may be underdiagnosed. One should maintain suspicion of HTLV-1 infection among individuals in or from endemic areas, recognizing the clinical features and prognostic implications of infectious dermatitis.
Atherosclerosis development is a complex process, with inflammation, indicated by elevated high-sensitivity C-reactive protein (hs-CRP), as a potential mediator. Obesity, physical activity, and ...depression have all been reported to affect hs-CRP. However, these factors are interconnected, and their relative individual importance remains unclear. From a separate prospective cohort study, 289 patients were selected for the present substudy. We assessed the relation of a variety of potential predictors and hs-CRP. Obesity, physical activity, and depression, in addition to several other potential factors, were analyzed in bivariate and multivariate linear regression models, adjusting for potential confounders. In unadjusted analyses, mild-to-moderate and severe depression were associated with increased hs-CRP compared to no or minimal depression. Vigorous physical activity was associated with decreased hs-CRP compared to no physical activity. All classes of obesity were associated with increased hs-CRP. In addition, attaining a college or graduate degree was associated with decreased hs-CRP compared to high school or less educational attainment. On multivariate analysis, depression was no longer associated with increased hs-CRP. Physical activity remained associated with decreased hs-CRP but only at vigorous levels. Educational attainment also remained associated but only at the collegiate or professional education level. Ultimately, obesity remained the greatest absolute predictor of elevated hs-CRP. In conclusion, in analyses of multiple factors potentially predictive of elevated hs-CRP in a large population of patients with subclinical coronary heart disease, we found the most important predictor to be obesity.
Objectives This article provides recommendations on the use of antithrombotic therapy in patients with stroke or transient ischemic attack (TIA). Methods We generated treatment recommendations (Grade ...1) and suggestions (Grade 2) based on high (A), moderate (B), and low (C) quality evidence. Results In patients with acute ischemic stroke, we recommend IV recombinant tissue plasminogen activator (r-tPA) if treatment can be initiated within 3 h (Grade 1A) or 4.5 h (Grade 2C) of symptom onset; we suggest intraarterial r-tPA in patients ineligible for IV tPA if treatment can be initiated within 6 h (Grade 2C); we suggest against the use of mechanical thrombectomy (Grade 2C) although carefully selected patients may choose this intervention; and we recommend early aspirin therapy at a dose of 160 to 325 mg (Grade 1A). In patients with acute stroke and restricted mobility, we suggest the use of prophylactic-dose heparin or intermittent pneumatic compression devices (Grade 2B) and suggest against the use of elastic compression stockings (Grade 2B). In patients with a history of noncardioembolic ischemic stroke or TIA, we recommend long-term treatment with aspirin (75-100 mg once daily), clopidogrel (75 mg once daily), aspirin/extended release dipyridamole (25 mg/200 mg bid), or cilostazol (100 mg bid) over no antiplatelet therapy (Grade 1A), oral anticoagulants (Grade 1B), the combination of clopidogrel plus aspirin (Grade 1B), or triflusal (Grade 2B). Of the recommended antiplatelet regimens, we suggest clopidogrel or aspirin/extended-release dipyridamole over aspirin (Grade 2B) or cilostazol (Grade 2C). In patients with a history of stroke or TIA and atrial fibrillation we recommend oral anticoagulation over no antithrombotic therapy, aspirin, and combination therapy with aspirin and clopidogrel (Grade 1B). Conclusions These recommendations can help clinicians make evidence-based treatment decisions with their patients who have had strokes.
Facial bacterial infections: Folliculitis Laureano, Ana Cristina, MD; Schwartz, Robert A., MD, MPH; Cohen, Philip J., MD
Clinics in dermatology,
11/2014, Letnik:
32, Številka:
6
Journal Article
Recenzirano
Abstract Facial bacterial infections are most commonly caused by infections of the hair follicles. Wherever pilosebaceous units are found folliculitis can occur, with the most frequent bacterial ...culprit being Staphylococcus aureus . We review different origins of facial folliculitis , distinguishing bacterial forms from other infectious and non-infectious mimickers. We distinguish folliculitis from pseudofolliculitis and perifolliculitis . Clinical features, etiology, pathology, and management options are also discussed.
Inefficient Batteries in Heart Failure Schwartz, Brian; Gjini, Petro; Gopal, Deepa M. ...
JACC. Basic to translational science,
November 2022, 2022-11-00, 2022-11-01, Letnik:
7, Številka:
11
Journal Article
Recenzirano
Odprti dostop
•Mitochondrial abnormalities have long been described in heart failure.•Reducing mitochondrial function to only a few measures limits our understanding of the entire mitochondrial ecosystem.•Systems ...biology approaches and comprehensive assessments of the multiple facets of mitochondrial function are needed to advance our understanding of the disturbed mitochondrial ecosystem in heart failure.
Mitochondrial abnormalities have long been described in the setting of cardiomyopathies and heart failure (HF), yet the mechanisms of mitochondrial dysfunction in cardiac pathophysiology remain poorly understood. Many studies have described HF as an energy-deprived state characterized by a decline in adenosine triphosphate production, largely driven by impaired oxidative phosphorylation. However, impairments in oxidative phosphorylation extend beyond a simple decline in adenosine triphosphate production and, in fact, reflect pervasive metabolic aberrations that cannot be fully appreciated from the isolated, often siloed, interrogation of individual aspects of mitochondrial function. With the application of broader and deeper examinations into mitochondrial and metabolic systems, recent data suggest that HF with preserved ejection fraction is likely metabolically disparate from HF with reduced ejection fraction. In our review, we introduce the concept of the mitochondrial ecosystem, comprising intricate systems of metabolic pathways and dynamic changes in mitochondrial networks and subcellular locations. The mitochondrial ecosystem exists in a delicate balance, and perturbations in one component often have a ripple effect, influencing both upstream and downstream cellular pathways with effects enhanced by mitochondrial genetic variation. Expanding and deepening our vantage of the mitochondrial ecosystem in HF is critical to identifying consistent metabolic perturbations to develop therapeutics aimed at preventing and improving outcomes in HF.
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Diurnal and nocturnal species are profoundly different in terms of the temporal organization of daily rhythms in physiology and behavior. The neural bases for these divergent patterns are at present ...unknown. Here we examine functional differences in the suprachiasmatic nucleus (SCN) and one of its primary targets in a diurnal rodent, the unstriped Nile grass rat (
Arvicanthis niloticus) and in a nocturnal one, the laboratory rat (
Rattus norvegicus). Grass rats and laboratory rats were housed in a 12:12 light:dark cycle, and killed at six time points. cFos-immunoreactive rhythms in the SCN of grass rats and laboratory rats were similar to those reported previously, with peaks early in the light phase and troughs in the dark phase. However, cFos-immunoreactivity in the lower subparaventricular zone (LSPV) of grass rats rose sharply 5 h into the dark phase, and remained high through the first hour after light onset, whereas in laboratory rats it peaked 1 h after light onset and was low at all other sampling times. Daily cFos rhythms in both the SCN and the LSPV persisted in grass rats, but not in laboratory rats, after extended periods in constant darkness. In grass rats, the endogenous cFos rhythm in the LSPV, but not the SCN, was present both in calbindin-positive and in calbindin-negative cells. Cells that expressed cFos at night in the region of the LSPV in grass rats were clearly outside of the boundaries of the SCN as delineated by Nissl stain and immunoreactivity for vasopressin and vasoactive intestinal peptide.
The LSPV of the grass rat, a region that receives substantial input from the SCN, displays a daily rhythm in cFos expression that differs from that of laboratory rats with respect to its rising phase, the duration of the peak and its dependence on a light/dark cycle. These characteristics may reflect the existence of mechanisms in the LSPV that enable it to modulate efferent SCN signals differently in diurnal and nocturnal species.
Abstract The effects of phosphodiesterase type 5 inhibitors on vasodilation mediated via nitric oxide–cyclic guanosine monophosphate are well described. Less is known about other mechanisms through ...which phosphodiesterase type 5 inhibitors benefit endothelial function, including normalization of serum biomarkers, increased levels of endothelial progenitor cells, ischemia–reperfusion protection mechanisms, and other actions specific to patients with diabetes. These various mechanisms are reviewed. Their impact on several cardiovascular diseases, including erectile dysfunction, pulmonary hypertension, heart failure, high-altitude pulmonary edema, Raynaud's phenomenon, coronary artery disease, diabetes, and atherosclerosis, is presented.
Purpose
Bone pain is a common side effect of pegfilgrastim and can interfere with quality of life and treatment adherence. This study investigated the impact of antihistamine prophylaxis on ...pegfilgrastim-induced bone pain.
Methods
This is a two-stage enrichment trial design. Patients receiving an initial dose of pegfilgrastim after chemotherapy were enrolled into the observation (OBS) stage. Those who developed significant back or leg bone pain (SP) were enrolled into the treatment (TRT) stage and randomized to daily loratadine 10 mg or placebo for 7 days. SP was defined by Brief Pain Inventory as back or leg pain score ≥5 and a 2-point increase after pegfilgrastim. The primary end point of TRT was reduction of worst back or leg bone pain with loratadine, defined as a 2-point decrease after treatment compared to OBS.
Results
Two hundred thirteen patients were included in the final analysis. Incidence of SP was 30.5 %. The SP subset had a worse overall Functional Assessment of Cancer Therapy-Bone Pain score (33.9 vs. 51.7,
p
< 0.001) and a higher mean white blood cell count (15.4 vs. 8.4 K/cm
3
,
p
= 0.013) following pegfilgrastim than those without SP. Forty-six patients were randomized in the TRT. Benefit was 77.3 % with loratadine and 62.5 % with placebo (
p
= 0.35). Baseline NSAID use was documented in four patients (18.2 %) in loratadine arm and two patients (8.3 %) in placebo arm, with baseline non-NSAID use documented in five (22.7 %) and six (25 %) patients, respectively. Eight additional patients used NSAIDS by day 8 compared to day 1 (six in the loratadine and two in the placebo arm). A total of six additional patients used non-NSAIDS by day 8 compared to day 1 (four in the loratadine and two in the placebo arm).
Conclusions
Administration of prophylactic loratadine does not decrease the incidence of severe bone pain or improve quality of life in a high-risk patient population.
ClinicalTrials.gov identifier: NCT01311336.
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