Breakfast, lunch, and dinner sign: a hallmark of flea and bedbug bites

Abstract: Human, dog, and cat fleas, as well as bedbugs, feed by biting their victims, causing acute prurigo, which is aggravated in sensitized victims (papular urticaria). The lesions appear in the classic "breakfast, lunch, and dinner" pattern. There are two main explanations: the parasites "map" the skin area in search of the best places to bite, and their removal when victim scratches, and then reattach to the skin. Treatments aim to control pruritus, as well as hypersensitivity reactions when necessary. Prevention is based on environmental control measures. The "breakfast, lunch, and dinner" sign is a definitive marker for diagnosis and the parasite´s identification and control.

Breakfast, lunch, and dinner sign: a hallmark of flea and bedbug bites.

Human, dog, and cat fleas, as well as bedbugs, feed by biting their victims, causing acute prurigo, which is aggravated in sensitized victims (papular urticaria). The lesions appear in the classic "breakfast, lunch, and dinner" pattern. There are two main explanations: the parasites "map" the skin area in search of the best places to bite, and their removal when victim scratches, and then reattach to the skin. Treatments aim to control pruritus, as well as hypersensitivity reactions when necessary. Prevention is based on environmental control measures. The "breakfast, lunch, and dinner" sign is a definitive marker for diagnosis and the parasite´s identification and control.

Glycated hemoglobin correlates with arterial stiffness and endothelial dysfunction in patients with resistant hypertension and uncontrolled diabetes mellitus.

This study aimed to evaluate the effects of glycated hemoglobin (HbA1c ) on flow-mediated dilation, intima-media thickness, pulse wave velocity, and left ventricular mass index in patients with resistant hypertension (RHTN) comparing RHTN-controlled diabetes mellitus and RHTN-uncontrolled type 2 diabetes mellitus. Two groups were formed: HbA1c <7.0% (RHTN-controlled diabetes mellitus: n = 98) and HbA1c ≥7.0% (RHTN-uncontrolled diabetes mellitus: n = 122). Intima-media thickness and flow-mediated dilation were measured by high-resolution ultrasound, left ventricular mass index by echocardiography, and arterial stiffness by carotid-femoral pulse wave velocity. No differences in blood pressure levels were found between the groups but body mass index was higher in patients with RHTN-uncontrolled diabetes mellitus. Endothelial dysfunction and arterial stiffness were worse in patients with RHTN-uncontrolled diabetes mellitus. Intima-media thickness and left ventricular mass index measurements were similar between the groups. After adjustments, multiple linear regression analyses showed that HbA1c was an independent predictor of flow-mediated dilation and pulse wave velocity in all patients with RHTN. In conclusion, HbA1c may predict the grade of arterial stiffness and endothelial dysfunction in patients with RHTN, and superimposed uncontrolled diabetes mellitus implicates further impairment of vascular function.

Disfunção Endotelial e Hipertensão Arterial / Endothelium Dysfunction and Arterial Hypertension

O papel do endotélio vascular na fisiopatologia das doenças cardiovasculares tem sido amplamente difundido. Alguns estudos demonstraram que a alteração da função endotelial constitui um importante mecanismo fisiopatogênico da hipertensão arterial, enquanto outros afirmam que hipertensão arterial provoca alteração da função endotelial. Disfunção endotelial (DE)caracteriza qualquer alteração de atividade normal do endotélio incluindo atividade vasomotora, proliferação celular, adesão/agregação plaquetária, permeabilidade vascular e a interação leucócitos­parede vascular. Contudo, em repouso o leito arterial exibe um estado basal de vasoconstrição (tônus vascular) modulado por mecanismos de controle central (sistema nervoso­simpático), periférico (sistema renina­angiotensina­aldosterona) e um mecanismo local (endotelial), cuja potência é superior às anteriores. DE na hipertensão está relacionada à diminuição da biodisponibilidade de NO por redução da síntese e liberação pela sintase endotelial do óxido nítrico (eNOS) influenciada por fatores genéticos e ambientais como hipóxia, hipofluxo, forças de cisalhamento, redução do substrato L-arginina e seus cofatores, ou inativação do NO resultado da sua ligação com diferentes moléculas como hemoglobina, albumina e, principalmente, sua interação com espécies reativas de oxigênio (estresse oxidativo). DE na hipertensão pode ainda, estar associada à liberação de substâncias vasoconstritoras derivadas do endotélio como tromboxano-A2, prostaglandina-H2, endotelina-1 e angiotensina-II.

The role of the vascular endothelium in the pathophysiology of cardiovascular disease has been widely discussed. Some studies have shown that changes in endothelial function are an important pathophysiological mechanism in hypertension, while others claim that high blood pressure causes changes in the endothelial function. Endothelial dysfunction (ED) includes any change in the normal activity of the endothelium including vasomotor activity, cell proliferation, platelet adhesion/aggregation, vascular permeability and leukocyte­vascular wall interactions. However, at rest, the arterial bed exhibits a baseline vasoconstriction (vascular tone) modulated by central control (sympathetic­nervous system), peripheral (renin­angiotensin­aldosterone system) and local mechanisms (endothelial); the effect of the latter is the greatest. ED in hypertension is related to decreased NO bioavailability due to reduced synthesis and release by endothelial NO synthase (eNOS). This condition is influenced by genetic and environmental factors such as hypoxia, low flow, shear stress, diminished L-arginine substrate and its cofactors or inactivation of NO after binding with molecules such as hemoglobin, albumin, and especially its interaction with reactive oxygen species (oxidative stress). ED in hypertension may also be associated with the release of vasoconstrictor endothelium-derived substances such as thromboxane-A2, prostaglandin-H2, endothelin-1 and angiotensin-II