Dengue infection - mechanisms, epidemiology, pathogenesis, diagnosis and management !

DENGUE:

"Dengue is the leading mosquito-borne viral illness infecting humans !"

Dengue is caused by infection with any of the four dengue virus serotypes. This review highlights the mechanisms underlying the clinical course of a dengue infection, which can range from mild febrile illness through to hemorrhagic fever and circulatory shock. It also outlines the epidemiology, pathogenesis, diagnosis and management of dengue infection.

Key phases of dengue infection

Dengue is a mosquito-borne disease caused by infection with dengue virus (DENV). Clinically, the disease can range from a mild febrile illness (previously called dengue fever) through to dengue with warning signs and severe dengue, which includes what were previously called dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS).

 

DENVs belong to the genus Flavivirus of the Flaviviridae family. The four serotypes are enveloped, spherical viral particles with a diameter of approximately 500 Å20. The genome of each serotype comprises approximately 11 kb of positive-sense, single-stranded RNA that encodes ten proteins. The three structural proteins encoded by the genome are the membrane (M) protein, envelope (E) protein and capsid (C) protein; the non-structural (NS) proteins are NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5.

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A Primeview on Sickle Cell Disease !

Primeview:

Sickle cell disease (SCD) is a group of inherited disorders caused by mutations in HBB, which encodes haemoglobin subunit β. Haemoglobin molecules that include mutant sickle β-globin subunits can polymerize; erythrocytes that contain mostly haemoglobin polymers assume a sickled form and are prone to haemolysis. Other pathophysiological mechanisms that contribute to the SCD phenotype are vaso-occlusion and activation of the immune system. SCD is characterized by a remarkable phenotypic complexity. Common acute complications are acute pain events, acute chest syndrome and stroke; chronic complications (including chronic kidney disease) can damage all organs. Hydroxycarbamide, blood transfusions and haematopoietic stem cell transplantation can reduce the severity of the disease. Early diagnosis is crucial to improve survival, and universal newborn screening programmes have been implemented in some countries but are challenging in low-income, high-burden settings.

Sickle cell disease (SCD) is an umbrella term that defines a group of inherited diseases (including sickle cell anaemia (SCA), HbSC and HbSβ-thalassaemia) characterized by mutations in the gene encoding the haemoglobin subunit β (HBB). Haemoglobin (Hb) is a tetrameric protein composed of different combinations of globin subunits; each globin subunit is associated with the cofactor haem, which can carry a molecule of oxygen. Hb is expressed by red blood cells, both reticulocytes (immature red blood cells) and erythrocytes (mature red blood cells). Several genes encode different types of globin proteins, and their various tetrameric combinations generate multiple types of Hb, which are normally expressed at different stages of life — embryonic, fetal and adult. Hb A (HbA), the most abundant (>90%) form of adult Hb, comprises two α-globin subunits (encoded by the duplicated HBA1 and HBA2 genes) and two β-globin subunits.

A single nucleotide substitution in HBB results in the sickle Hb (HbS) allele βS; the mutant protein generated from the βS allele is the sickle β-globin subunit and has an amino acid substitution. Under conditions of deoxygenation (that is, when the Hb is not bound to oxygen), Hb tetramers that include two of these mutant sickle β-globin subunits (that is, HbS) can polymerize and cause the erythrocytes to assume a crescent or sickled shape from which the disease takes its name. Hb tetramers with one sickle β-globin subunit can also polymerize, albeit not as efficiently as HbS. Sickle erythrocytes can lead to recurrent vaso-occlusive episodes that are the hallmark of SCD. SCD is inherited as an autosomal codominant trait; individuals who are heterozygous for the βS allele carry the sickle cell trait (HbAS) but do not have SCD, whereas individuals who are homozygous for the βS allele have SCA. SCA, the most common form of SCD, is a lifelong disease characterized by chronic haemolytic anaemia, unpredictable episodes of pain and widespread organ damage.

This primeview focuses on SCA and aims to balance such remarkable advances with the key major challenges remaining worldwide to improve the prevention and management of this chronic disease and ultimately to discover an affordable cure.

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Esophageal Cancer

Overview

Esophageal cancer starts at the inside lining of the esophagus and spreads outward through the other layers as it grows. The two most common forms of esophageal cancer are named for the type of cells that become malignant:

• Squamous cell carcinoma: Cancer that forms in squamous cells, the thin, flat cells lining the esophagus. This cancer is most often found in the upper and middle part of the esophagus, but can occur anywhere along the esophagus. This is also called epidermoid carcinoma.
• Adenocarcinoma: Cancer that begins in glandular (secretory) cells. Glandular cells in the lining of the esophagus produce and release fluids such as mucus. Adenocarcinomas usually form in the lower part of the esophagus, near the stomach.

The National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program estimates that some 16,980 people in the United States will be diagnosed with esophageal cancer and 15,590 will die of the disease in 2015. The average five year survival rate is just 17.9 percent.

Smoking, heavy alcohol consumption, and Barrett esophagus can increase the risk of developing esophageal cancer. Other risk factors include older age, being male, and being African-American.

Read more: Esophageal Cancer

The esophagus and stomach are part of the upper gastrointestinal (digestive) system.

Video link: Esophageal Cancer

Source: aacrfoundation

Colorectal cancer

Colorectal cancer had a low incidence several decades ago. However, it has become a predominant cancer and now accounts for approximately 10% of cancer-related mortality in western countries. The ‘rise’ of colorectal cancer in developed countries can be attributed to the increasingly ageing population, unfavourable modern dietary habits and an increase in risk factors, such as smoking, low physical exercise and obesity. New treatments for primary and metastatic colorectal cancer have emerged, providing additional options for patients; these treatments include laparoscopic surgery for primary disease, more-aggressive resection of metastatic disease (such as liver and pulmonary metastases), radiotherapy for rectal cancer, and neoadjuvant and palliative chemotherapies. However, these new treatment options have had limited impact on cure rates and long-term survival. For these reasons, and the recognition that colorectal cancer is long preceded by a polypoid precursor, screening programmes have gained momentum. This Primer provides an overview of the current state of the art of knowledge on the epidemiology and mechanisms of colorectal cancer, as well as on diagnosis and treatment.

Introduction

We live in an era with improved worldwide average living standards and increased access to adequate health care that has considerably improved the diagnosis and treatment of diseases. These measures have had an effect on the average life expectancy in most regions of the world. However, although death rates from communicable diseases have improved globally as a result of these medical improvements, cancer-related mortality has increased by almost 40% over the past 40 years. A further 60% increase is expected in the next 15 years, with 13 million people estimated to die of cancer in 2030. The main causes of cancer-related mortality have also changed, attributable to alterations in disease incidence, the introduction of screening programmes and therapeutic improvements. Colorectal cancer was rather rare in 1950, but has become a predominant cancer in western countries, now accounting for approximately 10% of cancer-related mortality. Reasons explaining this increased incidence include an ageing population and the preponderance of poor dietary habits, smoking, low physical activity and obesity in western countries. The change in incidence is not only apparent in the rates of sporadic disease but also in some familial cancer syndromes. Indeed, given that the rates of Helicobacter pyloriinfection (a causative factor of gastric cancer) have fallen dramatically, colorectal cancer is now the predominant presentation of Lynch syndrome (a hereditary non-polyposis type of colorectal cancer), whereas carriers of this syndrome used to be predominantly affected by gastric cancer.

Read more: Colorectal cancer

Source: krmc

Global epidemiology of gout: prevalence, incidence and risk factors.

Gout is a crystal-deposition disease that results from chronic elevation of uric acid levels above the saturation point for monosodium urate (MSU) crystal formation. Initial presentation is mainly severely painful episodes of peripheral joint synovitis (acute self-limiting 'attacks') but joint damage and deformity, chronic usage-related pain and subcutaneous tophus deposition can eventually develop. The global burden of gout is substantial and seems to be increasing in many parts of the world over the past 50 years. However, methodological differences impair the comparison of gout epidemiology between countries. In this comprehensive Review, data from epidemiological studies from diverse regions of the world are synthesized to depict the geographic variation in gout prevalence and incidence. Key advances in the understanding of factors associated with increased risk of gout are also summarized. The collected data indicate that the distribution of gout is uneven across the globe, with prevalence being highest in Pacific countries. Developed countries tend to have a higher burden of gout than developing countries, and seem to have increasing prevalence and incidence of the disease. Some ethnic groups are particularly susceptible to gout, supporting the importance of genetic predisposition. Socioeconomic and dietary factors, as well as comorbidities and medications that can influence uric acid levels and/or facilitate MSU crystal formation, are also important in determining the risk of developing clinically evident gout.

Gout is the most common form of inflammatory arthritis and is caused by chronic elevation of serum uric acid (SUA) levels above the saturation point for monosodium urate (MSU) crystal formation. The deposition of MSU crystals, which occurs predominantly in peripheral joints and surrounding tissues, defines gout. The characteristic presentation is of rapidly developing monoarticular synovitis in peripheral joints (an acute 'attack') that is extremely painful but self-limiting, with resolution within several days or 1–2 weeks. However, long-term deposition of MSU crystals can result in joint damage and disfiguring subcutaneous tophi. In addition, gout is also associated with many conditions that affect longevity and well-being,1 such as metabolic syndrome,2 cardiovascular diseases3, 4, 5, 6 and renal diseases. In particular, gout is increasingly recognised as an independent cardiovascular risk factor.

Read more: Global epidemiology of gout: prevalence, incidence and risk factors.

Figure 1: The estimated prevalence of gout across the world.

Source: NatureReviewsRheumatology