RESUMO
Dengue is a very serious public health problem that can manifest a wide range of symptoms from asymptomatic to fatal conditions, such as dengue shock syndrome (DSS). It is a life-threatening mosquito-borne viral infection widely spread in tropical areas. Dengue virus transmission occurs from an infected Aedes mosquito to humans. Various factors are responsible for the occurrence of the disease, such as viral load, age of the host, immune status of the host, and genetic variability. Dengue infection occurs in three phases: febrile, critical, and recovery. The febrile phase lasts for seven days and manifests symptoms such as high-grade fever, headache, arthralgia, and backache, and in some cases, the upper respiratory tract and gastrointestinal tract are also involved. Severe dengue is characterized by endothelial dysfunction that causes vascular permeability and plasma leakage. The fundamental mechanisms of these immune pathologies are not yet known. Dengue manifests various complications such as dengue encephalopathy, encephalitis, stroke, ocular involvement, acute transverse myelitis, myalgia, and cerebellar syndrome, but the most commonly seen is liver involvement. Dengue is managed supportively because there are no proven curative treatments. The cornerstone of care during the critical period of dengue is prudent fluid resuscitation. The first fluid of preference is a crystalloid. Prophylactic transfusion of platelets is not advised. The occurrence of four antigenically different dengue virus serotypes, each able to elicit a cross-reactive and disease-enhancing antibody response against the other three serotypes, has made the creation of the dengue vaccine a difficult undertaking. The development of a dengue vaccine has faced significant challenges due to a lack of the best animal models and a variety of immunological conditions in people, particularly in endemic locations. Dengvaxia is a live attenuated vaccine, which was developed by Sanofi. It is made up of four chimeric vaccine viruses produced by Vero cells.
RESUMO
Diabetes mellitus (DM) is the most common metabolic disease worldwide. Hence, the prevalence of the disease continues to increase across the globe. Metformin is used as a first-line oral hypoglycemic drug to keep control of type-2 DM (T2DM) in adults. Diabetic patients on metformin have been largely seen to be suffering from a deficiency of vitamin B12. It is a water-soluble vitamin mainly obtained from animal food like meat. At the basic cell level, it acts as a cofactor for enzymes essential for DNA synthesis and neuroprotection. As a result, vitamin B12 deficiency can show clinical effects such as progressive demyelination, peripheral neuropathy and haematological abnormalities (such as macrocytic anaemia and neutrophil hypersegmentation). Various studies also show a relation between vitamin B12 insufficiency and metformin-treated T2DM patients as decreased absorption of vitamin B12. There could be a severe complication of vitamin B12 deficiency in T2DM patients. The use of proton pump inhibitors, gastric bypass surgery, older patients and patients with a higher red blood cell turnover are factors that hasten the depletion of vitamin B12 reserves in the liver. Methylmalonic acid and homocysteine levels can be measured to identify vitamin B12 insufficiency at its early stage if blood vitamin B12 levels are borderline. The action of metformin on vitamin B12 absorption and its potential mechanisms of inhibition will be the main topics of discussion in this review. The review will also discuss how vitamin B12 deficiencies in T2DM patients using metformin affect their clinical results.
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Congestive heart failure (CHF) is a complex, heterogeneous medically ill condition that can occur due to diverse primary (cardiomyopathies, coronary artery diseases, and hypertension) and secondary causes (high salt intake and noncompliance toward treatment) and leads to significant morbidity and mortality. The approach toward managing the patient of CHF in the pediatric age group is more complex than in the adult population. Currently, in the adult group of the population of CHF, there are well-established guidelines for managing these patients, but in the case of children, there are no well-established guidelines; therefore, this systematic review gives more ideas for managing the pediatric population undergoing CHF. Treatment of the underlying cause, rectification of any advancing event, and management of pulmonary or systemic obstruction are the principles for management. The most widely used drugs are diuretics and angiotensin-converting enzyme (ACE) inhibitors, whereas beta-blockers are less commonly used in children than in adults. ACE inhibitors such as captopril, enalapril, and cilazapril are widely used in the pediatric age group. ACE inhibitors act on the renin-angiotensin-aldosterone system (RAAS) similar to those in the adult population. In children with heart failure (HF), ACE inhibitors reduce the pressure in the aorta, resistance in the systemic blood vessels, and upper left and right chamber pressures but do not appreciably influence pulmonary vascular resistance. We use a patient's initial perfusion and volume status assessment to decide further action for the supervision of acute HF. This paradigm was adopted from adult studies that showed higher rates of morbidity and mortality in patients with HF whose hemodynamic or volume status assessment results were stable with a pulmonary capillary wedge pressure >18 mmHg and a combined index (CI) of 2.2 L/minute/m2. ACE inhibitors, beta-blockers, and spironolactone are the most widely prescribed drugs for the chronic condition of CHF. This study shows the current status of medical therapy for critical as well as persistent pediatric HF.
RESUMO
Fever-induced seizures are referred to as febrile seizures (FSs). The most prevalent kind of epilepsy and neurological illness in infants and young children is FS. With a high occurrence seen between the ages of 12 and 18 months, they frequently affect children aged six months to five years. FS is a benign condition that seldom results in brain damage. Nevertheless, they cause stress and emotional anguish for the parents, who may believe that the death of their child is going to occur during the seizure. Lately, a more broad-based phrase has been used, fever-associated seizures or epilepsy that includes simple, complicated, and extended FSs. These are the three different kinds of FSs. Febrile status epilepticus is a subgroup of complex FS. The other kinds of FSs are FS plus, Dravet syndrome, hereditary epilepsy with FS plus, and febrile infection-related epilepsy syndrome. The most frequent, brief, and generalized simple FSs have a greater likelihood of causing temporal lobe epilepsy than complex FSs. These seizures are linked to the release of inflammatory mediators like interleukin (IL)-1, IL-6, and tumor necrosis factor, which are well-known fever inducers. This article details the factors that contribute to the occurrence of FSs, epidemiology, pathophysiology, evaluation, and management of the child.
