Recent Advances in the Management of Microangiopathic Hemolytic Anemias (MAHA): A Narrative Review.

Red blood cells (RBCs) start to break down early in hemolytic anemia, which can be chronic or life-threatening. It should be considered while determining if normocytic or macrocytic anemia is present. Hemolysis in the reticuloendothelial system may happen intravascularly, extravascularly, or both. It accounts for a broad spectrum of laboratory and clinical situations, both physiological and pathological. Whenever the frequency of RBC breakdown is rapid enough to lower hemoglobin levels below the normal range, hemolytic anemia occurs. Microangiopathic hemolytic anemia (MAHA) is a term used to describe non-immune hemolysis induced by intravascular RBC fragmentation caused by substances in the tiny blood arteries that generate schistocytes in the peripheral circulation. Microvasculature abnormalities, such as small arterioles and capillaries, are usually involved. Furthermore, MAHA can also be brought on by intravascular devices like a prosthetic heart valve or assistive technologies. Poor deformity results in entrapment, phagocytosis, antibody-mediated elimination through phagocytosis or direct complement activation, fragmentation brought about by microthrombi or acute mechanical stress, oxidation, or spontaneous cellular death. Hemolysis may cause acute anemia, jaundice, hematuria, dyspnea, tiredness, tachycardia, and possibly hypotension. This article aims to synthesize existing research, identify therapeutic strategies, and provide insights into current and emerging approaches for managing this complex hematological disorder.

Rasmussen's Encephalitis: A Literary Review.

Usually affecting one hemisphere of the brain, Rasmussen's encephalitis (RE) is a persistent inflammatory disease of unclear origin. Rasmussen and colleagues presumed a viral etiology of the sickness in their first description. Later, the condition was linked to autoantibodies that were in the blood. Recently, it was shown that the cause of RE was a cytotoxic T-cell reaction to neurons. RE may be identified histopathologically by cortical inflammation, neuronal degeneration, and cerebral hemispheric-specific gliosis. The hemisphere is affected by increasing multilocular inflammation. To diagnose patients sooner and to evaluate whether the aforementioned phenomena are primary or secondary, it is essential to continue the search for a primary immunological or viral component. This information is crucial for determining the effectiveness of immunotherapy. RE-related seizures can only now be managed surgically. The only procedure that works is complete hemispheric disconnection (hemidisconnection), which may be done as either a (functional) hemispherectomy or hemispherectomy. Although thalidomide has been anecdotally reported, its safety profile prevents it from being used as a first-line treatment despite having a noticeable effect on the frequency and severity of seizures. Finding the disease's root causes more quickly by combining descriptive clinical studies, genetic testing, and early histological evaluation of RE tissue specimens to check for viral and autoimmune pathogenesis. Creating appropriate in vitro or animal models will enable the study of causality, perhaps directing clinical trials.

A Narrative Review on the Effect of Maternal Hypothyroidism on Fetal Development.

The thyroid is a butterfly-shaped gland located in the human body's neck region. The thyroid produces three hormones that are essential for regulating body temperature, energy production, weight, hair and nail growth, and menstrual cycle maintenance. The production of these hormones is controlled by a feedback mechanism. Various factors cause changes in the stimulation and inhibition of these hormones, which ultimately causes either excessive release or a decrease in the levels of thyroid hormones. These causes can be physiological or pathological. One of the physiological causes is pregnancy. Pregnancy is a very complex process in which many changes occur in the body and its functioning. One of which is changes in the maternal thyroid gland. The inability to adequately adapt to the changes leads to the abnormal functioning of the thyroid gland. During pregnancy, there is a variation in the concentration of thyroid hormones which may cause a decrease in levels or inhibition in the production of thyroid hormones. This condition is called hypothyroidism. Hypothyroidism in pregnant mothers can either be gestational or may be a condition that is present way before her pregnancy. Often, gestational hypothyroidism reverts after delivery during the postpartum period but can also be present as subclinical hypothyroidism. In such cases, they pose a significant threat to development, cause growth hindrance to the infant in the womb, and cause abnormalities in the offspring in the future. Some of the changes occur in the gland because of enhancement in levels of thyroid binding globulin, increased clearance rate of iodine from the body in kidneys, altered effects in human chorionic gonadotropin hormone, and decreased consumption of iodine in meals. Iodine disbalance in maternal hypothyroidism is associated with severe health issues like cretinism and mental retardation. Thyroid hormones are crucial for the infant's neural, cognitive, and intelligence quotient development in the womb. Thus, the disturbances in the maternal hormone levels disturb typical early developmental characteristics. In the world of rapidly advancing scientific research, there are many ways in which this condition can be detected early, diagnosed correctly, and given apt and required attention and treatment for causing the least harm to the fetus and the mother.