In the Southern Hemisphere, the tropical cyclone year begins on July 1 and runs all year-round encompassing the tropical cyclone seasons, which run from November 1 until the end of April, with peaks in mid-February to early March.Of various modes of variability in the climate system, El Niño–Southern Oscillation has the largest impact on tropical cyclone activity. Most tropical cyclones form on the side of the subtropical ridge closer to the equator, then move poleward past the ridge axis before recurving into the main belt of the Westerlies. When the subtropical ridge position shifts due to El Niño, so will the preferred tropical cyclone tracks. Areas west of Japan and Korea tend to experience much fewer September–November tropical cyclone impacts during El Niño and neutral years. During La Niña years, the formation of tropical cyclones, along with the subtropical ridge position, shifts westward across the western Pacific Ocean, which increases the landfall threat to China and much greater intensity in the Philippines. The Atlantic Ocean experiences depressed activity due to increased vertical wind shear across the region during El Niño years. Tropical cyclones are further influenced by the Atlantic Meridional Mode, the Quasi-biennial oscillation and the Madden–Julian oscillation. Influence of climate change
Climate change can affect tropical cyclones in a variety of ways: an intensification of rainfall and wind speed, a decrease in overall frequency, an increase in the frequency of very intense storms and a poleward extension of where the cyclones reach maximum intensity are among the possible consequences of human-induced climate change.
Autoantibodies
A number of specific antibodies found in the blood (antinuclear antibody (ANA), anti-smooth muscle antibody (SMA), anti-liver kidney microsomal antibodies (LKM-1, LKM-2, LKM-3), anti soluble liver antigen (SLA), liver–pancreas antigen (LP), and anti-mitochondrial antibody (AMA)) are of use, as is finding an increased immunoglobulin G level. The presence of anti-mitochondrial antibody is more suggestive of primary biliary cholangitis. Hypergammaglobulinemia is also of diagnostic value. Histology
Autoimmune hepatitis can be characterized histologically by the following nonspecific findings:
Portal mononuclear cell infiltrate that invades the boundary surrounding the portal triad and infiltrates the surrounding lobule. Periportal lesions, also known as interface hepatitis, that spare the biliary tree (may include centrizonal necrosis). Bile duct abnormalities (cholangitis, ductal injury, ductular reaction) can be seen and should prompt evaluation for primary biliary cholangitis or sarcoidosis if granulomas are observed. Plasma cell infiltrate, rosettes of hepatocytes, and multinucleated giant cells. Varying degrees of fibrosis (except in the mildest form of autoimmune hepatitis). Bridging fibrosis that connects the portal and central areas can distort the structure of the hepatic lobule and result in cirrhosis. Diagnostic scoring
The Internal Autoimmune Hepatitis Group developed a standardized scoring system for clinical diagnosis in population studies but lacks value in individualized cases. A simplified scoring system for clinical use incorporates titers of autoantibodies, total IgG levels, liver histology, and the exclusion of viral hepatitis for diagnostic scoring. Classification
On the basis of detected autoantibodies, autoimmune hepatitis can be classified into three subtypes but have no distinct clinical presentations. Type 1 autoimmune hepatitis.