Vogt–Koyanagi–Harada disease at the University of Tokyo, in 1911. It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. Vogt–Koyanagi–Harada disease Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome, uveomeningitis syndrome and uveomeningoencephalitic syndrome, is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye. VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of
Glycogen storage disease type II Glycogen storage disease type II Glycogen storage disease type II, also called Pompe disease, is an autosomal recessive metabolic disorder which damages muscle and nerve cells throughout the body. It is caused by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid alpha-glucosidase enzyme. It is the only glycogen storage disease with a defect in lysosomal metabolism, and the first glycogen storage disease to be identified, in 1932 by the Dutch pathologist J. C. Pompe. The build-up of glycogen causes progressive muscle weakness (myopathy) throughout the body and affects various body tissues, particularly in the