As multiple studies have demonstrated both its efficacy and safety in a clinical setting, it is also used in different minimization regimens to reduce the application of higher risk immunosuppressive agents such as corticosteroids and calcineurin inhibitors (CNIs) in solid organ transplantation. Because both corticosteroids and CNIs have been found to potentially cause long-term adverse effects in the body, a multitude of studies have been conducted to examine the efficacy of thymoglobulin in SOT either with minimal usage or without the use of either agent. Findings have indicated that use of thymoglobulin alone minimizes risk of adverse effects and thus improves long-term outcomes for transplant patients.Thymoglobulin is also an effective agent for preventing graft-vs.-host disease in patients receiving haematopoietic stem cell transplantation (HSCT). GVHD is a condition in which immune cells within the graft attack host cells and cause tissue damage. It is considered a major obstacle to successful HSCT. The T-cell depleting activity of thymoglobulin has proved to be useful in preventing GVHD. Multiple studies have indicated that thymoglobulin is favored in comparison to other induction agents for patients who have increased risk of developing post-transplant complications, such as elderly patients, patients undergoing a repeat transplantation, and patients in which minimization of use of steroids or CNIs post-operation is  recommended. == References ==
Because ML I is classified as a sialidosis, it is sometimes referred to as sialidosis type II. A rarer form of sialidosis – sialidosis type 1– occurs in children and adolescents and is often referred to as the juvenile form of the disorder. Children usually begin to show symptoms during the second decade of life, and myoclonus and cherry-red macules are often the initial symptoms. Patients usually develop seizures and progressive deterioration of coordinated muscular and mental activities. Pathophysiology
The role of sialidase is to remove a particular form of sialic acid (a sugar molecule) from sugar-protein complexes (referred to as glycoproteins), which allows the cell to function properly. Because the enzyme is deficient, small chains containing the sugar-like material accumulate in neurons, bone marrow, and various cells that defend the body against infection. Diagnosis
The detection of high urinary sialyl oligosaccharides and the confirmation of lysosomal enzyme deficiency in leukocytes or cultured fibroblasts make the diagnosis. Management
Treatment of sialidosis is similar to the other progressive myoclonic epilepsy disorders, which consists of managing seizures and myoclonus along with palliative, supportive, and rehabilitative care. See also
Fucosidosis
Sialic acid
Neuraminidase
Mucolipidosis
Lysosomal storage disease

Notes
References
mucolipidoses at NINDS - article derived from detail sheet available here

External links

Sialidosis type 1 and 3 at NIHs Office of Rare Diseases
Sialidosis at NIHs Office of Rare Diseases