Specific codes in ICD-10 are unique alphanumeric designations used to identify and categorize diseases, disorders, and conditions. They consist of 3-5 characters, including both letters and numbers, that provide a high level of detail and specificity.
| Language | Translation |
|---|---|
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Multiple sclerosis |
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Sclérose en plaques |
| Level | Code | Title | |
|---|---|---|---|
| 1 | VI | Diseases of the nervous system | |
| 2 | G35-G37 | Demyelinating diseases of the central nervous system | |
| 3 | G35 | Multiple sclerosis |
| Code | Title | |
|---|---|---|
| G35.0 | ||
| G35.1 | ||
| G35.2 | ||
| G35.3 | ||
| G35.9 |
| Active Ingredient |
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Interferon beta-1b has been shown to possess both antiviral and immunoregulatory activity. The mechanisms by which interferon beta-1b exerts its actions in multiple sclerosis are not clearly understood. However, it is known that the biological response-modifying properties of interferon beta-1b are mediated through its interactions with specific cell receptors found on the surface of human cells. |
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Ocrelizumab is a recombinant humanised monoclonal antibody that selectively targets CD20-expressing B cells. The precise mechanisms through which ocrelizumab exerts its therapeutic clinical effects in MS is presumed to involve immunomodulation through the reduction in the number and function of CD20-expressing B cells. Following cell surface binding, ocrelizumab selectively depletes CD20-expressing B cells through antibody-dependent cellular phagocytosis (ADCP), antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis. The capacity of B-cell reconstitution and preexisting humoral immunity are preserved. |
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Tetracosactide acetate consists of the first 24 amino acids occurring in the natural corticotropic hormone (ACTH) sequence and displays the same physiological properties as ACTH. In the adrenal cortex, it stimulates the biosynthesis of glucocorticoids, mineralocorticoids, and, to a lesser extent, androgens, which explains its therapeutic effect in conditions responsive to glucocorticoid treatment. |