**16.2. Striae**

**15. Myopathy**

• Potential delay of diagnosis

**Lymphocytes**

reduction)

immune response

• Reduced cytokine production • Impaired formation of nitric oxide • Defective adherence to endothelium, extravasation,chemotaxis • Inhibition of apoptosis

• Inhibition of prostaglandin production • Inhibition of host's inflammatory response

**Neutrophils**

burst

**Other effects**

• Reversible lymphopenia, CD4 depletion (>50%

• Impaired delayed-type hypersensitivity • Impaired natural killer cell cytotoxicity

TNFα,interleukin-12, interferon γ)

and increased Th2 cytokine production)

• Decreased proliferation and migration of lymphocytes

110 Pharmacokinetics and Adverse Effects of Drugs - Mechanisms and Risks Factors

• Decreased lymphokine production (interleukin-2,

• Th1/Th2 dysregulation of T-helper cells (decreased Th1

• Impaired phagocyte effector cell function and cellular

• Impaired phagocytosis, degranulation, and oxidative

• Attenuation of clinical (i.e. fever) and radiological signs of infection

**Table 9.** Immunosuppressive effects of glucocorticoids (adapted from [126]).

GCs have direct catabolic effects on skeletal muscles. These catabolic effects are mediated by several cellular mechanisms. GCs inhibit the glucose uptake in skeletal muscles, by this way stimulate protein catabolism and inhibit protein synthesis in muscles. These direct effects causes muscle weakness. Besides, it was shown that GCs increase the transcription of genes encoding components of the ubiquitin-proteasome pathway, thereby increasing the proteolytic capacity of muscle cells. Transactivation of certain genes through glucocorticoid receptors also contributes to muscle atrophy. GCs inhibit the production by the muscle of IGF-I, a growth factor that stimulates the development of muscle mass by increasing protein synthesis and myogenesis, while decreasing proteolysis and apoptosis. In addition, GCs stimulate the production of myostatin, a growth factor that inhibits the muscle mass development by

**Monocytes/macrophages**

inflammation

• Reversible monocytopenia (>40% reduction) • Impaired phagocytosis and oxidative killing • Decreased chemotaxis and migration to sites of

• Impaired maturation of monocytes to macrophages

• Decreased counts for alveolar dendritic cells, central nervous system microglial cells, and Langerhans'

• Impaired antigen-presenting capacity of dendritic and Langerhans' cells (decreased expression of

• Defective microglial cell-killing capacity (impaired

• Impaired formation of nitric oxide

**Other immune effector cells**

MHC II on their surface)

nitric oxide formation)

epidermal cells

• Inhibition of pro-inflammatory cytokine production(interleukin-1, interleukin-6, TNFα)

Myopathy usually develops over several weeks to months with the use of GCs. The typical clinical features are proximal muscle weakness and atrophy in both the upper and lower

downregulating the proliferation and protein synthesis [132–135].

These are visible linear scars that form in areas of dermal damage, presumably during mechanical stress. Stria means scar tissue. For this reason, once developed, they are permanent. In the differential diagnosis, excessive weight gain and pregnancy should be excluded [141].
