Elevated creatine kinase (CK) levels in the blood (at most ~10 times normal) are typical in sIBM but affected individuals can also present with normal CK levels. Electromyography (EMG) studies usually display abnormalities such as increased insertional activity and short duration motor unit potentials. Muscle biopsy may display several common findings including; inflammatory cells invading muscle cells, vacuolar degeneration, and<unk>  bodies of aggregations of multiple proteins. sIBM is a challenge to the pathologist and even with a biopsy, diagnosis can be ambiguous. A diagnosis of<unk>  was historically dependent on muscle biopsy results. Antibodies to cytoplasmic 5'-nucleotidase (cN1A; NT5C1A) have been strongly associated with the condition. In the clinical context of classic history and positive antibodies, a muscle biopsy might be unnecessary. Differential diagnosis<unk>  is often initially misdiagnosed as polymyositis. A course of prednisone is typically completed with no improvement and eventually, sIBM is confirmed. sIBM weakness comes on over months or years and progresses steadily, whereas polymyositis has an onset of weeks or months. Other forms of muscular dystrophy (e.g. limb girdle) must be considered as well. Classification * The common type is sIBM; it strikes individuals apparently at random. * There is a type that has been observed in multiple siblings in the same generation in several families, termed familial inflammatory sIBM, but it is not passed on from generation to generation. * There are also several very rare forms of hereditary<unk>  body myopathy (hIBM) that are linked to specific genetic defects and that are passed on from generation to generation, each inherited in different ways.
Inclusion body myositis
Dermatomyositis
Nemaline myopathy
Polymyositis
Dermatopolymyositis
Centronuclear myopathy
Hereditary inclusion body myopathy
Brody myopathy