[3][9] LGMD may be triggered or worsened in genetically susceptible individuals by statins, because of their effects on HMG-CoA reductase.

[11] Usually, the hip girdle is the first area to exhibit weakness,[2] manifesting as difficulty walking, going up and/or downstairs, rising from a chair, bending at the waist, or squatting.

[2][4] The disease commonly leads to dependence on a wheelchair within years of symptom onset, although some patients maintain mobility.

[16] HMG CoA Reductase homozygous mutation leads to a form of LGMD that may respond to treatment with the downstream metabolite mevalonolactone in the cholesterol synthesis pathway.

[4] The 2014 Evidence-based guideline summary: Diagnosis and treatment of limb-girdle and distal dystrophies indicates that individuals suspected of having the inherited disorder should have genetic testing.

[6] Also in the differential are Emery–Dreifuss muscular dystrophies, Pompe disease, later-onset congenital myasthenic syndromes, and proximal-predominant hereditary motor neuropathies.

Careful attention to lung and heart health is required, corticosteroids in LGMD 2C-F individuals, show some improvement.

[25] In terms of the prognosis of limb–girdle muscular dystrophy in its mildest form, affected individuals have near-normal muscle strength and function.

LGMD isn't typically a fatal disease, though it may eventually weaken the heart and respiratory muscles, leading to illness or death due to secondary disorders.

[26] The prevalence of individual LGMDs, as studied in the United States, in descending order, are those due to mutation of 1) calpain, 2) dysferlin, 3) collagen VI, 4) sarcoglycans, 5) anoctamin 5, and 6) fukutin-related protein.

[3] With the new definition, several diseases were removed from the LGMD category: There is a variety of research underway targeted at various forms of limb-girdle muscular dystrophy.

[28] According to a review by Bengtsson et al., some success with AAV-mediated gene therapies (for different disorders) has increased interest in researchers, with CRISPR/Cas9 and exon-skipping helping these therapeutic goals along.