Careful attention to lung and heart health is required, corticosteroids in LGMD 2C-F individuals, shows some improvement. Additionally individuals can follow management that follows:
Occupational therapy
Respiratory therapy
Speech therapy
Neutralizing antibody to myostatin should not be pursuedThe sarcoglycanopathies could be possibly amenable to gene therapy. Prognosis
In terms of the prognosis of limb–girdle muscular dystrophy in its mildest form, affected individuals have near-normal muscle strength and function. LGMD isnt typically a fatal disease, though it may eventually weaken the heart and respiratory muscles, leading to illness or death due to secondary disorders. Epidemiology
The minimum prevalence of limb–girdle muscular dystrophy, as a group, likely ranges from 2.27-10 per 100,000 (1:44,000 to 1:10,000). LGMD is the fourth most common muscular dystrophy, after the dystrophinopathies, myotonic dystrophies, and facioscapulohumeral muscular dystrophy. 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. It is difficult to calculate the worldwide prevalence of even the most common LGMD types, due to the founder effect causing varying prevalence by region. The less common types are very rare, often only described is limited regions of the world. History
The term limb girdle muscular dystrophy was published in 1954, describing a group of heterogeneous conditions that clinicians noticed to be distinct from Duchenne muscular dystrophy, facioscapulohumeral muscular dystrophy, and myotonic dystrophy.
The genetics of LGMDs began to be understood in the late 1900s, which led the European Neuromuscular Centre (ENMC) to establish a consensus on classification of LGMDs in 1995. The classification scheme at that time denoted autosomal dominant LGMDs as LGMD1 and autosomal recessive LGMDs as LGMD2. A letter was appended to the names of LGMDs according to the order of discovery of the causal genetic mutation. As LGMD2Z was established, the question arose of what letter to assign the next discovered LGMD2. With this issue, among other motives, the ENMC established a new consensus on the classification and definition of LGMD in 2017. With the new definition, several diseases were removed from the LGMD category:

Research
There is a variety of research under way targeted at various forms of limb–girdle muscular dystrophy. Among the treatments thought to hold promise is gene therapy, which is the delivery of genetic material, often a copy of a healthy gene, into cells.According to a review by Bengtsson et al. some success with AAV-mediated gene therapies (for different disorders) have increased interest in researchers, with CRISPR/Cas9 and exon-skipping helping these therapeutic goals along. Limb–girdle muscular dystrophies have many different types which are due to different gene mutations. LGMD2D is caused by a mutation in the α-sarcoglycan gene.