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.
Some have tried prescription vitamin-D with success. Ultraviolet A (UVA) light, with or without psoralens have also been tried. UVA-1, a more specific wavelength of UVA light, is able to penetrate the deeper portions of the skin and thus, thought to soften the plaques in morphea by acting in two fashions: by causing a systemic immunosuppression from UV light, or by inducing enzymes that naturally degrade the collagen matrix in the skin as part of natural sun-aging of the skin. [1] However, there is limited evidence that UVA‐1 (50 J/cm2), low‐dose UVA‐1 (20 J/cm2), and narrowband UVB differ from each other in effectiveness in treating children and adults with active morphea. Epidemiology
Morphea is a form of scleroderma that is more common in women than men, in a ratio 3:1. Morphea occurs in childhood as well as in adult life. Morphea is an uncommon condition that is thought to affect 2 to 4 in 100,000 people. Adequate studies on the incidence and prevalence have not been performed. Morphea also may be under-reported, as physicians may be unaware of this disorder, and smaller morphea plaques may be less often referred to a dermatologist or rheumatologist. See also
List of cutaneous conditions

References
Further reading
JAMA Dermatology Patient Page. Morphea (Localized Scleroderma. Nicole M. Fett, MD. JAMA Dermatol. 2013;149(9):1124. doi:10.1001/jamadermatol.2013.5079. September 2013


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