Duchenne muscular dystrophy (DMD) is a severe X-linked recessive disorder caused by mutations, most commonly deletions, in the DMD gene, which encodes the dystrophin protein. The absence or dysfunction of dystrophin leads to progressive muscle degeneration and myonecrosis, which are central to the disease's pathophysiology. DMD predominantly affects males, with clinical manifestations typically appearing between the ages of 3 and 5 years. Life expectancy is generally limited to 20 to 30 years without therapeutic intervention. The clinical presentation of DMD is characterized by progressive motor deficits, including gait disturbances, kyphoscoliosis, pseudohypertrophy of the calves, and the hallmark Gower's sign, indicative of proximal muscle weakness. Over time, the disease progresses to involve the cardiorespiratory system, with dilated cardiomyopathy and respiratory muscle weakness becoming the leading causes of mortality. Management of DMD requires a multidisciplinary approach. Physiotherapy and corticosteroid therapy are the primary treatments to preserve muscle strength and function for as long as possible. In advanced stages, when cardiorespiratory complications arise, non-invasive ventilation is often required, and pharmacologic interventions, such as angiotensin-converting enzyme (ACE) inhibitors and beta-blockers, are used to manage cardiac dysfunction. This report discusses the case of a 10-year-old male presenting with classic DMD symptoms in a low-resource setting. The challenges and strategies for managing such patients in resource-limited environments are explored, emphasizing the importance of timely diagnosis, physiotherapy, and appropriate pharmacologic management to mitigate disease progression and improve quality of life.

Keywords: Duchenne muscular dystrophy, X-linked recessive, myonecrosis, corticosteroids, Gower sign, Pseudo calf hypertrophy, Paresis, Creatinine kinase (CK-MB)

Abbreviations: Duchenne muscular dystrophy (DMD); angiotensin-converting enzyme (ACE); Creatinine kinase (CK-MB)