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Paeds SAQsneurology-neurodisability-and-neuromuscular

Paeds SAQs · neurology-neurodisability-and-neuromuscular

Duchenne and Becker muscular dystrophy: SAQ

Short-answer questions on Duchenne and Becker muscular dystrophy covering the creatine kinase and the genetic confirmation, the glucocorticoid backbone with prednisolone or deflazacort started at the motor plateau, the cardiac and respiratory surveillance, the reading-frame hypothesis, and the precision therapies of exon-skipping and adeno-associated-virus gene therapy, with the FOR-DMD and EMBARK trial evidence.

20 marks30 min4 min readVerification in progress

Target exams

RACP DWEMRCPCH TheoryABP General Pediatrics
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Study tools

Target exams

RACP DWEMRCPCH TheoryABP General Pediatrics
Prompt
A 4-year-old boy is referred by his general practitioner because he cannot keep up with his peers, walks on his toes, falls often, and cannot jump. He walked at twenty months. On examination he has firm, large calves, a waddling gait, and a Gowers sign that takes six seconds. His deep tendon reflexes are reduced. His creatine kinase is 28,000 units per litre. His liver transaminases are mildly raised with a normal bilirubin and a normal synthetic function. His weight is 17 kilograms.

This boy has the classic presentation of Duchenne muscular dystrophy, with the delayed walking, the toe-walking, the calf pseudohypertrophy, the Gowers sign, the reduced reflexes, and a creatine kinase of 28,000 units per litre that is off the scale. The mildly raised transaminases are muscle-derived, not liver-derived, because the bilirubin and the synthetic function are normal. The creatine kinase above 10,000 points to a dystrophic process, and the first step after it is the DMD genetic test. [3]

Question 1 (10 marks)

Outline the diagnostic confirmation and the immediate management plan for this boy, justifying each step with the relevant evidence. [3]

A full-mark answer addresses the genetic confirmation, the glucocorticoid decision, the systems surveillance, and the family counselling, each with the correct number or dose. [4]

Genetic confirmation (3 marks). The creatine kinase of 28,000 units per litre confirms a dystrophic process, and the diagnosis is now settled by genetic testing rather than a muscle biopsy. The first-line test is multiplex ligation-dependent probe amplification, which detects the exon deletions and duplications that account for the majority of cases, and if it is normal, whole-gene sequencing finds the point and splice mutations. The reading-frame hypothesis of Koenig predicts that an out-of-frame deletion produces Duchenne, while an in-frame deletion produces Becker, and the mutation type also decides the eligibility for the precision therapies. [2][3]

The glucocorticoid decision (3 marks). The boy is four years old and showing the motor plateau, the point at which the care considerations say to start the glucocorticoid, typically between four and seven years. The FOR-DMD trial established prednisolone 0.75 mg per kg per day and deflazacort 0.9 mg per kg per day as equivalent and superior to placebo, with deflazacort producing less weight gain, so either is started now and continued through the loss of ambulation. For this 17 kg boy, prednisolone is about 13 mg per day. The bone protection with calcium and vitamin D begins at the same time, and the family is taught the sick-day rule for stress-dose hydrocortisone. [7][4]

Systems surveillance and counselling (4 marks). A baseline electrocardiogram and echocardiogram are done at diagnosis and repeated at least annually, and an angiotensin-converting-enzyme inhibitor is started by the age of ten even before symptoms, because the cardiomyopathy is progressive and silent in the young boy. Spirometry begins from age five or six and the forced vital capacity is tracked. The family is counselled that the disease is X-linked recessive, that about two thirds are inherited and one third new, and that the mother, the sisters, and the maternal aunts are offered genetic testing and cardiac surveillance. The multidisciplinary neuromuscular centre coordinates the neurology, the cardiology, the respiratory, the rehabilitation, the endocrine, and the psychosocial care. [5]

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References5ShowHide
  1. [3]Bushby K, Finkel R, Birnkrant DJ Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Lancet Neurol, 2010.PMID 19945913
  2. [4]Birnkrant DJ, Bushby K, Bann CM Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management. Lancet Neurol, 2018.PMID 29395989
  3. [5]Birnkrant DJ, Bushby K, Bann CM Diagnosis and management of Duchenne muscular dystrophy, part 2: respiratory, cardiac, bone health, and orthopaedic management. Lancet Neurol, 2018.PMID 29395990
  4. [7]Griggs RC, Miller JP, Greenberg CR Efficacy and safety of deflazacort vs prednisone and placebo for Duchenne muscular dystrophy. Neurology, 2016.PMID 27566742
  5. [2]Koenig M, Beggs AH, Moyer M The molecular basis for Duchenne versus Becker muscular dystrophy: correlation of severity with type of deletion. Am J Hum Genet, 1989.PMID 2491009
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