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Lint: hunter-syndrome

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"Hunter syndrome is an X-linked recessive disorder caused by mutations in the iduronate 2-sulfatase (IDS) gene, responsible for the degradation of heparan and dermatan sulfate. Mutations of IDS lead to accumulation of proteoglycan products in tissues, leading to organ dysfunction and growth abnormalities 3."

Line 19:104 · Italics should be used only in exceptional circumstances: '<em>IDS</em>) gene, responsible for the degradation of heparan and dermatan sulfate. Mutations of <em>IDS</em>'
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"The mainstay of treatment for mucopolysaccharidoses is enzyme replacement therapy (ERT). For Hunter syndrome, this consists of replacement with idursulfase or tividenofusp alfa-eknm administered via intravenous infusions. Enzyme replacement therapy in Hunter syndrome has been shown to produce symptomatic improvement in somatic symptoms and appears to slow disease progression 6. However, because idursulfase does not cross the blood-brain barrier, it does not affect cognitive decline 7; tividenofusp alfa-eknm does cross the blood-brain barrier but its clinical benefits are not yet certain (c.2026). Haematopoietic cell transplantation has been shown to improve clinical outcomes but also does not prevent cognitive decline 8,9."

Line 41:628 · Check the abbreviation form against the style guide: 'c.2026'.
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"The mainstay of treatment for mucopolysaccharidoses is enzyme replacement therapy (ERT). For Hunter syndrome, this consists of replacement with idursulfase or tividenofusp alfa-eknm administered via intravenous infusions. Enzyme replacement therapy in Hunter syndrome has been shown to produce symptomatic improvement in somatic symptoms and appears to slow disease progression 6. However, because idursulfase does not cross the blood-brain barrier, it does not affect cognitive decline 7; tividenofusp alfa-eknm does cross the blood-brain barrier but its clinical benefits are not yet certain (c.2026). Haematopoietic cell transplantation has been shown to improve clinical outcomes but also does not prevent cognitive decline 8,9."

Line 41:629 · Check the number format against the style guide: '.2026'.
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Expected headings

  • H1 Terminology
  • H1 Usage
  • H1 Epidemiology
  • H2 Risk factors
  • H2 Associations
  • H1 Clinical presentation
  • H2 Complications
  • H1 Diagnosis
  • H2 Diagnostic criteria
  • H2 Diagnostic clues
  • H1 Pathology
  • H2 Aetiology
  • H2 Location
  • H2 Classification
  • H2 Macroscopic appearance
  • H2 Microscopic appearance
  • H2 Immunophenotype
  • H2 Markers
  • H2 Genetics
  • H1 Radiographic features
  • H2 Plain radiograph
  • H2 Mammography
  • H2 Antenatal ultrasound
  • H2 Transoesophageal echocardiography
  • H2 Ultrasound
  • H2 CT
  • H3 Dual-energy CT
  • H2 Angiography (DSA)
  • H2 MRI
  • H2 CT/MRI
  • H2 Nuclear medicine
  • H3 PET-CT
  • H3 PET-MRI
  • H1 Radiology report
  • H1 Treatment and prognosis
  • H2 Complications
  • H1 History and etymology
  • H1 Differential diagnosis
  • H2 Clinical differential diagnosis
  • H1 Practical points
  • H1 See also

"MRI"

Line 32:1 · " <sup>​</sup>MRI" is not a recognised heading for this article type.
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"The mainstay of treatment for mucopolysaccharidoses is enzyme replacement therapy (ERT). For Hunter syndrome, this consists of replacement with idursulfase or tividenofusp alfa-eknm administered via intravenous infusions. Enzyme replacement therapy in Hunter syndrome has been shown to produce symptomatic improvement in somatic symptoms and appears to slow disease progression 6. However, because idursulfase does not cross the blood-brain barrier, it does not affect cognitive decline 7; tividenofusp alfa-eknm does cross the blood-brain barrier but its clinical benefits are not yet certain (c.2026). Haematopoietic cell transplantation has been shown to improve clinical outcomes but also does not prevent cognitive decline 8,9."

Line 41:521 · Use semicolons judiciously.