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Scleroderma, Pediatric


Basics


Description


  • Scleroderma means "hard skin. "  It can be systemic or localized.
  • Systemic sclerosis (SSc) or progressive systemic sclerosis (PSS)
    • Diffuse cutaneous SSc: affects skin and internal organs (lungs, GI tract)
    • Limited cutaneous SSc, also known as CREST: a variant form of SSc characterized by calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiectases
  • Localized
    • Morphea
    • Linear scleroderma
    • En Coup de Sabre/Parry-Romberg syndrome

Epidemiology


  • Systemic
    • Age of onset: 30 " “50 years; very rare in children
    • Sex ratio
      • <7 years, male = female
      • >7 years, female > male (3:1)
      • 15 " “44 years, female > male (15:1)
  • CREST
    • Earlier age of onset than SSc
    • Almost nonexistent in children
    • Female > male

Incidence
  • Systemic: 0.27 per million annually
  • CREST: affects ’ ˆ Ό1/2 of patients with systemic disease
  • Localized: approximately 10 ƒ — more common than SSc in childhood

Pathophysiology


  • Systemic involvement
    • Vasculopathy: based on high association with Raynaud phenomenon; vascular injury leading to fibrotic changes as a part of overcorrection
    • Serum factors: overexpression of endothelin, a potent vasoconstrictor with profibrotic activity
    • Immune dysfunction: autoimmunity directed against connective tissue antigen such as laminin or type IV collagen, platelet-derived growth factor receptors stimulating fibrosis
  • Localized form
    • Alteration of normal glycosylation and hydroxylation of collagen
    • May represent distinct early and late processes
      • Early: increased hydrophilic glycosaminoglycan; increased T cells, macrophages, and plasma cells; mast cell hyperplasia
      • Late: increased collagen content; collagen is embryonic with narrow fibrils and immature cross-banding; atrophy of rete pegs, epithelial tissue projecting into underlying connective tissue

Diagnosis


History


  • Thickening of skin
  • Tightness of joints
  • Discoloration of skin
  • Often insidious onset
  • Morning stiffness
  • Heartburn, dysphagia, reflux, cough with swallowing

Signs and symptoms: ‚  
  • SSc
    • Diagnostic criteria (1 major criterion or 2 minor criteria required)
    • Major: sclerodermatous changes (tightness, thickening, induration) proximal to metacarpophalangeal or metatarsophalangeal joints
    • Minor: sclerodactyly-sclerodermatous changes limited to digits (unable to pinch skin over the digit), digital pitting, bibasilar pulmonary fibrosis not due to primary lung disease
    • CREST
      • More severe calcinosis
      • Distal symptoms more severe
      • Associated with anti-centromere antibody
      • Occasional evolution into another connective tissue disease such as mixed connective tissue disease (MCTD) or systemic lupus erythematosus (SLE)
  • Localized
    • Fibrosis limited to skin, subcutaneous (SC) tissue, and muscle
    • Systemic features including Raynaud phenomenon and visceral involvement are extremely rare except in Parry-Romberg.
    • Forms:
      • Morphea: ≥1 oval or round indurations that become hard and whitish early on, have active inflammatory border with violaceous color. Various forms: plaque or guttate (limited number of lesions); generalized (extensive); nodular (SC)
    • Linear: ≥1 linear areas affecting SC tissue, muscle, and bone; can cross joint lines and also affect limb growth
    • En Coup de Sabre: involves face or scalp; may be associated with seizures
    • Parry-Romberg syndrome: form of linear scleroderma; congenital dysplasia of SC tissue; neurologic changes such as transient ischemic attacks (TIAs) in brain matter under lesion, without its direct extension into the skull

Physical Exam


  • Findings in SSc:
    • Skin
      • Stage 1: Edema " ”tense, nonpitting; perhaps warm or tender but often asymptomatic
      • Stage 2: Sclerosis " ”waxy, hard texture; bound to SC structures, back of digits, face (loss of forehead wrinkles, reduced mouth orifice)
      • Stage 3: Atrophy " ”shiny appearance, hypopigmented or hyperpigmented, calcium deposits in SC tissue
      • Telangiectasias: macular dilatations that fill slowly, unlike spider telangiectasias
      • Loss of SC tissue pulp of the fingers and ulcerations on fingertips with prolonged healing in SSc
    • Raynaud phenomenon
      • Primary phenomenon or Raynaud disease: not associated with underlying disease; milder; 75% are female.
      • Secondary Raynaud phenomenon: associated with underlying disease such as SSc, SLE, Sj ƒ Άgren syndrome, MCTD, dermatomyositis, and polymyositis; more serious. Present in ’ ˆ Ό90% of SSc patients.
      • Triple phase: blanching of digits with sharp border to normal-colored skin (arterial vasoconstriction) followed by cyanosis (venostasis) then erythema; tingling/numb sensation of the digits (reflex hyperemia to vasodilatation)
      • Usually fingers; also toes, nose, ears, and tongue; often spares thumb
    • Calcinosis, especially over extensor joint surfaces in systemic form only
    • Pitfalls
      • Failure to recognize limited mouth opening in SSc
      • Failure to evaluate periungual nailfold changes with Raynaud phenomenon: capillary dropout and dilated loops; occasional redundant cuticular growth and digital pitting
    • Musculoskeletal
      • "Creaking "  of thickened tendons
      • Contractures, especially proximal interphalangeal joints and elbows
      • Associated arthritis
      • Muscle inflammation in ’ ˆ Ό30% of cases
    • GI
      • Mucosal telangiectasias of mouth
      • Decreased incisor distance/mouth opening secondary to skin tightness of the lips
      • Sicca syndrome with parotitis
      • Loosening of teeth secondary to periodontal membrane disease
      • Esophageal disease: esophagitis, occasional ulceration or stricture
      • Large-bowel disease less common
    • Cardiac
      • Primary cause of morbidity
      • Possibly due to Raynaud phenomenon of coronary arteries and pulmonary artery hypertension
      • Myocarditis possible
    • Pulmonary
      • Interstitial fibrosis with gradual obliteration of vascular bed and resulting cor pulmonale
      • Parenchymal disease is almost universal; frequently asymmetric; may have hacking cough, dyspnea on exertion, pleural rub.
      • Combined pulmonary vascular and pulmonary parenchymal disease
      • Primary pulmonary vascular disease with right ventricular failure
    • Renal: due to decreased renal plasma flow, proteinuria, hypertension, renal crisis
    • CNS: cranial nerve involvement, especially sensory branch of trigeminal nerve
    • Sicca syndrome
      • Xerostomia (dry mouth)
      • Keratoconjunctivitis sicca (dry eyes)

Diagnostic Tests & Interpretation


Lab
There are no specific diagnostic tests. ‚  
  • Nonspecific tests
    • Systemic form
      • Antinuclear antibody (ANA): often positive
      • Hemoglobin: 25% have anemia due to chronic disease or vitamin B12 and folate deficiencies resulting from chronic malabsorption in sclerodermatous gut.
      • Eosinophilia: present in 50%
      • Sclero-70 (Scl-70 or topoisomerase 1) antibodies: present in 26% of adults; more common with diffuse disease than with peripheral vascular disease
      • Anti-centromere antibody: present in 22%, almost exclusively with CREST
      • Muscle biopsy
    • Localized forms
      • Eosinophilia: present in 25 " “50% during active disease
      • ANA: positive in 37 " “67%

Imaging
  • Chest radiograph
    • Bibasilar pulmonary fibrosis
    • Rib notching
    • Calcifications (in CREST)
  • High-resolution chest CT
    • Ground-glass attenuation
    • Honeycombing
  • Bone radiograph
    • Acro-osteolysis: resorption of tufts of distal phalanges, especially with severe Raynaud phenomenon
    • Periarticular or SC calcification (15 " “25% patients)
    • Bony erosions

Diagnostic Procedures/Other
  • For sicca syndrome
    • Schirmer test for dry eyes
    • Lip biopsy
    • Rose bengal staining of cornea
  • ECG
    • 1st-degree block
    • Right and left bundle-branch block
    • Premature atrial contractions (PACs) and premature ventricular contractions (PVCs): nonspecific T-wave changes, ventricular hypertrophy
  • Pulmonary function tests
    • Restrictive lung disease: present in 34% of patients with SSc
    • Earliest changes are decreased forced vital capacity (FVC) and small airway disease.
    • Decreased diffusing capacity of the lung for carbon monoxide (DLCO): present in 18% of patients with SSc at the time of diagnosis

Pathologic Findings
  • Histologic
    • Skin: loss of SC fat, increased amount of fibroblasts
    • Muscle: increased collagen and fat; negative immunofluorescence
    • Esophagus: Atrophic muscle replaced by fibrous tissue more commonly affects smooth muscle of lower 2/3 of esophagus.
  • Esophageal manometry and pH probe: decreased or absent peristalsis of distal esophagus " ”distal dilatation, hiatal hernia, stricture
  • Dilatation of second and third part of duodenum and proximal jejunum

Differential Diagnosis


  • Graft-versus-host disease (GVHD)
  • Phenylketonuria
  • Borrelia infection: acrodermatitis chronica atrophicans
  • Porphyria cutanea tarda
  • Scleredema
  • Stiff skin syndrome (mucin deposition in the dermis, hardening of the subcutaneous tissue with normal-looking epidermis)
  • Eosinophilic fasciitis

Treatment


Medication


Disease modification: Many agents have been tried; however, there are few controlled trials, and no proven treatment exists. Medications include the following: ‚  
  • Localized
    • Imiquimod, calcitriol ointment, psoralen ultraviolet A light (PUVA) therapy, methotrexate, mycophenolate mofetil, cyclosporine
  • Systemic
    • Colchicine: inhibits fibroproliferative process
    • Immunosuppressives
      • Steroids, chlorambucil, methotrexate, mycophenolate mofetil, cyclosporine, cyclophosphamide, rituximab
  • Pitfall: Avoid excessive use of immunosuppressive therapy late in disease when inflammatory component has resolved.

Additional Treatment


General Measures
  • Supportive care: Avoid trauma and excessive cold; keep extremities warm AND dry.
  • Management of Raynaud phenomenon:
    • Avoid beta-blockers, caffeine, and stimulating ADHD medications.

Additional Therapies


  • Physical therapy
    • Helps retard development of contractures and muscle atrophy
    • Pitfall: insufficient physical therapy resulting in permanent joint contractures

Ongoing Care


Follow-up Recommendations


Patient Monitoring
  • Localized forms
    • Physical exam for joint mobility, muscle bulk, and growth
    • Difficult to follow slow disease progression, thus photography of lesions every 3 " “6 months is recommended
  • Systemic forms
    • Physical exam for digital ulcerations, joint mobility, muscle bulk, and growth
    • Yearly pulmonary function tests
    • Yearly barium swallow
    • ECHO

Prognosis


  • In localized forms, natural course includes several phases:
    • Initial: inflammation
    • Late: sclerosis
    • Occasional regression over 3 " “5 years
  • Contractures and limb size difference can persist with linear scleroderma.
  • Systemic form is progressive and ultimate prognosis depends on severity of skin tightness, joint contracture, and visceral involvement.
  • Mortality with SSc
    • Males > females
    • Non-whites > whites
  • Most common cause of death in pediatric patients with SSc is secondary to cardiac, renal, and pulmonary complications.

Complications


  • Localized
    • Skin thickening
    • Joint contractures
    • Leg length discrepancies
    • CNS bleed in Parry-Romberg

Additional Reading


  • Fain ‚  ET, Mannion ‚  M, Pope ‚  E, et al. Brain cavernomas associated with en coup de sabre linear scleroderma: two case reports. Pediatr Rheumatol Online J.  2011;9:18. ‚  [View Abstract]
  • Fitch ‚  PG, Rettig ‚  P, Burnham ‚  JM, et al. Treatment of pediatric localized scleroderma with methotrexate. J Rheumatol.  2006;33(3):609 " “614. ‚  [View Abstract]
  • Foeldvari ‚  I. Methotrexate in juvenile localized scleroderma. Arthritis Rheum.  2011;63(7):1779 " “1781. ‚  [View Abstract]
  • Foeldvari ‚  I. Update on pediatric systemic sclerosis: Similarities and differences from adult disease. Curr Opin Rheumatol.  2008;20(5):608 " “612. ‚  [View Abstract]
  • Herrick ‚  AL, Ennis ‚  H, Bhushan ‚  M, et al. Incidence of childhood linear scleroderma and systemic sclerosis in the UK and Ireland. Arthritis Care Res.  2010;62(2):213 " “218. ‚  [View Abstract]
  • Martini ‚  G, Foeldvari ‚  I, Russo ‚  R, et al. Systemic sclerosis in childhood: Clinical and immunologic features of 153 patients in an international database. Arthritis Rheum.  2006;54(12):3971 " “3978. ‚  [View Abstract]
  • Zulian ‚  F. New developments in localized scleroderma. Curr Opin Rheumatol.  2008;20(5):601 " “607. ‚  [View Abstract]

Codes


ICD09


  • 710.1 Systemic sclerosis
  • 517.8 Lung involvement in other diseases classified elsewhere

ICD10


  • M34.9 Systemic sclerosis, unspecified
  • M34.1 CR(E)ST syndrome
  • L94.0 Localized scleroderma [morphea]
  • L94.1 Linear scleroderma
  • M34.83 Systemic sclerosis with polyneuropathy
  • M34.81 Systemic sclerosis with lung involvement
  • M34.82 Systemic sclerosis with myopathy
  • M34.0 Progressive systemic sclerosis
  • M34.89 Other systemic sclerosis

SNOMED


  • 89155008 systemic sclerosis (disorder)
  • 62382002 Calcinosis, Raynauds phenomenon, sclerodactyly, and telangiectasia syndrome (disorder)
  • 201048007 Localized morphea (disorder)
  • 22784002 Linear scleroderma (disorder)
  • 7513007 Generalized morphea
  • 196133001 Lung disease with systemic sclerosis (disorder)
  • 236502006 Renal involvement in scleroderma
  • 128460000 systemic sclerosis, diffuse (disorder)
  • 299276009 Limited systemic sclerosis (disorder)

FAQ


  • Q: Is a biopsy necessary?
  • A: Biopsy is often useful to confirm diagnosis and assess degree of inflammation.
  • Q: Is the sclero-70 antibody useful?
  • A: Not for diagnosis; it is positive only in a subset of individuals with the systemic form and, therefore, useful for predicting more severe disease.
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