Complications
Prevalence: over 60% of patients.[69][70]
Aetiology: growth hormone/insulin-like growth factor 1 excess.
Monitoring: ECG, echocardiography.
Treatment: standard medical care.[26]
Left ventricular hypertrophy, cardiomyopathy, arrhythmia, valvular heart disease, and ischaemic heart disease can all be consequent to acromegaly.[26]
Cardiomyopathy can occur in the absence of hypertension even in young patients. After effective treatment of acromegaly, normal diastolic and systolic functions are best restored in younger patients and in patients with a shorter duration of acromegaly.[71] However, cardiac comorbidities might persist despite successful control of acromegaly.[69]
Cardiovascular complications significantly affect patient survival.[26]
Prevalence: 30% to 60% of patients.[26]
Aetiology: growth hormone/insulin-like growth factor 1 excess.
Monitoring: serial blood pressure measurement.
Treatment: standard medical care.
Prevalence: 25% to 80% of patients.[26][70]
Aetiology: derangement of central respiratory control mechanism and/or upper airway obstruction (macroglossia, soft-tissue swelling, and mandibular overgrowth secondary to growth hormone/insulin-like growth factor 1 excess).[4][26]
Monitoring: polysomnography.
Treatment: continuous positive airway pressure, mouth guard, and uvulopalatoplasty.[4]
Sleep apnoea is a likely co-determinant of cardiovascular mortality, if untreated.
The condition generally improves following or during successful control of acromegaly.[26]
Prevalence: joint pain affects more than 75% of patients.[4]
Aetiology: articular cartilage hypertrophy, joint laxity, bone enlargement due to growth hormone/insulin-like growth factor 1 excess.
Monitoring: clinical examination, bone and joint x-rays.
Treatment: standard medical care for degenerative joint disease. Corrective surgery may be required to treat bone enlargement or joint pathology.[4]
Articular cartilage hypertrophy decreases with GH/IGF-1 normalisation. Once bone damage has occurred, it is irreversible with arthritis developing.[26]
Prevalence: about 50% of patients.[26][70]
Aetiology: insulin resistance due to growth hormone excess.
Monitoring: fasting and post-oral glucose tolerance test plasma glucose measurements.
Treatment: standard medical care. The presence of diabetes influences the choice of acromegaly medical therapy: octreotide and lanreotide have a neutral effect on glucose control; pasireotide has a high-risk for developing hyperglycaemia in patients with uncontrolled diabetes; pegvisomant treatment improves glucose metabolism.[26]
Aetiology: growth hormone/insulin-like growth factor 1 (IGF-1) excess.
Monitoring: colonoscopy at diagnosis of acromegaly. There is no consensus between guidelines on the interval for ongoing surveillance, which ranges from every 3 to 10 years, pending initial colonoscopy findings and IGF-1 levels.[72]
Prevalence: up to 64% of patients.[4]
Aetiology: soft-tissue swelling with median nerve compression (can be bilateral) due to growth hormone/insulin-like growth factor 1 excess.
Monitoring: clinical examination, electromyogram.
Treatment: surgical intervention is usually not required.
The condition generally improves with successful control of acromegaly.[26]
Aetiology: compression of the normal pituitary gland by the adenoma or secondary to treatment (surgery and/or radiotherapy).
Monitoring: measurement of pituitary hormones 2 to 3 months after treatment and yearly thereafter.
Treatment: replacement hormone therapy when appropriate.
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