HGH abuse in sports is widespread due to perceived, though mainly unproven, benefits and the difficulty of detection [4, 7, 9]. Exogenous GH administration, in matured and healthy adults with sufficient GH secretions from pituitary gland, is strongly condemned due to the many adverse effects that can take place in both short-term and long-term use. Doses used by athletes are estimated to an average daily dose of 1–2 mg GH, which is three times higher than the normal endogenous secretions [10]. Current evidence lacks certain recommendations for the overdose level of GH. Acute HGH overdose can cause tremors, drowsiness, dizziness and nausea, although critical acute intoxication in the manner of other drugs like alcohol and opioids have not been reported and has remained unknown. In the long-term setting, excessive administrations of HGH can be a mimicker of acromegaly and its manifestations [6]. GH contributes to collagen and muscle mass increase in heart and leads to cardiomyopathy [11]. Interstitial fibrous tissue proliferation in myocardium is provoked by GH [12]. Such alterations are associated with arrythmias and heart failure [13, 14]. Electrocardiography studies and Holter recordings have documented abnormalities of cardiac rhythm in patients with acromegaly [14]. Left ventricular hypertrophy (LVH) is common in acromegaly patients as a result of volume overload. Since LVH is associated with increased risk for adult sudden death; cardiomegaly secondary to chronic HGH misuse may heightens the risk of sudden cardiac arrest in athletes [15].
Systemic hypertension is promoted via the activation of renin–angiotensin–aldosterone-system (RAAS) advancing oxidative stress as well as sodium and water retention that are stimulated by HGH. Elevated blood pressure have had correlations with the severity of acromegaly cardiopathy [16, 17].
GH impact on neurocognition has been controversial; while GH secretions regulate metabolic and growth function, overexpression of GH in a rodent model caused impairments in memory [18]. Although hallucinations as an aftermath of abundant use of GH are not mentioned as the side effects, few episodes of psychosis in the context of acromegaly were seen [19].
Aspiration pneumonia seen on chest CT scan is probably stemmed from his decreased level of consciousness prior to his intubation. On account of the mere left atrial (LA) abnormality that was seen in the electrocardiograms, and no reflection of acute myocardial infarction, therefore rhabdomyolysis is supposed to be responsible for the elevated troponin level. In our case, acute skeletal muscle hypertrophy and destruction might have resulted in rhabdomyolysis [20]. Hypertensive crisis and the pleural effusion are concluded to be directly ensued from his somatropin toxicity which were supposedly brought about by its fluid retention effect. The high d-dimer could have been suggestive of a probable pulmonary embolism (PE), however in light of his rapid deterioration, chest CT angiography could not be performed. Eventually the cardiovascular collapse is deemed to be attributed to PE. On the other hand, based on his chronic use of HGH, an increased ventricular mass and acromegaly related cardiomyopathy might had been accountable for the sudden cardiac arrest.
As far as we know, this is a first lethal case of HGH acute toxicity considering the amount of abused GH and the extent of severity. Clinicians and in particular; endocrinologists and sport medicine specialists are increasingly confronted with the complications of HGH misuse. Thus, public awareness about its deleterious side effects should be raised.
