Systemic inflammatory response with rhabdomyolysis and consequent multiorgan failure is a known sequela of psychotropic drug abuse. However, in cases with uncertain past medical history the initial diagnosis can be challenging. Here we report the case of a 21-year-old male who was admitted to the intensive care unit with severe neurological impairment caused by amphetamine intoxication. First laboratory investigations revealed extremely high serum procalcitonin (PCT) levels reaching a maximum concentration of 1640？ng/mL on the second day of observation. Although PCT has high sensitivity and specificity in differentiating bacterial sepsis from nonbacterial inflammation, our case report shows for the first time that it can be extremely elevated following serious amphetamine intoxication without bacterial infection. 1. Introduction Procalcitonin (PCT) is a well-known biomarker for the diagnosis of sepsis. Although its absolute value and its kinetics over time have high sensitivity and specificity for differentiating bacterial infection from systemic inflammation in the critically ill [1, 2] but it is also important to interpret the results of the first measurement in the context of the full medical picture. One has to take into account that one cut-off value for PCT cannot be applied in all circumstances. Indeed, “elevated” PCT levels were described in surgical and trauma patients without proven infection but this increment was generated by the systemic inflammatory response syndrome (SIRS) in answer to the injurious insult [3, 4]. Severe SIRS can also be present in various medical conditions including amphetamine overdose [5]. We report the case of an extreme elevation of PCT without bacterial sepsis in a young man who presented with altered level of consciousness due to amphetamine intoxication which was initially thought to be infectious meningitis. 2. Case Report The 21-year-old male was found unconscious by his parents at home. The attending ambulance crew measured severe hypoglycaemia. After the serum glucose level was normalised by iv. glucose infusion the patient was transferred to the Accident and Emergency Department with oxygen supplementation via a face mask. Regarding his medical history he was fit and well, not on any regular medication. On the first assessment he was tachypnoeic (30/min) and had a SpO2 of 98%, sinus tachycardia (135/min), and a blood pressure of 96/67？mmHg. His neurological examination showed a Glasgow Coma Scale of 9 with no meningeal signs, dilated, equal pupils reacting for light, bulbs fixed to the left, and right sided
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