Cerebroprotein hydrolysate allergy in patients with traumatic brain injury

Dear Editor,

Case 1

A 22-year-old male patient had RTA. He was intubated in causality in view of low GCS (E1V1M2), PEARL-2 mm. He has been diagnosed to have diffuse axonal injury, subarachnoid hemorrhage around the brainstem, and fracture of the left femur. He was transfused with two units of PRBCs and hemodynamics maintained with an infusion of noradrenaline (0.1 μg/kg/min). All other routine investigations were normal. He was treated with ceftazidime, levetiracetam 500 mg i.v. tds, and mannitol with 0.25gm/kg/body wt. The patient had a history of allergy for ingestion of goat intestine which has been revealed later by the informant.

On day 2, the patient received injection: cerebroprotein hydrolysate 10 ml (each milliliter contains 215.2 mg of cerebroprotein hydrolysate). Before the commencement of the infusion, his blood pressure was around 120–130 mmHg/70–80 mmHg, with noradrenaline support of 0.1 μg/kg/min. After 30 min of infusing 10 ml of cerebroprotein hydrolysate diluted in 100 ml normal saline, the patient had hypotension (systolic BP lowered to 60 mmHg) and after 3 min developed rashes all over the body. His saturation dropped from 99 to 85%; auscultation of the chest had bilateral extensive rhonchi. He was receiving only cerebroprotein at that time; hence, it was stopped immediately and was managed with i.v. fluids, increasing the dose of noradrenaline infusion to 0.4 μg/kg/min, hydrocortisone i.v. 200 mg, ranitidine 50 mg i.v., and pheniramine maleate 25 mg i.v. There was persistent hypotension, hence inj.adrenaline 200 μg bolus given and infusion started at 0.2 μg/kg/min. Thereafter, vitals showed improvement, BP-100/60 mmHg, and SpO₂-96%, and inotropes were tapered and reached the initial state from 0.4 μg/kg/min to 0.1 μg/kg/min over 6 h of the onset of the event and stopped after 24 h of the event.

Case 2

A 48-year-old male had RTA with left frontotemporal SDH and right temporal EDH with GCS 7/15, PEARL-2 mm. Pt had a history of drug allergy to amoxicillin and food allergy for chana dal (split chick peas) (Cicer arietinum (botanical name)). The patient was given cefoperazone + sulbactam 1.5 g i.v. ATD, and no drug reactions were observed. Inj. cerebroprotein infusion was started in a 100-ml infusion immediately; after 1 ml of i.v. infusion, the patient developed rash over the arm and face. The infusion was stopped. A dose of pheniramine maleate 25 mg i.v., inj. hydrocortisone 200 mg, and inj. ranitidine 50 mg i.v. was administered slowly.

Discussion

The neurotrophic factors are small proteins that exert trophic actions on neuronal cells. They are nerve growth factor, glial cell-derived neurotrophic factor, brain-derived neurotrophic factor, neurotrophin 3, growth-associated protein, and ciliary neurotrophic factor. Cerebroprotein enhances the neuronal survival by enhancing the effect through calfin. It provides neuromodulatory action and repair of neurons and has neuroimmunotrophic action (Sharma et al. 2010). It decreases the beta amyloid deposition used in Alzheimer’s disease (Plosker and Gauthier 2009); it modulates the neuronal plasticity and is used in traumatic brain injury (Wong et al. 2005) and vascular injury. It helps in the differentiation of neurons and protects against ischemia and neurotoxic injury. Common side effects include headache, agitation, fever, chills, flu-like syndrome, hallucination, and confusion. There is drug interaction with monoamine oxidase inhibitors. The neurotropic activity in plasma is detected after 24 h after a single injection (Hartbauer et al. 2001).

Conclusions

It is always better to give cerebroprotein after an intradermal test dose, and it is better avoided in patients with known allergies for protein.