Most adverse effects in clinical trials were mild and transient.The European Medicines Agency has listed a number of safety concerns to be evaluated on a post-marketing basis, most notably the theoretical possibilities of spleen rupture and tumor cell mobilisation. The first concern has been raised because splenomegaly was observed in animal studies, and G-CSF can cause spleen rupture in rare cases. Mobilisation of tumor cells has occurred in patients with leukaemia treated with plerixafor. Interactions
No interaction studies have been conducted. The fact that plerixafor does not interact with the cytochrome system indicates a low potential for interactions with other drugs. Pharmacology
Mechanism of action
In the form of its zinc complex, plerixafor acts as an antagonist (or perhaps more accurately a partial agonist) of the alpha chemokine receptor CXCR4 and an allosteric agonist of CXCR7. The CXCR4 alpha-chemokine receptor and one of its ligands, SDF-1, are important in hematopoietic stem cell homing to the bone marrow and in hematopoietic stem cell quiescence. The in vivo effect of plerixafor with regard to ubiquitin, the alternative endogenous ligand of CXCR4, is unknown. Plerixafor has been found to be a strong inducer of mobilization of hematopoietic stem cells from the bone marrow to the bloodstream as peripheral blood stem cells. Additionally, plerixafor inhibits CD20 expression on B cells by interfering with CXCR4/SDF1 axis that regulates its expression. Pharmacokinetics
Following subcutaneous injection, plerixafor is absorbed quickly and peak concentrations are reached after 30 to 60 minutes. Up to 58% are bound to plasma proteins, the rest mostly resides in extravascular compartments.
), ruptured aortic aneurysm, superior mesenteric artery syndrome, etc. Severe dehydration
Third spacing, e.g. malignant pleural effusion, ascites, severe peripheral oedema due to kidney failure
Rapid fluid shift due to dialysis
Cardiogenic shock
Myocardial infarction
Severe cardiac arrhythmia, e.g. ventricular fibrillation, sea water poisoning
Failed heart transplant or artificial heart; in those with cardiovascular disease who are just being treated with medical therapy or oxygen, pacing, cardioversion, or defibrillation using an implantable cardioverter-defibrillator, or else implantation of an intra-aortic balloon pump, or a unilateral or bilateral ventricular assist device, may help matters, as could the use of stenting and/or coronary artery bypass surgery and/or the removal of atherosclerotic plaques. Eventually, a heart transplant or artificial heart may be needed, and these can be replaced when they are no longer performing as well as they did. If necessary, while waiting for a transplant or device, extracorporeal membrane oxygenation (ECMO) or mechanical ventilation using a ventilator, or other less invasive methods, can be used to help compensate. If other systems get impaired, renal dialysis, liver dialysis, and artificial nutrition and hydration (including total or partial parenteral nutrition) can also be used. Congenital heart defects
Obstructive shock
Pulmonary embolism
Cardiac tamponade
Aortic dissection
Tension pneumothorax
Hypertrophic cardiomyopathy
Constrictive pericarditis
Distributive shock
Septic shock
Anaphylactic shock
Acute pancreatitis
Hypotension due to medications
Intoxicative inhalants
Combined
Dengue fever

Effects
The effects of a circulatory collapse vary based on the type of collapse it is.