History
Captopril, the first ACE inhibitor, is a functional and structural analog of a peptide derived from the venom of the jararaca, a Brazilian pit viper (Bothrops jararaca). Enalapril is a derivative, designed by scientists at Merck to overcome the rash and bad taste caused by captopril. : 12–13 
Enalapril is actually a prodrug; the active metabolite is enalaprilat.The di-acid metabolite of enalapril, enalaprilat, and its lysine analogue lisinopril are potent inhibitors of angiotensin converting enzyme (ACE); they do not contain sulphydryl groups. Both drugs can be assayed by high pressure liquid chromatography and by radioimmunoassay and plasma ACE inhibition remains stable under normal storage conditions. It is therefore possible to study their pharmacokinetics as well as their pharmacodynamic effects in humans. Enalaprilat and lisinopril as well as ACE activity have been measured in blood taken during the course of two studies of the effects of these drugs on blood pressure and autonomic responsiveness. Lisinopril is a synthetic peptide derivative of captopril. Scientists at Merck created lisinopril by systematically altering each structural unit of enalaprilat, substituting various amino acids. Adding lysine at one end of the drug turned out to have strong activity and had adequate bioavailability when given orally; analogs of that compound resulted in lisinopril, which takes its name from the discovery with lysine. Merck conducted clinical trials, and the drug was approved for hypertension in 1987 and congestive heart failure in 1993.The discovery posed a problem, since sales of enalapril were strong for Merck, and the company did not want to diminish those sales.
If the findings still remain unclear, microscopic examination of fine needle asperates taken from the tumor will, when combined with the imaging findings, the lesion’s natural history, and its clinical presentation, likely confirm the diagnosis of FMC in virtually all cases. Treatment and prognosis
Prompt diagnosis and treatment of FMS is crucial for avoiding the impairments that may follow long-term mal-positioning of infants head such as permanent facial asymmetry, flattened head, loss of neck mobility, and scoliosis. About 95% of infants with minimal limitations in their heads mobility show improvements in this mobility after 4 weeks of an active home stimulation program (i.e. observation, massage, and active and passive stretching) while ~91% of infants with more severe movement limitations show good results after 3 sessions of targeted physiotherapy over a 3–4 month period. The recommended treatment for infants who show no improvements in mobility after 1 year of physical therapy or who initially present at >12 months of age is surgical tenotomy (i.e. cutting) of one of the tendons on the involved sternocleidomastoid muscle. Tenotomy may use the open surgical (i.e. cutting of skin) approach or endoscopic (i.e. percutaneous) approach. The overall prognosis of FMS tumors is good using these treatment measures.Infants presenting with FMS should be examined for the presence of hip dysplasia. See also
Skin lesion


== References ==