This is due to the high likelihood of recurrence as well as the difficulty in distinguishing a benign from malignant growth with a hemithyroidectomy alone. The benign mucocutaneous lesions observed in Cowden syndrome are typically not treated unless they become symptomatic or disfiguring. If this occurs, numerous treatment options, including topical agents, cryosurgery, curettage, laser ablation, and excision, may be utilized. History
Cowden Syndrome was described in 1963, when Lloyd and Dennis described a novel inherited disease that predisposed to cancer. It was named after the Cowden family, in which it was discovered. They described the various clinical features including "adenoid facies; hypoplasia of the mandible and maxilla; a high-arch palate; hypoplasia of the soft palate and uvula; microstomia; papillomatosis of the lips and oral pharynx; scrotal tongue; [and] multiple thyroid adenomas. "The genetic basis of Cowden Syndrome was revealed in 1997, when germline mutations in a locus at 10q23 were associated to the novel PTEN tumor suppressor. See also
List of cutaneous neoplasms associated with systemic syndromes

References
Further reading
External links

GeneReviews/NCBI/NIH/UW entry on PTEN Hamartoma Tumor Syndrome (PHTS)
MORM syndrome is an autosomal recessive congenital disorder characterized by mental retardation, truncal obesity, retinal dystrophy, and micropenis". The disorder shares similar characteristics with Bardet–Biedl syndrome and Cohen syndrome, both of which are autosomal recessive genetic disorders. MORM syndrome can be distinguished from the above disorders because symptoms appear at a young age. The disorder is not dependent on sex of the offspring, both male and female offspring are equally likely to inherit the disorder. The syndrome is caused by a mutation in the INPP5E gene which can be located on chromosome 9 in humans. Further mapping resulted in the identification of a MORM syndrome locus on chromosome 9q34.3 between the genetic markers D9S158 and D9S905. Presentation
For individuals with MORM syndrome, symptoms do not appear until about one year of age. From conception to birth, individuals with MORM syndrome appear asymptotic, with no abnormal characteristics. Vision is negatively affected within the first year of life, particularly night vision. Individuals with MORM syndrome experience decreased visual acuity, meaning their ability to see distinct sharp lines decreases. Vision quality continues to deteriorate until age three. Any further reduction in vision acuity is not observed until the individual is between the ages thirty to forty. Delayed sentence processing and intellectual disability is associated with individuals with MORM syndrome, primarily observed at age four. Individuals continue to develop and grow until they are five to twelve years old.