Some tumors secrete more than one hormone, the most common combination  being GH and prolactin, which present as unexpected bone growth and unexpected lactation (in both men and women).A patient with pituitary adenoma may present with visual field defects, classically bitemporal hemianopsia. It arises from the compression of the optic nerve by the tumor. The specific area of the visual pathway at which compression by these tumours occurs is at the optic chiasma. The anatomy of this structure causes pressure on it to produce a defect in the temporal visual field on both sides, a condition called bitemporal hemianopsia. If originating superior to the optic chiasm, more commonly in a craniopharyngioma of the pituitary stalk, the visual field defect will first appear as bitemporal inferior quadrantanopia, if originating inferior to the optic chiasm the visual field defect will first appear as bitemporal superior quadrantanopia. Lateral expansion of a pituitary adenoma can also compress the abducens nerve, causing a lateral rectus palsy.Also, a pituitary adenoma can cause symptoms of increased intracranial pressure. Prolactinomas often start to give symptoms especially during pregnancy, when the increased hormone level estrogen can increase the tumors growth rate.Various types of headaches are common in patients with pituitary adenomas. The adenoma may be the prime causative factor behind the headache or may serve to exacerbate a headache caused by other factors.
This means the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. DNA repair
RECQL4 has a crucial role in DNA end resection that is the initial step required for homologous recombination (HR)-dependent double-strand break repair. When RECQL4 is depleted, HR-mediated repair and 5’ end resection are severely reduced in vivo. RECQL4 also appears to be necessary for other forms of DNA repair including non-homologous end joining, nucleotide excision repair and base excision repair. The association of deficient RECQL4-mediated DNA repair with accelerated aging is consistent with the DNA damage theory of aging. Diagnosis
Management
History
The condition was originally described by August von Rothmund (1830–1906) in 1868. Matthew Sydney Thomson (1894–1969) published further descriptions in 1936. See also
Poikiloderma vasculare atrophicans
List of cutaneous conditions
List of radiographic findings associated with cutaneous conditions

References
External links
GeneReviews/NCBI/NIH/UW entry on Rothmund-Thomson Syndrome
Poikiloderma of Rothmund-Thomson at NIHs Office of Rare Diseases