Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0851184 (
thinning
)
11,252
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Three cases of symptomatic Rathkes' cleft cyst are described. Case 1. A 51-year-old man was admitted to the hospital for evaluation of intermittent headache, in April, 1985. He was neurologically free, but skull films disclosed a ballooning of the sella with
thinning
of the dorsum sellae. CT scan showed enlargement of the sella, but no abnormal density area in the sellar region. MRI revealed a round mass with high signal intensity located just posteriorly to the pituitary body. By a transsphenoidal approach, a thin-walled cyst was found at the posterior portion of the sella. Turbid mucinous fluid and the capsule of the cyst were subtotally removed. Histologic section of the specimen demonstrated that its wall was composed of a loose fibrous tissue lined by a single layer of ciliated cuboidal epithelium containing some goblet cells. Electron microscopy showed ciliated cuboidal cells, cells with microvilli, cells with light and large granules, and basal cells abutting on the basal lamina. Case 2. A 33-year-old female was referred to the hospital with complaints of severe headache and decreased visual acuity 0.02 in the left and 0.1 in the right, in July, 1985. Visual field examination revealed bitemporal hemianopsia. She had amenorrhea,
galactorrhea
and polyuria. CT scan and metrizamide CT cisternography detected a low density mass in the suprasellar region. Endocrinological studies disclosed hyperprolactinemia with partial hypopituitarism. She had a right frontal craniotomy and a suprasellar cyst was subtotally removed. Histologically, a cystic wall was lined by pseudostratified columnar epithelium supported by a loose fibrous tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Rathke's cleft cyst--report of three cases]. 361 39
Androgenetic alopecia (AGA), also known in women as female pattern hair loss, is caused by androgens in genetically susceptible women and men. The
thinning
begins between ages 12 and 40 years, the inheritance pattern is polygenic, and the incidence is the same as in men. In susceptible hair follicles, dihydrotestosterone binds to the androgen receptor, and the hormone-receptor complex activates the genes responsible for the gradual transformation of large terminal follicles to miniaturized follicles. Both young women and young men with AGA have higher levels of 5alpha reductase and androgen receptor in frontal hair follicles compared to occipital follicles. At the same time, young women have much higher levels of cytochrome p-450 aromatase in frontal follicles than men who have minimal aromatase, and women have even higher aromatase levels in occipital follicles. The diagnosis of AGA in women is supported by early age of onset, the pattern of increased
thinning
over the frontal/parietal scalp with greater density over the occipital scalp, retention of the frontal hairline, and the presence of miniaturized hairs. Most women with AGA have normal menses and pregnancies. Extensive hormonal testing is usually not needed unless symptoms and signs of androgen excess are present such as hirsutism, severe unresponsive cystic acne, virilization, or
galactorrhea
. Topical minoxidil solution is the only drug available for promoting hair growth in women with AGA. Efficacy has been shown in double-blind studies using hair counts and hair weight.
...
PMID:Androgenetic alopecia in women. 1289 91