Instead, researchers would turn to much more potent synthetic progestogens for use in oral contraception in the future. Progestins to prevent ovulation
Pincus asked his contacts at pharmaceutical companies to send him chemical compounds with progestogenic activity. Chang screened nearly 200 chemical compounds in animals and found the three most promising were Syntexs norethisterone and Searles noretynodrel and norethandrolone.Chemists Carl Djerassi, Luis Miramontes, and George Rosenkranz at Syntex in Mexico City had synthesized the first orally highly active progestin norethisterone in 1951. Frank B. Colton at Searle in Skokie, Illinois had synthesized the orally highly active progestins noretynodrel (an isomer of norethisterone) in 1952 and norethandrolone in 1953.In December 1954, Rock began the first studies of the ovulation-suppressing potential of 5–50 mg doses of the three oral progestins for three months (for 21 days per cycle—days 5–25 followed by pill-free days to produce withdrawal bleeding) in fifty of his patients with infertility in Brookline, Massachusetts. Norethisterone or noretynodrel 5 mg doses and all doses of norethandrolone suppressed ovulation but caused breakthrough bleeding, but 10 mg and higher doses of norethisterone or noretynodrel suppressed ovulation without breakthrough bleeding and led to a 14% pregnancy rate in the following five months. Pincus and Rock selected Searles noretynodrel for the first contraceptive trials in women, citing its total lack of androgenicity versus Syntexs norethisterone very slight androgenicity in animal tests.
Gallbladder and sphincter of Oddi disorders

E1. Biliary pain
E1a. Functional gallbladder disorder
E1b. Functional biliary sphincter of Oddi disorder
E2. Functional pancreatic sphincter of Oddi disorderF. Anorectal disorders

F1. Fecal incontinence
F2. Functional anorectal pain
F2a. Levator ani syndrome
F2b. Unspecified functional anorectal pain
F2c. Proctalgia fugax
F3. Functional defecation disorders
F3a. Inadequate defecatory propulsion
F3b. Dyssynergic defecationG. Childhood functional GI disorders: Neonate/Toddler

G1. Infant regurgitation
G2. Rumination syndrome
G3. Cyclic vomiting syndrome (CVS)
G4. Infant colic
G5. Functional diarrhea
G6. Infant dyschezia
G7. Functional constipationH. Childhood functional GI disorders: Child/Adolescent

H1. Functional nausea and vomiting disorders
H1a. Cyclic vomiting syndrome (CVS)
H1b. Functional nausea and functional vomiting
H1b1. Functional nausea
H1b2. Functional vomiting
H1c. Rumination syndrome
H1d. Aerophagia
H2. Functional abdominal pain disorders
H2a. Functional dyspepsia
H2a1. Postprandial distress syndrome
H2a2. Epigastric pain syndrome
H2b. Irritable bowel syndrome (IBS)
H2c. Abdominal migraine
H2d. Functional abdominal pain ‒ NOS
H3. Functional defecation disorders
H3a. Functional constipation
H3b. Nonretentive fecal incontinence

Epidemiology
Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16–26% of the population. Research
There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. A role for mast cell activation has been proposed as one of the factors. See also
Allergy
Food intolerance
Functional indigestion
Histamine intolerance

References


== External links ==