Hyperplasia therapy

Saw palmetto (cabbage palm, fan palm, scrub palm) Serenoa repens %mptoms of benign prostatic hyperplasia Generally well-tolerated occasional gastrointestinal effects May interact with hormones such as oral contraceptive drugs and hormone replacement therapy. 

The expression of TRPVl in the bladder is, however, not restricted to afferent nerves urothelium, detrusor muscle and fibroblasts also express TRPVl in the human bladder [140]. The implication of these findings for intravesical vanilloid therapy is unclear [141], but the increase in TRPVl immunoreactivity in the urothelium in patients with neurogenic detrusor overactivity (that occurs in concert with increased TRPVl in bladder af-ferents) is a very intriguing finding [142]. In the male urogenital system, TRPVl is also present in testicles, prostate and scrotal skin [143], and it was postulated that TRPVl ligands may be beneficial in the treatment of benign prostatic hyperplasia [144]. 

Chappie CR. Pharmacological therapy of benign prostatic hyperplasia/ lower urinary tract symptoms an overview for the practicing clinician. BJU Int 2004 94 738-744. 

McConnell JD, Roehrborn CG, Bautista OM et al. The long term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl 1 Med 2003 349 2387-2398. 

Because data suggest that doxazosin (and probably other oq-receptor blockers) are not as protective against CV events as other therapies, they should be reserved as alternative agents for unique situations, such as men with benign prostatic hyperplasia. If used to lower BP in this situation, they should only be used in combination with primary antihypertensive agents. 

Low-dose hormone therapy (conjugated equine estrogen 0.45 mg and medroxyprogesterone acetate 1.5 mg/day) has demonstrated equivalent symptom relief and bone density preservation without an increase in endometrial hyperplasia. Whether such lower doses will be safer (cause less venous thromboembolism and breast cancer) remains to be seen. 

The effects of pure antiestrogens in the uterus have also been extensively studied, since it is an estrogen-dependent organ and the target of the main side effects of tamoxifen therapy, such as endometrial hyperplasia, hypertrophy of glandular epithelium, or even focal cellular atypia (Sourla et al. 1997). 

Endometrial hyperplasia Prolonged unopposed estrogen therapy may increase risk... 

Long-term maintenance therapy for patients with bilateral micronodular or macronodular adrenal hyperplasia (idiopathic hyperaldosteronism). 

Hormone replacement therapy PO 5-lOmgfor 12-14 consecutive days a month, beginning on day 1 or 16 of cycle given as parf of regimen with conjugated estrogens. Endometrial hyperplasia PO 2.5-10 mg/day for 14 days. 

Substitution therapy for deficiency states acute or chronic adrenal insufficiency, congenital adrenal hyperplasia, and adrenal insufficiency secondary to pituitary insufficiency, nonendocrine disorders arthritis rheumatic carditis allergic, collagen, intestinal tract, liver, ocular, renal, shin diseases bronchial asthma cerebral edema malignancies PO 5-60 mg/day in divided doses. Intra-articular, Intralesional (acetate) 4-100 mg, repeated as needed. Intra-articular, Intralesional (sodium phosphate) 2-30 mg, repeated at 3-day to 3-week intervals, as needed. IM (acetate, sodium phosphate) 4-60 mg a day. 

Substitution therapy in deficiency states acute or chronic adrenai insufficiency, congenital adrenal hyperplasia, and adrenal insufficiency secondary to pituitary insufficiency nonendocrine disorders arthritis rheumatic carditis aiiergic, coiiagen, intestinai tract, liver, ocular, renal, shin diseases bronchiai asthma cerebrai edema maiignancies PO... 

The causes of airway narrowing in acute asthmatic attacks (or "asthma exacerbations") include contraction of airway smooth muscle inspissation of viscid mucus plugs in the airway lumen and thickening of the bronchial mucosa from edema, cellular infiltration, and hyperplasia of secretory, vascular, and smooth muscle cells. Of these causes of airway obstruction, contraction of smooth muscle is most easily reversed by current therapy reversal of the edema and cellular infiltration requires sustained treatment with antiinflammatory agents. 

Most of the synthetic androgens and anabolic agents are 17-alkyl-substituted steroids. Administration of drugs with this structure is often associated with evidence of hepatic dysfunction. Hepatic dysfunction usually occurs early in the course of treatment, and the degree is proportionate to the dose. Bilirubin levels may increase until clinical jaundice is apparent. The cholestatic jaundice is reversible upon cessation of therapy, and permanent changes do not occur. In older males, prostatic hyperplasia may develop, causing urinary retention. 

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