Carbidopa/levodopa/entacapone, sold under the brand name Stalevo among others, is a dopaminergic fixed-dose combination medication that contains carbidopa, levodopa, and entacapone for the treatment of Parkinsons disease. It is marketed by Swiss-based Novartis Pharmaceuticals and manufactured by Finnish drugmaker Orion Corporation. Medical uses
Carbidopa/levodopa/entacapone was approved by the U.S. Food and Drug Administration (FDA) in June 2003, to treat adults with Parkinsons disease of unknown cause in two scenarios. First, to substitute with equivalent strength of each of the three components for immediate-release carbidopa/levodopa and entacapone previously administered as individual products. Second, to replace immediate-release carbidopa/levodopa therapy (without entacapone) when people experience the signs and symptoms of end-of-dose "wearing-off" but only for people taking a total daily dose of levodopa of 600 mg or less and not experiencing dyskinesias.It may help decrease a change of response to Parkinsons medications.In the European Union it is indicated for the treatment of adults with Parkinsons disease and end-of-dose motor fluctuations not stabilized on levodopa/dopa decarboxylase (DDC) inhibitor treatment. Side effects
Sometimes a wearing off effect may occur at the end of the dosing interval, where a patient may feel Parkinsons symptoms. Urine, saliva, or sweat may be discolored (dark color such as red, brown, or black) after taking carbidopa/levodopa/entacapone. Prostate cancer
On March 31, 2010, the United States Food and Drug Administration (FDA) stated it was evaluating long-term clinical data from STRIDE-PD which found that a greater number of patients taking Stalevo had prostate cancer compared to those taking carbidopa/levodopa.
Low levels of oestrogen effect the HPG axis with no feedback to the anterior pituitary to inhibit the secretion of FSH and LH. FSH and LH are secreted at abnormal elevated levels. Improper levels of these hormones will cause a failure to initiate puberty, undergo menarche, and develop secondary sex characteristics. If sufficient functional ovarian tissue is present, limited menstrual cycles can occur.The pathogenesis of 46,XX gonadal dysgenesis is unclear, as it can manifest from a variety of dysregulations. Interruption during ovarian development in embryogenesis can cause 46,XX gonadal dysgenesis with cases of abnormalities in the FSH receptor
and mutations in steroidogenic acute regulatory protein (StAR protein) which regulates steroid hormone production. 46,XY gonadal dysgenesis
46,XY gonadal dysgenesis is characteristic of male hypogonadism with karyotype 46,XY.In embryogenesis, the development of the male gonads is controlled by the testis determining factor located on the sex-determining region of the Y chromosome (SRY). The male gonad is dependent on SRY and the signalling pathways initiated to several other genes to facilitate testis development.The aetiology of 46,XY gonadal dysgenesis can be caused by mutations in the genes involved in testis development such as SRY, SOX9, WT1, SF1, and DHH. If a single or combination of these genes are mutated or deleted, downstream signalling  is disrupted, leading to malformation of male external genitalia.SRY acts on gene SOX9 which drives Sertoli cell formation and testis differentiation. An absence in SRY causes SOX9 to not be expressed at the appropriate time or concentration, leading to a deficiency in testosterone and anti-Müllerian hormone production.