The suppository is more effective after a long-term follow-up than terconazole as a cream or other intravaginal treatments. Side effects
The most common side effects of terconazole include headaches, vulvar/vaginal irritation, rash, itching, burning or discomfort. Other side effects may include abdominal pain or cramps, dysmenorrhea, chills, fever and allergic reactions. Flu-like symptoms have been recorded in those that take suppositories greater than 160 mg. May cause birth defects if used in the first trimester.Terconazole is not considered hazardous when handled under normal conditions. It is generally non-flammable and non-carcinogenic. Generally is non-toxic, however, can emit toxic fumes when dust is set alight. Can cause respiratory distress as dust. Can be absorbed by embryo within the first trimester of pregnancy and cause birth defects. Cross inhibition shows that there may be some toxicity. Interactions
Terconazole may interact with the spermicide nonoxynol-9. A precipitate is formed upon combination of both drugs. Terconazole may weaken latex-based condoms. Chemistry
Terconazole is a triazole ketal with broad-spectrum antifungal/antimycotic tendencies. Terconazole synthesis synologous with ketoconazole except for the fact that triazole and not imidazole heterocyclic ring is used, and that isopropyl group instead of acetamide. Terconazole has the chemical formula C26H31Cl2N5O3. The chemical name for terconazole is 1-{[(2S,4S)-2-(2,4-dichlorophenyl)-4-{[p-(4-isopropyl-1-piperazinyl)phenoxy]methyl}-1,3-dioxolan-2-yl]methyl}-1H-1,2,4-triazole. Terconazole has a melting point of 126.3 °C (259.34 °F). The molecular weight of terconazole is 532.462 g/mol. Terconazole is synthesized using two chemical compounds: cis-[2(bromomethyl)-2-(2,4-dichlorophenyl)-1,3-dioxolan-4-yl] methyl benzoate and the sodium salt of triazole, created by mixing triazole with sodium hydride.
In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Adrenal and thyroid gland problems could also be a cause.Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinsons disease and multiple system atrophy. It may occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis. Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining. Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.People with gastroparesis are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.