You are on page 1of 61

DESLORATAD, LEVOCETIRIZINE AND FEXOFENADINE Desloratadine (5 mg), a major metabolite of loratadine, has a selective and peripheral H1-antagonist action.

It does not readily enter the central nervous system. Unlike other antihistamines, desloratadine is also effective in relieving nasal congestion, particularly in patients with allergic rhinitis. Most common sideeffects are fatigue, dry mouth, headache, painful menstruation, and gastrointestinal disturbances. Fexofenadine HCl (180 mg), a second generation antihistamine, is an active metabolite of terfenadine. Levocetirizine is metabolized to a lesser extent than desloratadine, and has higher specificity for histamine-1 receptors. Onset of action and Effectivity in histamine-induced wheal-and-flare suppression : Fexofenadine > Levocetirizine > Desloratadine Drowsiness/sedation : Levocetirizine > Desloratadine > Fexofenadine ILAPRAZOLE (5, 10, and 20 mg) Ilaprazole is not significantly influenced by CYP2C19, compared to the available PPIs and is as tolerable, safe, and efficacious as omeprazole in the treatment of duodenal ulcers. The pharmacological characteristics of ilaprazole confer theoretical advantages that are expected to translate into an improved acid control, particularly at night time. But none of the trials indicated superiority of ilaprazole over the existing PPIs. Ilaprazole has shown higher suppression of gastric acid secretion, more prolonged plasma half-life, and similar safety as omeprazole when taken in equivalent doses (10 mg/d ilaprazole vs. 20 mg/d omeprazole). Studies also showed that ilaprazole significantly prevented the development of reflux oesophagitis. Ilaprazole can cause mild to moderate GI discomfort with anorexia, fatigue, weight loss, nausea or vomiting

and indigestion. Ilaprazole may interact with Clarithromycin, midazolam, ketoconazole and amoxicillin. GEMCITABINE (Gemzar - vials contain either 200mg or 1g gemcitabine HCl) Gemcitabine 1-1.2 g/m2 of body surface area over 30 minutes intravenously. For cancer of pancreas it is given once a week up to 7 weeks to start, then a week without treatment; after that, once a week for 3 weeks followed by a week off. For breast or ovarian cancer, it’s usually once a week for 2 weeks, then 1 week off. For lung cancer or other cancer patients, it usually is given weekly for 3 weeks with 1 week off. It is also not as debilitating as some other forms of chemotherapy. Anemia is usual a few weeks after starting treatment. Severe nausea and vomiting, flu-like symptoms , temporary hair loss. Serious side effects include chest pain, jaw/left arm pain, weakness on one side of the body, slurred speech, vision changes, confusion, dizziness/lightheadedness, fainting, mouth sores, numbness/tingling of hands/feet, sudden weight gain, swelling of ankles/feet, severe stomach/abdominal pain, easy bleeding/bruising, cough, shortness of breath/ wheezing, unusual tiredness, fast/irregular heartbeat, change in amount of urine, dark urine, yellowing of the eyes/skin. PIRANULIN (Pirasun - alpha glycerylphosphorylcholine 250 mg, piracetam 800 mg) Piranulin is a cyclic derivative of GABA. Piranulin is Nootropics & Neurotonics/Neurotrophics in the class of other agents used as CNS stimulant. It appears to enhance cognition and memory, slow brain aging, increase blood flow and oxygen to the brain, aid stroke recovery, and ameliorate Alzheimer's, Down's syndrome, dementia, and dyslexia, among other diseases and conditions.

PO Adjunct in treatment of cortical myoclonus 7.2 g/day in 2-3 divided doses, increase if needed. Max: 20 g/day. Cognitive enhancer 2.4 g/day in 2-3 divided doses. Severe: Up to 4.8 g/day. IV/IM Cognitive enhancer 1-2 g 3 times/day. May be taken with or without food. Take w/a glass of water or soft drink after taking the undiluted soln to mask bitter taste. Special precaution - Avoid abrupt withdrawal. Impaired renal function. Cardiac disorders. Haemostatic disorders. Patients who have recently undergone major surgery. Elderly. C/I - Hepatic and severe renal impairment. Cerebral haemorrhage. Pregnancy and lactation. Adverse effects - Hyperkinesia, nervousness, depression, diarrhoea, rashes. CNS stimulation, sleep disturbances, dizziness, excitement, insomnia, somnolence, wt gain. May increase prothrombin time in patients who are on warfarin. DAPOXETINE HYDROCHLORIDE Dapox (30 mg) Ranbaxy Laboratories Ltd Rs. 144/6 Duralast (30 mg) Sun Pharmaceutical Industries Ltd Rs. 96/4 Ejalong (30 mg) and Sustinex (30 mg) Emcure Pharmaceuticals Ltd Rs. 144/6 Dapoxetine hydrochloride, a member of SSRI, is taken at least two hours before sexual intercourse to achieve maximum treatment benefits. Its fast acting property makes it suitable for the treatment of PE but not as an antidepressant. Other SSRIs such as fluoxetine, paroxetine, sertraline, fluvoxamine, and citalopram have been used as off label drugs to treat PE. Waldinger’s meta analysis shows that the use of these conventional antidepressants increasing IELT from two to ninefold above base line in comparison of three to eightfold when dapoxetine is used. However, these SSRIs must be taken daily in order to achieve meaningful efficacy, and the long half-life

and telithromycine. If a patient stops taking one of these drugs. or tricyclic antidepressant. Ethanol doesn’t affect the pharmacokinetics of dapoxetine. followed by nausea. permanent pacemaker. It works by inhibiting the serotonin transporter over 12 weeks more than a three-to-four fold increase in mean IELT generally well tolerated. The most common adverse events reported with both 30 mg and 60 mg doses of dapoxetine were nausea.7 and 21. serotonin-norepinephrine reuptake inhibitors. on the other hand. If a patient stops taking dapoxetine. or other significant ischemic heart disease.increases the risk of the drug accumulation and as a consequence increased of adverse effects such as decreasing sexual libido and causing erectile dysfunction. Dapoxetine does not alter the pharmacokinetic of tadalafil (Cialis) or sildenafil. dizziness. Dapoxetine. It is rapidly absorbed and eliminated from the body within a few hours (terminal half-life of 18. 2011. Caution is advised in men receiving thioridazine. SSRIs. monoamine oxidase inhibitors. dry mouth. Dapoxetine should not be used in men with moderate to severe hepatic impairment and in those receiving CYP3A4 inhibitors such as ketoconazole. ritonavir. he should wait for 14 days before taking dapoxetine.9 hours for a single dose of 30 mg and 60 mg respectively). the US FDA approved the supplementation of hydroxyprogesterone caproate during pregnancy to reduce the risk . is a fast-acting SSRI. with most side effects of mild-to-moderate severity. headache. diarrhea. Progesterone Supplementation and the Prevention of Preterm Birth On February 3. Dapoxetine can also not be used in patients with heart failure. he should wait for 7 days before receiving these drugs. and insomnia.

respectively. but is predictive of delivery prior to 28 weeks and 32 weeks in 90% and 60% of cases. the pregnancy is at a sixfold increased risk of delivery prior to 35 weeks. The primary value of this test lies in its negative predictive value (99% of patients with a negative fFN test will not deliver within 7 days). However. Progesterone produced by the corpus luteum is critical to the maintenance of early pregnancy until the placenta takes over this function at 7 to 9 weeks of gestation (hence its name Pro-gesterone). If the cervical length is < 10th percentile for gestational age in the midsecond trimester. the positive predictive value of a positive fFN test at 22 to 24 weeks of gestation for spontaneous preterm delivery prior to 28 weeks and 37 weeks of gestation is only 13% and 36%. The single greatest risk factor for preterm birth is a history of a prior unexplained spontaneous preterm delivery. Although the ability of obstetric care providers to identify women at high risk for preterm birth has improved (due to the introduction of transvaginal cervical length measurements and cervicovaginal fetal fibronectin testing). efforts to prevent preterm birth have been largely unsuccessful. respectively. A strong inverse correlation exists between residual cervical length as measured by transvaginal ultrasound and preterm birth.of recurrent preterm birth in women with a history of at least one prior spontaneous preterm delivery. Preterm birth refers to any delivery occurring prior to 259 days of gestation. A cervical length of < 15 mm at 22 to 24 weeks occurs in < 2% of low-risk women. in a low-risk population. which may prevent unnecessary hospitalization and medical intervention. Elevated levels of fetal fibronectin (fFN) in cervicovaginal secretions (defined as > 50 ng/mL) at 22-0/7 through 34-6/7 weeks of gestation are associated with an increased risk of preterm birth. .

oxytocin and prostaglandin receptors.Recent data suggest that progesterone may be important in maintaining uterine quiescence in the latter half of pregnancy by limiting the production of stimulatory prostaglandins and inhibiting the expression of contraction-associated protein genes (ion channels. which was a theoretical concern of this therapy. 250 asymptomatic women with a short cervix (≤ 15 mm) on transvaginal ultrasound at 20 to 25 weeks of gestation were treated with either vaginal progesterone (200 mg each night) or placebo. very low birth weight infants.4% in controls. need for supplemental oxygen and overall neonatal morbidity and mortality. Weekly injection of 17P is able to extend gestation in women presenting with preterm premature rupture of the membranes (PPROM) at 20 to 30 weeks of gestation. a significant reduction in respiratory distress syndrome. Progesterone administration significantly reduced the rate of spontaneous preterm birth before 34 weeks (19. infants born to mothers treated with 17P had less perinatal morbidity and significantly reduced rates of necrotizing enterocolitis. intraventricular hemorrhage. There was no evidence of virilization of female offspring. Studies suggest that the rate of recurrent preterm birth with the use of prophylactic progestational agents is approximately 25% to 31% compared with 33% to 47% in placebo controls. randomized. Moreover. Whether progesterone acts by attenuating further cervical shortening is not yet clear. placebo-controlled trial. In a high-profile.2% vs 34. and gap junctions) within the myometrium. There is no information on use of progesterone supplementation in women with a positive cervicovaginal fFN test. The observation that progesterone supplementation does not prevent preterm birth in multiple pregnancy suggests that the mechanism leading to preterm labor and delivery in multiples— . It is not clear whether 17P provides additional benefit to women (with a history of prior midtrimester pregnancy losses due to cervical insufficiency) with a cervical cerclage in place.

61 Indeed. although patients were enrolled in trials up to 26. which are key regulators of myometrial contractility.namely excessive uterine stretch—is different from that in singletons. Progesterone does not inhibit stretch-induced MAPK activation or gene expression in myometrial cells in vitro.9 weeks. At best. and treatment should be continued through 36 weeks of gestation. Progesterone supplementation does not appear to significantly alter circulating steroid levels and basal levels of 17P in the maternal circulation far exceed that of the dissociation constant for the progesterone receptor. early discontinuation of therapy appears to increase the risk of recurrent preterm birth. and the long-term benefits of progesterone supplementation are not yet clear. It interferes with oxytocin binding and signaling in a nongenomic fashion by binding directly with the transmembrane oxytocin receptor. And . PR-A and PR-B. leading at term to a PR-A/PR-B ratio that favors myometrial contractility and cervical effacement. progesterone supplementation prevents only one-third of recurrent preterm births. It alters the expression of PR coactivators and histone acetylation within myometrial cells. If used. progesterone supplementation should generally be initiated between 16 and 20 weeks of gestation. It alters immune function both systemically and at the maternal-fetal interface. Women with a history of a prior preterm delivery of twins are at risk of a recurrent preterm birth even if the subsequent pregnancy is a singleton. and should be considered as candidates for progesterone supplementation. How then does progesterone act to prevent preterm labor and delivery? Progesterone differentially regulates the expression of the two major isoforms of the progesterone receptor (PR) gene. Levels of progesterone in the maternal circulation during labor are not different from that measured 1 week prior.

it has been shown to modulate myometrial expression of a number of miRNA-200 family members and their targets. which has been implicated as the “placental clock” regulating the timing of labor. the most important of which is placental corticotropin-releasing hormone (CRH). The advantage of vaginal progesterone is its high uterine bioavailability because uterine exposure occurs before the first pass through the liver. dose. . directly regulate the expression of key contraction-associated genes. which is present in high concentrations in amniotic fluid. One third of preterm birth occurs in the setting of PPROM. formulation. Progesterone has been shown to interfere with cortisol-mediated regulation of placental gene expression. It also has fewer systemic side effects. including the oxytocin receptor and connexin-43. thereby preventing PPROM and subsequent preterm birth. Progesterone has been shown to upregulate an endogenous inhibitor of phospholipase A2.most recently. These data suggest that progesterone may block proinflammatory cytokine-induced apoptosis within the fetal membrane. The type of progestin. ZEB1 and ZEB2. It is possible for progesterone supplementation to maintain uterine quiescence and prevent preterm birth without altering circulating progesterone levels by acting directly at the level of the uterus and cervix to circumvent the functional withdrawal seen in these tissues. which. High levels of such an inhibitor would serve to limit the availability of arachidonic acid and thereby the production of prostaglandins. and route of delivery may have a significant impact on efficacy. Recent studies have shown that progesterone is able to inhibit apoptosis (programmed cell death) in term fetal membranes both under basal conditions and in the setting of inflammation. in turn. although vaginal irritation can be bothersome.

Dose and Route of Administration . Recommendations for Progesterone Supplementation to Prevent Preterm Birth Indication Progesterone Indicated? Formulation. Moreover.Several studies have suggested that the risk of miscarriage and stillbirth may be increased in women exposed to progestins. even if real. and yet others have suggested that progestins may be protective in this regard. this risk is limited to exposure prior to 11 weeks of gestation and. is not relevant to the current discussion. however. Appropriate candidates should be counseled about the potential benefits of progesterone supplementation from 16 to 20 weeks through 36 weeks of gestation to prevent preterm birth in any subsequent pregnancy. The only concern that persists is a possible increased risk of hypospadias in male offspring exposed to exogenous progestins. but none of these differences reached statistical significance. as such. not all studies were able to confirm this observation.

Prior spontaneous preterm birth Yes 17a-hydroxyprogesterone caproate. 250mg i.m. 90-200mg vaginally each night from time of diagnosis through 36 weeks of gestation Cervical shortening (15mm prior to 24weeks) Yes Multiple pregnancy Premature rupture of membranes Positive fetal fibronectin (fFN) test Cervical cerclage in place Undelivered after an episode of preterm labor No No No No Unclear STRATEGIES FOR THE PREVENTION OF PRETERM BIRTH Strategies That Have Limited or N0 Proven Efficacy Bed rest Pelvic rest (avoidance of intercourse) Intensive education and prenatal care Screening and treatment of asymptomatic lower genital tract Infections Treatment of gingival disease Empirical broad-spectrum antibiotic therapy Prophylactic tocolytic therapy Strategies That May Have Some Benefit  Prevention and early diagnosis of sexually transmitted and  genitourinary infections  Treatment of symptomatic lower genital tract infection . weekly from 16-20 week through 36 weeks of gestation Progesterone suppository.

20% of women stop having periods after 1 year of use. Most of the hormone stays inside the uterus. Cramping or backache can occur at insertion. Cessation of smoking and illicit substance use  Prevention of multiple pregnancies  Elective (prophylactic) cervical cerclage. After insertion Mirena is effective for 5 years. Itcan be used while breastfeeding. and only a small amount is absorbed into the rest of the body. It also reports concerns about potential effects on the infant's liver and brain development in the first six weeks postpartum. citing increased expulsion rates.7%. but this diminishes to about four days at 12 months. but this usually improves after 3 to 6 months. The first year failure rate for the hormonal IUD is 0. These rates are comparable to tubal sterilization. The average user reports 16 days of bleeding or spotting in the first month of use. However. Blood levels of levonorgestrel in Mirena users are half those found in Norplant users and one-tenth those found in users of levonorgestrel-only pills. it recommends offering Mirena as a contraceptive option beginning at six weeks postpartum even to nursing women.2% and the five year failure rate is 0. as such its effects are mostly paracrine rather than systemic. . Irregular periods and spotting between periods often occurs after insertion. although some studies have shown that it may be effective through 7 years. less likely to interact with other medications and safe for women with medical problems. WHO recommends it against immediate postpartum insertion. if indicated  Folic acid supplementation Mirena The hormonal IUD releases the levonorgestrel directly into the uterus.

which further implies that IUDs prevent fertilization through several contraceptive effects: Cervical mucus thickens Sperm's survival and ability to penetrate the egg is inhibited Endometrium is suppressed In some women. IUDs also decrease the risk of ectopic pregnancy. tar products. If PID does occur. Methotrexate cannot be used by people: With blood disorders or severe anemia. but no fertilized eggs were found in women using IUDs. it will most likely happen within 21 days of insertion. In one experiment involving tubal flushing. fertilized eggs were found in half of women not using contraception. With liver or kidney diseases. although some may be accompanied by pelvic pain or dyspareunia. ointments. IUDs primarily prevent fertilization. Enlarged follicles (ovarian cysts) have been diagnosed in about 12% of the subjects using a hormonal IUD.Insertion of an IUS is not recommended for women having had a D&E abortion (second-trimester abortion) within the past four weeks or had pelvic inflammatory disease within the past 3 month. It may also be given as a shot once a week. It is taken orally once a week or in 3 divided doses at 12-hour intervals. In most cases the enlarged follicles disappear spontaneously after two to three months. . and phototherapy have not worked or cannot be used. The device itself does not increase the risk of infection. Most of these follicles are asymptomatic. With stomach ulcers. ovulation is inhibited METHOTREXATE Methotrexate slows the rapid growth of skin cells in psoriasis and is used to treat psoriatic arthritis or severe psoriasis (more than 20% of the skin is affected) when creams. not implantation.

Common temporary side effects include: Nausea.With an infectious disease. PPIs might affect the body’s absorption of calcium. The PPI actually lowers the acidity of the stomach so much that the C. Researchers found a link between long-term use of PPIs and hip fractures. FDA recently issued a safety alert about these drugs and diarrhea that doesn’t go away. Who cannot return to the doctor for tests to check for side effects of the medicine. With the change in pH in your stomach. L anzoprazole has the potential to be an . fatigue. The body can’t absorb vitamin B12 without stomach acid to uncouple the vitamin from protein in food. CYP2C19 plays a major role in the primary metabolism of both omeprazole and diazepam . difficile diarrhea. By lowering stomach acid levels. loss of appetite. The reduction of vitamin B12 may also increase bone fragility by raising homocysteine. Who drink alcohol frequently. acid-sensitive drugs and nutrients like iron and calcium can just pass through your system unabsorbed. PROTON PUMP INHIBITORS (PPI) An analysis of research into the side-effects of PPIs has found between half and two-thirds of prescriptions are 'inappropriate. difficile bacteria — normally kept at bay by the acid in your stomach — proliferate out of control. One of the most serious side effects of PPI is C. phenytoin. such as tuberculosis. and R-warfarin. Esomeprazole showed a slightly weaker inhibitory potency on CYP2C19 than omeprazole.

lansoprazole. Pantoprazole showed the highest inhibition potency on CYP2C9 of the five PPIs (i. telmisartan should be administered with caution and a lower dose should be considered.equally or more potent inhibitor than omeprazole or esomeprazole. Production of angiotensin II can occur through non-ACE pathways as well as through the primary ACE pathway. leaving AT2 receptor unblocked.. and these alternative pathways are unaffected by ACE inhibition. omeprazole. ACE is a relatively nonspecific enzyme that has substrates in addition to angiotensin I. esomeprazole.e. inhibition of ACE may result in accumulation of these substrates. ARBs may offer more complete angiotensin II inhibition by interacting selectively with the receptor site. ARBs act to prevent the action of angiotensin II at the AT1 receptor. . Specific adverse effects are associated with ACE inhibitor effects on the enzyme. Most of the antihypertensive effect of telmisartan is apparent within 2 weeks and maximal reduction is generally attained after 4 weeks. However. In patients with possible intravascular volume depletion. and rabeprazole). including bradykinin and other tachykinins. ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS) ARBs were developed to overcome several of the deficiencies of ACE inhibitors: Competitive inhibition of ACE results in a reactive increase in renin and angiotensin I levels. pantoprazole. which may overcome the blockade effect. administered intravenously would avoid a potential influence on the liver enzymes by the first pass metabolism of pantoprazole. and thus.

Elderly hypertensives with diabetes mellitus exhibits higher response to levamlodipine therapy than non-diabetic patients.No initial dosage adjustment is necessary for elderly patients or patients with renal impairment. Orthostatic hypotension is indicated if there is a drop in 20 mmHg of SBP (and a 10 mmHg drop in DBP in some facilities) and a 20 beats/minute increase in HR between seated and standing (with a two-minute delay in between each position change) positions. The studies also reported a significant reduction in total cholesterol and triglyceride levels with levamlodipine. . Telmisartan 40/80 mg is superior to losartan 50/100 mg in controlling DBP and SBP during the last 6 h of the 24-h dosing interval. Asomex.5 mg of levamlodipine was found to be equivalent in its blood pressure lowing efficacy to 5 mg of amlodipine. dizziness. Levamlodipine is an effective switch-over option for the elderly patients who experience oedema and other adverse events with racemic amlodipine as it is rarely associated with peripheral edema and other side effects like headache.etc) Out of the two forms only the (S)-enantiomer of amlodipine binds to and blocks L-type calcium channels. which was not seen with amlodipine. Espin. including those on hemodialysis. Levoamlodipine or S-amlodipine Besylate .(Eslo. 2. Patients with biliary obstructive disorders or hepatic insufficiency can be expected to have reduced clearance. flushing and abdominal pain.

chemicals). As catecholamines induce platelet activation via alpha 2-receptors on platelet membrane. and thereby producing further vasodilatation. Whereas L-type Ca2+ channel blockade produces vasodilation of peripheral resistance vessels akin to amlodipine. The inhibitory effect on the N-type Ca2+channel may bestow an additional clinical advantage for the treatment of hypertension. Cilnidipine acts through dual blockade of L-type and Ntype Ca2+ channels. This unique mechanism of action results in vasodilation of both preand post-capillary resistance vessels reducing capillary hypertension and consequent hyperfiltration of fluid into the interstitium. CILNIDIPINE ' suppresses the development of proteinuria greater than amlodipine through inhibiting N-type calcium channeldependent podocyte injury. telmisartan 40mg) Amlodipine acts primarily through blockade of L-type Ca2+ channels. quantitative evaluations did not reveal significant volume gains. such as suppression of reflex tachycardia. Cilnidipine has 50 times higher selectivity for Ntype of calcium channels than amlodipine.Cilnidipine Cilacar (Cilnidipine 10 mg/15 mg j.b. CILNIDIPINE significantly decreased urinary albumin excretion without affecting serum creatinine concentration in hypertensive patients. inhibition of neuronal N-type Ca2+ channels disrupts sympathetic nervous outflow. CILACAR-T tab (Cilnidipine 5 mg. CILNIDIPINE leads to less activation of the RAAS compared with amlodipine and therefore cilnidipine might be expected to be superior in organ protection in addition to the . decrease in norepinephrine level by cilnidipine (absent in amlodipine) causes attenuation of platelet activation. The dual mechanisms of cilnidipine can explain the low incidence of ankle edema (as it dilates the venules and hence the pressure in the capillary bed is reduced). Although physical examinations showed leg edema in 16% of the patients. lowering plasma catecholamine levels.

thirst. While its analgesic actions have been compared to tramadol and oxycodone. Adult: 100 mg tid. Cilnidipine inhibits proliferation of vascular smooth muscle cells through inhibition of DNA/ RNA synthesis induced by growth-promoting factors released during atherosclerosis. abdominal pain. S/E . resulting in a reducted secretion of water and electrolytes in the intestinal lumen. This leads to a reduction in cAMP mucosal levels.Vomiting. is an antidiarrheal drug which acts as a peripherally acting enkephalinase inhibitor.Within 30 minutes.with or without food Onset . also known as acetorphan. its general potency is somewhere between tramadol and morphine in effectiveness. racecadotril has an antisecretory effect—it reduces the secretion of water and electrolytes into the intestine. INOTROPES Inotropes increase intracellular levels of c-AMP (class I). up to 7 days. nausea. TAPENTADOL Tapentadol (TAPAL) is a centrally acting analgesic with a dual mode of action as an agonist of the μ-opioid receptor and as a norepinephrine reuptake inhibitor. Ecadotril is s-racecadotril. vertigo and headache.anti-albuminuric effect. These enkephalins activate δ-opioid receptors in the GI tract. Racecadotril increases the availability of endogenous opioids (enkephalins) by inhibiting the membrane-bound enkephalinase. affect ion channels or pumps (class II). RACECADOTRIL Racecadotril. which reduce intestinal motility. constipation. Unlike other medications used to treat diarrhea. modulate intracellular calcium .

Desirable: < 14 mg/dL (< 35 nmol/l) Borderline risk: 14 . Vegetarians have higher levels of Lp-a than fish eaters in one homogeneous tribal population of Tanzania raising the possibility that pharmacologic amounts of fish oil supplements may be helpful to lower the levels of Lp-a. which translates into an estimated 60% decrease in the number of cardiac events and a 17% reduced risk of stroke after long-term treatment.8 mmol/l (70 mg/dl). .75 nmol/l) High risk: 31 . generally in an extended release form.50 mg/dL (75 . 1-3 grams daily.125 nmol/l) Very high risk: > 50 mg/dL (> 125 nmol/l) Currently. Aspirin may be beneficial as well. Statins Statins can lower LDL cholesterol by 1. the recommended treatment for an elevated LP(a) is niacin. They have less effect than the fibrates or niacin in reducing triglycerides and raising HDL-cholesterol. and augment contractility through multiple pathways (class IV).30 mg/dL (35 . Niacin therapy can reduce LP(a) levels by 20-30%. A recent meta-analysis suggests that atorvastatin may also lower Lp(a) levels. Some studies have shown that regular consumption of moderate amounts of alcohol leads to significant decline in plasma levels of Lp-a while other studies have not.regulation (class III). Lipoprotein(Lpa) Lp(a) : .

the risk of myopathy was suggested to be lowest with pravastatin and fluvastatin. found. at commonly prescribed doses.000 patients treated with statins other than cerivastatin. such as fluvastatin. and pravastatin.A comparison of atorvastatin. Ubiquinol is the antioxidant form of CoQ10 and plays an important role in energy production within the body as well as protecting cells against free radical damage. Some researchers have suggested hydrophilic statins. but other studies have not found a connection. Possible adverse effects include cognitive loss.44 per 10. or if standard statins (atorvastatin. . pravastatin. Statin Drugs are known to lower the levels of Ubiquinol in the the heart. are less toxic than lipophilic statins. no statistically significant differences among agents in reducing cardiovascular morbidity and mortality.4). rosuvastatin. In randomized trials. fluvastatin. two-thirds of these were myalgia or raised liver enzymes. statins increased the risk of an adverse effect by 39% compared to placebo (odds ratios 1. such as atorvastatin. lovastatin. pancreatic and hepatic dysfunction. The incidence of rhabdomyolyis was 0. lovastatin. or simvastatin) were combined with fibrate (fenofibrate or gemfibrozil) treatment. the risk was over 10fold greater if cerivastatin was used. However. probably because they are more hydrophilic and as a result have less muscle penetration. Cerivastatin was withdrawn by its manufacturer in 2001. CoQ10 supplements are sometimes used to treat statin-associated myopathy. neuropathy. and sexual dysfunction. based on their effectiveness against placebos. and simvastatin. with serious adverse effects similar to placebo. pravastatin and simvastatin.

Lovastatin induces the expression of gene atrogin-1. Studies have shown greater LDL and total cholesterol reductions in the short-acting simvastatin taken at night rather than . simvastatin. so statins with short half-lives are usually taken at night to maximize their effect. Protease inhibitors and statins taken together may raise the blood levels of statins and increase the risk for myopathy. it is a major inhibitor of only lovastatin. atorvastatin) and some other medications (flavonoids (i.e. bergamottin and dihydroxybergamottin) inhibit the cytochrome P450 enzyme CYP3A4. although the trialists warned the number needed to treat would approximate 5000. this effect was not exhibited by fibrates. with higher doses appearing to have a larger effect. This increases the levels of the statin.e. increasing the risk of dose-related adverse effects (including myopathy/rhabdomyolysis). which is believed to be responsible in promoting muscle fiber damage. Statins may slightly increase the risk of diabetes. naringin) were thought to be responsible). Consumption of grapefruit or grapefruit juice inhibits the metabolism of certain statins. including one which showed patients taking statins for over five years reduced their risk of colorectal cancer by 50%. Several case-control studies have found statins reduce cancer incidence. Most physicians have now abandoned routine monitoring of liver enzymes and creatine kinase. making statins unlikely tools for primary prevention. Cholesterol synthesis appears to occur mostly at night. Furanocoumarins in grapefruit juice (i. and to a lesser degree. Bitter oranges may have a similar effect. which is involved in the metabolism of most statins (however.

calcium hydroxide or calcium oxide with citric and malic acids in aqueous solution. . C. some calcium sources are not as pure as other sources.the morning. calcium malate. which generally includes the elderly and those on medications that decrease gastric acid secretion. In addition. CCM can be consumed with or without food. For example. The mixture is dried and grounded to reduce the particle size for easier tabletting or adding to foods and beverages.des-F(6)-quinolone The fluoroquinolones are usually active against the majority of the Gram-negative and Gram-positive pathogens of the upper and lower respiratory tract as well as the organisms associated with atypical community-acquired pneumonia (CAP) such as M. One of the problems with supplementation of the diet with calcium is that all sources of calcium are not equally soluble or bioavailable. or other biological origins contains trace amounts of lead and other minerals. Unlike other calcium sources that necessitate supplementation be used with a meal to ensure an appreciable benefit. pneumoniae. The chemistry of CCM makes it a particularly beneficial calcium source for individuals with hypochlorydia or achlorydia. calcium carbonate derived from bone meal. which is considerably more soluble than calcium citrate.The salt is prepared by the reaction of calcium carbonate. The calcium citrate malate/metastable salt represents a soluble form of calcium. Calcium citrate malate (CCM) . and in fact it protects against stone-forming poten Garenoxacin mesylate monohydrate . In addition. CCM is also recognized as a calcium source that does not increase the risk of kidney stones. oyster shell. Some calcium carbonates also contain silica. but have shown no difference in the long-acting atorvastatin. the calcium citrate malate is considerably more soluble in dilute acid solutions. or calcium carbonate.

So far only clinafloxacin and sitafloxacin appear to meet the criteria for dual target inhibition i. The major issue for garenoxacin is drug-related hypotension. some activity against organisms resistant to existing agents and/or fewer safety issues compared to marketed products. Based on the Committee for Medicinal Products for Human Use (CHMP) review of the data regarding safety and efficacy (risk/benefit). often defined as similar inhibition of DNA gyrase and Topo IV as determined by resistance mutation emergence patterns and by in-vitro enzyme inhibition.DNA gyrase and DNA topoisomerase IV (Topo IV). Nevertheless. 2006) for approval of the antibiotic Garenoxacin. the CHMP considered the application for Garenoxacin to be unapprovable. reliance on comparisons of mean values may hide significant changes in individual subjects that might occur if the interaction is at the level of renal excretion. Schering-Plough withdrew its application to the US. The European Medicines Agency (EMEA) had also been formally notified by Schering-Plough Europe (July 28 2007) of its decision to withdraw the application for a centralized marketing authorization for Garenoxacin as well.positive pathogen . (August 20. FDA. Very detailed investigations of possible risk factors identified several that included both host . A new quinolone or fluoroquinolone would not be likely to represent a major step forward unless it had some exceptional features related to its antibacterial spectrum. doubt has been cast on the in-vivo efficacy of ciprofloxacin against pneumococcal pneumonia. The 4quinolones act by inhibiting two bacterial tetrameric enzymes of the type II topoisomerase class . The applicant dismissed the observations made from the interaction study with digoxin. However. In contrast. Due to reports of pneumococcal pneumonia developing despite ciprofloxacin oral therapy.e.pneumoniae and Legionella pneumophila. there are some marked differences between compounds in their in-vitro activities against the major gram.Streptococcus pneumoniae. levofloxacin and moxifloxacin appear to be effective.

For garenoxacin patients the frequency of QTc change >60 ms on Day 1 was 1% for both genders. In addition. histamine sensitisation and some affinity of garenoxacin for β-adrenergic receptors may be involved. It was proposed that IV garenoxacin may trigger hypotensive events in some individuals probably by causing histamine release (although in healthy subjects plasma histamine was similar between garenoxacin and placebo groups).blockers were more likely to have a hypotensive event than those who did not. PK/PD considerations suggested that activity might also be dubious against some of the enterobacterial species even when quinolone-susceptible.adrenoceptors. Garenoxacin-treated subjects who received diuretics. 2% for those with hypokalaemia or on concomitant anti-arrhythmic drugs treatment. However. The applicant has proposed that histamine release. 1% for those <65 years and 2% for those ≥ 65 years. The laboratory data in patients suggest an association between raised/worsening creatinine and urea with garenoxacin. These issues merit further investigation and discussion by the . garenoxacin may have a secondary effect to decrease heart rate or prevent a reflex stimulated increase in heart rate possibly due to its affinity for β.characteristics and concomitant medications. Evidence generally pointed to cross-resistance between other quinolones and garenoxacin. for pneumococci and staphylococci with certain mutations. aeruginosa. inotropic agents or beta. nitrates. the data suggest that garenoxacin likely has a low potential to prolong the QTc interval among the quinolones. perhaps. The applicant has not conducted a study to investigate effects on the QT interval in accordance with the CHMP guidance. There may also be some association with worsening LFTs and hypoglycaemia. including P. digoxin. some anaerobic species and organisms that have reduced susceptibility to ciprofloxacin and other quinolones except. The in-vitro data suggested that garenoxacin was very unlikely to have useful clinical activity against the difficult to treat non-fermenters.

tobramycin. Common side effects are Prolongation of bleeding time. vomiting. MEROPENEM/MERONEM (1 gm vial) Meropenem is an ultra-broad-spectrum beta-lactam injectable antibiotic and belongs to the subgroup of carbapenem. cefoxitin. atracurium. Doses of 1 g may also be administered as an intravenous bolus injection (5 to 20 mL) over approximately 3-5 minutes. diarrhea. Compared to other quinolones the risk of phototoxicity seems to be low. The applicant should perform a well-designed study in diabetic persons (Types 1 and 2 diabetes) to further evaluate this matter.applicant. anaphylaxis. similar to imipenem and ertapenem. Tazobactam may interfere with birth control pills. When used empirically. Piperacillin binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall and inhibits the third and last stage of bacterial cell wall synthesis. .5G IV (Piperacillin 4g + Tazobactam 0. probenecid. Caution should be exercised in patients with history of convulsive diseses.5 g 6hrly via infusion over 30 minutes. floxacillin. chloramphenicol. Piperacillin is known to interact with arbekacin.5g) 4. combination with an aminoglycoside or antipseudomonal fluoroquinolone is recommended.aeruginosa) 8 hrly for skin and skin structure infections and 1 g 8 hrly for intra-abdominal infections. including comparisons between garenoxacin and individual comparators and by indication and dose. PIPZO/TAZAR 4. warfarin. nausea. methotrexate. thrombophlebitis.V. should be administered as infusion over 15 to 30 minutes. MERREM I. 500 mg (1g for P. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.

another kallikrein-related peptidase. PSA PSA (Prostate-specific antigen). Zinc ions have a strong inhibitory effect on the activity of PSA and on that of KLK2. where it is bacteriostatic. headache (2. injection-site inflammation (2. also known as gammaseminoprotein or kallikrein-3. although meropenem is more active against Enterobacteriaceae and less active against Gram-positive bacteria. PSA is secreted as an inactive pro-form by the epithelial cells of the prostate gland. so that PSA is totally inactive.6%). PSA is activated through the action of KLK2.4%). In the prostate.9%). Meropenem also has a reduced potential for causing seizures in comparison with imipenem. is a member of the kallikrein-related peptidase family. In fertile couples.8%). The most common adverse effects are diarrhea (4. It may be more susceptible to metallo-beta-lactamases. This condition frequently occurs in patients with hematological malignancies and cancer patients receiving anticancer drugs that cause bone marrow suppression. Several cases of severe hypokalemia have been reported. nausea and vomiting (3. the final vaginal pH . and thrombophlebitis (0. The spectrum of action includes many Gram-positive and Gram-negative bacteria (including Pseudomonas) and anaerobic bacteria.3%). Clostridium difficile associated diarrhea (CDAD) happened in 3.10ml and 20ml water is adde to 500 mg and 1 g vial respectively. Meropenem is frequently given in the treatment of febrile neutropenia. Meropenem is bactericidal except against Listeria monocytogenes. The overall spectrum is similar to that of imipenem. zinc ion concentrations are ten times higher than in other bodily fluids.9%).6% of the patients on meropenem. rash (1.

The activated PSA in the ejaculate liquefies semen in the seminal coagulum and allows sperm to swim freely. such as PSAP and CD57. Only 30 percent of patients who have high PSA level are cancer prostate positive after biopsy. The lowest level is referred to as the PSA nadir. It also dissolves cervical mucus. After radiation therapy PSA levels may continue to decrease for several years. PSA levels between 4 and 10 ng/mL are considered to be suspicious. S ome drugs—including finasteride and dutasteride. A subsequent increase in PSA levels by 2. and recent ejaculation. which are used to treat BPH—lower a man’s PSA level.0 ng/dL above the nadir is the currently accepted definition of prostate cancer "biochemical recurrence" after radiation therapy. irritation. Large doses of certain chemotherapy medications can .after coitus approaches the 6-7 levels." and treatments involve risks of complications including erectile dysfunction and incontinence. Approximately 15% of prostate cancers can occur in men with a “normal” PSA. Histological analysis to identify such cases usually uses PSA in combination with other antibodies. PSA levels can be increased by prostatitis. FDA has approved the PSA test for annual screening of prostate cancer in men of age 50 and older. noting that the test may result in “overdiagnosis” and “overtreatment” because "most prostate cancer is asymptomatic for life. BPH. c atheter tube recently placed into your bladder to drain urine. Obesity has been reported to reduce serum PSA levels. The United States Preventive Services Task Force (USPSTF. Certain drugs used to treat BPH or urinary conditions may lower PSA levels. which coincides well with reduced zinc inhibition of PSA. and is the cause of elevated blood levels of PSA. Disruption of prostatic epithelium may lead to some diffusion of the antigen into the tissue around the epithelium. allowing the entry of sperm into the uterus. 2012) does not recommend PSA screening.

3 8.5 The "normal" reference ranges for prostate-specific antigen increase with age. Age-Adjusted PSA According to the American Cancer Society.3 2. the effect is clinically insignificant.3 0.2 17. since DRE causes the most substantial increases in patients with PSA levels already elevated over 4.3 4. Individual prostate cancer cells produce less PSA than healthy cells.69 >70 Cancer No cancer Cancer No cancer Cancer No cancer Cancer No cancer 5th percentile 0.5 Men older than 70 years: PSA level less than 6.3 (ng/mL) 95th percentile 163.5 0.59 years: PSA level less than 3.69 years: PSA level less than 4. However.also lower PSA levels. the raised serum levels in prostate cancer patients is due to the greatly increased number of such cells.7 1. indicates a 25% chance of it being related to prostate cancer.2 0.4 0. A PSA level higher than 10. not their individual activity.8 . as do the usual ranges in cancer: Age(yrs) <50 50 . increases the likelihood of having prostate cancer to 50% or more.0 ng/mL.5 1. No ejaculation at least two days prior to test. Older men typically have slightly higher PSA levels than younger men. Normal ranges by age group commonly used include:     Men below age 50: PSA less than 2.2 372.5 Men 50 .0 2.5 Men 60 . Digital rectal examination (DRE) has been shown in several studies to produce an increase in PSA. a PSA level between 4 and 10.4 613.59 60 .7 253.

For instance. PSA Density .5 ng/ml for patients in their the rate of change of the PSA over a period time. (even if the rise exceeds the “safe” velocities) may not always be reason for alarm.35 ng/mL per year is cause for concern. a rise from 5 to 5. Some organizations (AUA) recommend that screening isn't necessary for men age 75 and older or those who aren't expected to live more than 10 years. The transition zone is the interior part of the prostate that surrounds the urethra. So while a rise in PSA from 1 to 1.4 ng/ml for men under the age of 50 and 6.The free PSA circulates in the bloodstream not attached to a carrier protein. Percentage of Free PSA (PSA-f) . the more likely the patient is to have prostate cancer. The higher the PSA density.5 may not. The higher the percentage of free PSA. a free PSA of 0-10% is associated with a 56% chance of cancer while a free PSA greater than 25% is only associated with an 8% risk of cancer.5 may be a cause for concern.75 ng/ml. PSA Velocity . Some groups recommend earlier discussions for men in high-risk groups — those with a family history of prostate cancer and African Americans and Asian Americans. returning slowly to baseline levels within 24 hours. Both total (free plus bound) and free PSA increase immediately after the PSA divided by the volume of the transition zone of the prostate. This test is primarily used for men with a PSA level in the . The American Urological Association (AUA) recommends that men consider getting a baseline prostate cancer screening. Patients with a PSA of 4-10 have reasons for concern when the PSA velocity is greater than 0. including a PSA test and DRE. An isolated rise of the PSA. a velocity of greater than 0.Accepted age-adjusted PSA rates are below 2. For patients whose PSA is less than 2. Three successive PSA determinations over an 18month period represents a meaningful velocity. the lower the risk of cancer. beginning at age 40.

PANTOPRAZOLE An analysis of research into the side-effects of proton pump inhibitors (PPI) has found between half and two-thirds of such prescriptions are 'inappropriate.borderline range between 4 and 10. the reliability of the test has improved. PPIs might affect the body’s absorption of calcium. RABIPRAZOLE. S-OMEPRSZOLE. which in turn could lead to osteoporosis and fractures. With the introduction of the ratio of free to total PSA. Researchers found a link between long-term use of PPIs and hip fractures. Risk of prostate cancer in two age groups based on Free PSA as % of Total PSA OMEPRAZOLE. By lowering stomach acid levels. PPIs may also affect vitamin B12 levels because the body can’t absorb the vitamin without stomach acid to uncouple the vitamin .

The fact that stomach acid is sometimes coming up in your mouth suggests to me that the ra is causing what we call “rebound acid hypersecretion. The reduction of vitamin B12 may also increase bone fragility by raising homocysteine. With the change in pH in your stomach. Methotrexate cannot be used by people: With blood disorders or severe anemia. The PPI actually lowers the acidity of the stomach so much that the C. One of the most serious side effects of proton pump inhibitors (PPI) is C. It may also be given as a shot once a week. It is also used to treat psoriatic arthritis and taken orally once a week or in 3 divided doses taken at 12-hour intervals during a 24-hour period (for instance.m. and then again at 8 a. acid-sensitive drugs and nutrients like iron and calcium can just pass through your system unabsorbed. With stomach ulcers.).. METHOTREXATE Methotrexate slows the rapid growth of skin cells in psoriasis. at 8 p. and phototherapy have not worked or cannot be used.from protein in food.m. Food and Drug Administration recently issued a safety alert about these drugs and diarrhea that doesn’t go away.” That’s where your stomach starts secreting everincreasing amounts of acid to compensate for the drug’s action to slow it down. . taken at 8 a. tar products. Methotrexate is used to treat severe psoriasis (more than 20% of the skin is affected) when creams. ointments. The PPI also may be causing your anemia.m.. difficile diarrhea. difficile bacteria — normally kept at bay by the acid in your stomach — proliferate out of control.

as well as being an antipsychotic. heartburn. relatively cardioselective. nebivolol. At a dosage of 25mg three times daily. metoprolol.With liver or kidney diseases. therefore. the correct drug name is Levosulpiride and it has several medical uses. fatigue. have less effect on the β2 (bronchial) receptors and are. IBS. Who cannot return to the doctor for tests to check for side effects of the medicine. LEVOSULPRIDE Levosulpride is actually just a misspelling. With an infectious disease. . but they are not cardiospecific. loss of appetite. conferring this drug with a cholinergic effect. Common temporary side effects include: Nausea. levosulpiride accelerates gastric and gallbladder emptying. BISOPROLOL Bisoprolol is a selective type β1 adrenergic receptor blocker. gastritis and GERD. Who drink alcohol frequently. such as tuberculosis. so it enhances gastrointestinal motility and can treat problems such as bloating. and (to a lesser extent) acebutolol. It acts as a prokinetic agent. Bisoprolol. Levosulpiride is a sulpiride isomer that exerts its prokinetic action through a dual mechanism: 1) as a D(2) dopamine receptor antagonist and 2) as a serotonin 5HT(4) receptor agonist. They have a lesser effect on airways resistance but are not free of this side effect.

is not approved by Health Canada nor by the USA’s FDA). Erythromycin. * It may cause dizziness or drowsiness. has numerous documented cases of sudden death due to cardiac toxicity. These side effects included severe diarrhea needing IV . Novartis received approval to market tegaserod to women with irritable bowel syndrome.Neuroleptic malignant syndrome. like cisapride.Absence of menstrual period.and magnesiumcontaining antacids. Avoid alcohol. breast enlargement in male.Reduced bioavailability with sucralfate. aluminium. and changes in libido. Attempts were made to bring itopride to the North American market by Axcan Pharma but failed to progress beyond a Phase III trial. the FDA issued a warning related to reports of severe side effects associated with tegaserod. which in some cases led to deaths. The "risk of this occurrence is greatly increased when erythromycin is taken with other drugs that also have a propensity for cardiac toxicity. and intestinal obstruction. Potentially Fatal . Cisapride was voluntarily pulled from the market by Janssen Pharmaceutica in July 2000 (in the United States) due to the risk of rare but serious cardiac events. when used at antibiotic dosage levels. In July. Contraindicated in patients with gastrointestinal bleeding. spontaneous milk secretion. do not drive a car or operate machinery while taking this medication. In April 2004. 2002. (Note: Levosulpiride. Side Effects : Genitourinary . Effect on GI motility may be antagonised by anticholinergic agents. narcotics and analgesics.

has been reported to the FDA. arms. These animal studies are part of the data that must be prepared for regulatory premarket submissions. hand. a central nervous system side effect resulting in possibly irreversible involuntary muscle movement of the face. increased risk of angina. a syndrome trigged by an imbalance to the autonomic nervous system. It can cause ambulatory disability. people over 65 years of age. Immediate discontinuation of the medication can resolve the symptoms.fluid replacement. legs. Prucalopride (Resolor®) is now available and on the market in the UK and EU countires for the treatment of chronic constipation. and/or those who have taken high dosages of the drug. . or in other parts during your treatment or for up to several months afterward. and strokes. By March 2007. those who have used the offending drug long term. Metoclopramide possesses the greatest risk for tardive dyskinesia (TD). trunk or hands. A mortality rate of 10% occurs with this syndrome. the back of ankle. which causes blood pressure instability. low blood pressure with episodes of passing out. The results of an FDA re-analysis of clinical trial data on tegaserod showed a slight. but definite. MOXIFLOXACIN Moxifloxacin increases the risk of developing tendinitis or a tendon rupture in shoulder. Those at greatest risk for TD are women. which have shown up in the obligatory chronic (long-term) studies conducted in animals. Metoclopramide-induced neuroleptic malignant syndrome. and ischemic colitis. heart attacks. the FDA asked Novartis to stop marketing tegaserod. fever and a stuporous-like state. The risk is highest in people over 60 years of age. It is doubtful it will come to the North American market due to reports of carcinogenic problems.

1-6 years: 20mg. 8 hourly. Paracetamol 500mg). SOS. DROTIN PLUS (Drotaverine HCI 80mg. It reduces the incidence of traumatic postpartum haemorrhage by reducing the incidence of cervical tear. more effective when given in more dilated cervix than with less dilatation and more effective in multigravida than in primigravida. 6-12 years: 40mg. but the results have been conflicting. 8 hourly. A study at the R. There was no interference with uterine contractility and no increase in operative delivery. and has no anticholinergic effects. Kar Medical College and Hospital concluded that drotaverine is highly effective in reducing the duration of active phase of labour by hastening cervical dilatation. Together with rimantadine it is used as a treatment for influenza. Irritable bowel syndrome patients presenting with predominant diarrhea are more likely to benefit from Buscopan. Accelerates labor by speeding up cervical dilation. didanosine. SOS. Drotaverine DROTIN 40mg/DROTIN-DS 80mg. G. Drotaverine is a selective inhibitor of phosphodiesterase4. sucralfate. or vitamin supplements that contain iron or zinc. It is a safe drug for the mother as well as for the baby. Mefenamic acid 250mg) 40-80 mg Tab 3 times/day. Tamsulosin . DROTIN-M (Drotaverine HCI 80mg.Moxifloxacin should be taken at least 4 hours before or at least 8 hours after any of these medications: antacids containing magnesium or aluminum.

kidney stones through urination. Tamsulosin may also be used to help your body "pass. Its muscle relaxant properties may be due to a direct action on the smooth muscle rather than by antagonizing muscarinic receptors. urethritis. nocturia. Tamsulosin contains a sulfa moiety. Contiflo XL. Flomaxtra. urgency. Flavoxate Flavoxate (Urispas) is an anticholinergic with antimuscarinic effects. frequency and incontinence in cystitis. Women should not take tamsulosin. Urimax and Pradif. It has also been used to help treat bladder problems in women." or get rid of. dysuria. Capsule is usually taken once a day 30 minutes after the same meal. prostatitis. suprapubic pain.Tamsulosin is an α1a-selective alpha blocker in the prostate versus the α1B receptor in the blood vessels. Treatment with the combination of dutasteride and tamsulosin provides greater symptom benefits compared to monotherapy with either agent alone for treatment of benign prostatic hyperplasia.Prone to a complication known as floppy iris syndrome during cataract surgery. Tamsulosin is used in the symptomatic treatment of benign prostatic hyperplasia (BPH). Tamsulosin hydrochloride extended-release capsules are marketed under the trade names Flomax. It can cause males to experience retrograde ejaculation. .urethrocystitis/urethrotrigonitis. Flavoxate is indicated in interstitial cystitis. thus causing typical reactions to sulfa drugs.

. Aspirin Low-dose.g. It has higher intrinsic anticoagulant potency than warfarin. the plasma concentrations of acenocoumarol are substantially lower than those for warfarin in patients receiving longterm treatment. So. achalasia. heart failure). long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. Contraindicated in pyloric or duodenal obstruction. Nicoumaline Nicoumaline is an international brand name for Warfarin Half-life: Acenocoumarol: 8 to 11 hour Warfarin: 6 to 12 hour Acenocoumarol is a short-lived oral anti-coagulant.Can potentially cause.and increased sensitivity of your eyes to light.glaucoma. fast/irregular heartbeat. dry mouth or throat. gastrointestinal hemorrhage and obstructive uropathies of the lower urinary tract. obstructive intestinal lesions or ileus. upset stomach. eye pain. functions by inhibiting vitamin K epoxide reductase.It is best to take these tablets after meals. vomiting. heart problems (e. .200 mgTablet is taken three or four times a day with or without food. blurred vision. producing an inhibitory effect on platelet aggregation. which. like warfarin. The clearance of acenocoumarol is ~20-fold faster than that for warfarin.

prasugrel or ticagrelor) for at least 12 months while EU guidelines recommend DAPT for 6–12 months after drug eluting stent. The recovery of adults with the syndrome is generally complete.a rare but severe illness characterized by acute encephalopathy and fatty liver.aspirin combined with an ADP receptor inhibitor. such as clopidogrel.can occur when children or adolescents are given aspirin for a fever or other illnesses or infections. (jaundice is not usually present) . with liver and brain function returning to normal within two weeks of onset. However. US guidelines recommend dual anti-platelet therapy (DAPT .WHO study said regular low dose (75 or 81 mg) aspirin female users had a 25% lower risk of death from cardiovascular disease and a 14% lower risk of death from any cause. In children. as opposed to the antipyretic action of aspirin seen with lower doses. Some authors have suggested testing regimes to identify those patients who are resistant to aspirin or other anti-thrombotic drugs (such as clopidogrel). It has also been established that low doses of aspirin may be given immediately after a heart attack to reduce the risk of another heart attack or of the death of cardiac tissue. with rash. mild to severe permanent brain damage is possible. Multiple meta-analyses and reviews have concluded that regular use of aspirin reduces colorectal cancer (CRC). they agree that aspirin be continued indefinitely after DAPT is complete. When high doses of aspirin are given. it may actually cause fever. however. owing to the heat released from the electron transport chain (aspirin buffers and transports the protons). Documented cases of Reye’s syndrome in adults are rare. vomiting. especially in . Reye's syndrome .

Cannabis The terms cannabis or marijuana generally refer to the dried flowers and subtending leaves and stems of the female cannabis plant. Even if none of these conditions is present. manufacturers recommend people with peptic ulcers. a metabolite of aspirin. unless it is on the advice of a doctor. or simply hash) is a concentrated resin produced from the flowers of the female cannabis plant. US FDA now recommends aspirin (or aspirin-containing products) should not be given to anyone under the age of 12 who has a fever. This is the most widely consumed form. . the risk of stomach bleeding is still increased when aspirin is taken with alcohol or warfarin. have been proposed to cause tinnitus. Quitting cannabis did not appear to reverse the loss. Hash can often be more potent than marijuana and can be smokedor chewed. It varies in color from black to golden brown depending upon purity. attention and memory. hashisha. mild diabetes. dependent use of marijuana before age 18 show lasting harm to a person's intelligence.infants. Hashish (also spelled hasheesh. and the British Medicines and Healthcare products Regulatory Agency recommends children who are under 16 years of age should not take aspirin. The persistent. Over thirty percent of the cases reported in the United States from 1981 through 1997 resulted in fatality. or gastritis seek medical advice before using aspirin. containing 3% to 22% Tetrahydrocannabinol (THC). Large doses of salicylate. Owing to its effect on the stomach lining.

The high lipid-solubility of cannabinoids results in their persisting in the body for long periods of time. Even after a single administration of THC, detectable levels of THC can be found in the body for weeks or longer . CB1 receptor is found primarily in the brain as well as in some peripheral tissues, and the CB2 receptor is found primarily in peripheral tissues, but is also expressed in neuroglial cells as well. Via CB1 activation, THC indirectly increases dopamine release and produces psychotropic effects. Cannabidiolalso acts as an allosteric modulator of the mu and delta opioid receptors. THC also potentiates the effects of the glycine receptors. The role of these interactions in the "marijuana high" remains elusive. While commentators have warned that greater cannabis "strength" could represent a health risk, others have noted that users readily learn to compensate by reducing their dosage, thus benefiting from reductions in smoking side-hazards such as heat shock or carbon monoxide. L- Carnitine There is no evidence that L- Carnitine as an ingredient in weight loss supplements is more effective than other ingredients. There has not been enough large scale clinical trials undertaken to back up the claims made for L-Carnitine by some manufacturers of weight loss products. L-Carnitine is found in red meat and dairy products, you do not necessarily need to buy supplements. There is no evidence that L-Carnitine as a standalone supplement procures superior results in achieving weight loss than other stand alone supplements available for sale.

Tamsulosin Tamsulosin is a selective a1 receptor antagonist that has preferential selectivity for the a1A receptor in the prostate versus the a1 B receptor in the blood vessels. When alpha 1 receptors in the bladder neck and the prostate are blocked, this causes a relaxation in smooth muscle and therefore less resistance to urinary flow. Due to this the pain associated with BPH can be reduced. Normally, the sphincter of the bladder contracts and the ejaculate goes to the urethra, the area of least pressure. In retrograde ejaculation, this sphincter does not function properly. Calcium and vitD

Vitamin D3

activated 7-dehydrocholesterol

Cholecalciferol is calciol, an inactive, unhydroxylated form of vitamin D3.

It is structurally similar to steroids such as testosterone, cholesterol, and cortisol (though vitamin D3 itself is a secosteroid). Forms Vitamin D3 has several forms:  Cholecalciferol, (sometimes called calciol) is an inactive, unhydroxylated form of vitamin D3). It is either synthesized in the skin from the precursor hormone 7-dehydrocholesterol, or acquired through diet or supplements. It is then hydroxylated in the kidneys or by the macrophages in your immune system to form calcitriol.  Calcifediol (also called calcidiol, hydroxycholecalciferol, 25hydroxyvitamin D3, etc. and abbreviated 25(OH)D is one of the forms measured in the blood to assess vitamin D status; blood levels of this molecule largely reflect the amount of vitamin D3 produced in the skin or the vitamin D2 or D3 ingested.  Calcitriol (also called 1,25-dihydroxyvitamin D3) is the active form of D3. Cholecalciferol is the only one that is ingested either through food, supplements or by way of sun absorption. Metabolism 7-dehydrocholesterol, precursor of vitamin D3, undergoes an electrocyclic reaction in the epidermis as a result of UVB radiation, resulting in the opening of the vitamin precursor B-ring through a conrotatory pathway. Following this, the previtamin D3 undergoes a antarafacial sigmatropic rearrangement and therein finally isomerizes to form vitamin D3. It reaches an equilibrium after several minutes depending on several factors including conditions of sunlight (latitude, season, cloud cover, altitude), age of skin, and color of skin.

. These are removed by various techniques. Calcitriol is the most active hormone form of vitamin D3. Some unwanted isomers are formed during irradiation. cholesterol is extracted from wool grease and wool wax alcohols obtained from the cleaning of wool after shearing.Cholecalciferol is then hydroxylated in the endoplasmic reticulum of hepatocytes by 25-hydroxylase to become calcifediol (25hydroxyvitamin D3). This hydroxylation is loosely regulated. The 7-dehydrocholesterol is then irradiated with ultra violet light. The cholesterol undergoes a four step process to make 7-dehydrocholesterol. calcitriol.000 International Units per gram. Industrial production Cholecalciferol is produced industrially for use in vitamin supplements and to fortify foods by the ultraviolet irradiation of 7dehydrocholesterol extracted from lanolin found in sheep's wool.000 to 30.000. if at all. Calcifediol is again hydroxylated in the kidney by 1-alphahydroxylase and becomes calcitriol (1.25-dihydroxyvitamin D3). This hydroxylation is tightly regulated (stimulated by either parathyroid hormone or hypophosphatemia) and serves as the major control point in production of the most active circulating form. leaving a resin which melts at about room temperature and usually has a potency of 25. Paraphrasing a more detailed explanation. the same compound that is stored in the skin of animals.000.

000 IU daily. (Recommendations in Europe: 5µg/d. 20 µg/d (800 IU/d) is recommended.In foods where animal products are not desired.000 IU. in France: 25 µg).025 µg.000 IU.000-IU figure is more of an estimate than a number based on evidence of toxicity above 4. female. Recommendations vary depending on the country. pregnant/lactating women) under the age of 70 yrs-old. particularly for individuals deprived of regular sun exposure or those at higher risk such as those with higher melanin content in the skin (i. A growing body of researchers question whether the current recommended adequate levels are sufficient to meet physiological needs. The 4.000. and those who live far from the equator. Latin American.000-IU cut-off was determined by the Institute of Medicine in 2010 after reviewing the then-current medical literature. or Asian).e.000 IU after more than 7 years of daily intake. Middle Eastern. For all individuals older than 70 years. The Institute of Medicine did not find evidence of toxicity between 4. and that there was a single case of toxicity above 10..000 IU and 10. Patients . the obese. those whose ancestors are African. this case of toxicity occurred under circumstances that have led other researchers to dispute it as a credible case to consider when making vitamin D intake recommendations.000 (40x106)IU. finding that the dose for lowest observed adverse effect level is 40. The upper limit (UL) for vitamin D has been recommended as 4. an alternative compound is ergocalciferol (also known as vitamin D2) derived from the fungal sterol ergosterol. In the they are: 15 µg/d (600 IU per day) for all individuals (males. Dose One gram is 40. equivalently 1 IU is 0.. so the 4.000 IU daily for at least 12 weeks.

Chronic hypercalcemia may lead to serious or even life-threatening complications. somnolence. particularly affecting the kidneys. its magnitude can be calculated based on the actual serum 25-hydroxy-vitamin D level and body weight.0 ng/ml. orhistoplasmosis. metallic taste. and metastatic calcifications may occur. or in two to four divided doses. and may lead to hypercalcemia and excess bone loss. however. weakness. vertigo. with some studies suggesting less efficacy of D2.5 mg). headache. dry mouth. and ataxia . and anorexia (appetite/weight loss). Individuals at particular risk include those with hyperparathyroidism. followed by polyuria n). sarcoidosis. Also. There are conflicting reports concerning the absorption of cholecalciferol (D3) versus ergocalciferol (D2). in a single dose.000 IU (7.0 to 74. kidney disease. The normal range of calcifediol is 30.500 µg) to 500. fatigue. there is a therapy for rickets utilizing a single dose. there also exists a hypothesis that dis-advises supplementing vitamin D if not really necessary: Vitamin D might support the emergence of allergies and adulterate already existing allergies and autoimmune diseases. and should be managed by a physician. However. called stoss therapy in Europe.000 IU (12. tuberculosis. At . vomiting. taking from 300.with severe vitamin D deficiency will require treatment with a loading dose. and others showing no difference. Treatment involves stopping the intake of vitamin D or calcium. Vitamin D toxicity can result from regular excess intake. Early symptoms of hypercalcemia may include nausea. The 25-hydroxy vitamin D (calcifediol) blood test is used to determine how much vitamin D is in the body. tinnitus . Acidification of urine and corticosteroids may be necessary. polydipsia . that is merely an unproven hypothesis.500 µg = 12. Kidney function may become impaired.

However. In humans. Interactive pathway map . and cholecalciferol has been used in poison bait for the control of these pests. break down to form sura-sterols. with 400 IU daily. in practice it has been found that use of cholecalciferol in rodenticides represents a significant hazard to other animals. Stability Cholecalciferol is very sensitive to UV radiation and will rapidly. but reversibly.present. D2 and D3 doses are frequently considered interchangeable. such as dogs and cats. and cholecalciferol has been used as the active ingredient in lethal gel baits and cereal pellet baits "DECAL" for possum control. In New Zealand. Toxicity Rodents are somewhat more susceptible to high doses than other species. possums have become a significant pest animal. which can further irreversibly convert to ergosterol. Preventative application A 2008 study published in Cancer Research has shown the addition of vitamin D3 (along with calcium) to the diet of some mice fed a regimen similar in nutritional content to a new Western diet with 1000 IU cholecaliferol per day prevented colon cancer development. but more research is needed to clarify this. there was no effect. It has been claimed that the compound is less toxic to non-target species.

Vitamin D Synthesis Pathway Vitamin D is not a true vitamin.25-dihydroxycholecalciferol. D3 or D2. including egg yolk. . it must be metabolized within the body to the hormonally-active form known as 1. Rather. There are also dietary sources of vitamin D. because individuals with adequate exposure to sunlight do not require dietary supplementation. fish oil and a number of plants. The plant form of vitamin D is called vitamin D2 or ergosterol. does not have significant biological activity. However. natural diets typically do not contain adequate quantities of vitamin D.


the effect is to activate transcription. pigs. horses. The major inducer of 1-alpha-hydroxylase is parathyroid hormone. it is also induced by low blood levels of phosphate. In contrast. and blood levels of this molecule largely reflect the amount of amount of vitamin D produced in the skin or ingested. Hepatic synthesis of 25-hydroxycholecalciferol is only loosely regulated. In most cases studied. The vitamin D receptor binds several forms of cholecalciferol. while that of 1.25-dihydroxycholecalciferol is only a few hours. which explains their relative biological potencies. Like the receptors for other steroid hormones and thyroid hormones. cattle and sheep contain adequate quantities of 7dehydrocholesterol . It turns out that vitamin D receptors are present in most if not all cells in the body. In contrast. Its affinity for 1. Its most dramatic effect is to facilitate intestinal absorption of calcium. the skin of dogs and cats constains significantly lower quantities of 7-dehydrocholesterol. the activity of 1-alpha-hydroxylase in the kidney is tightly regulated and serves as the major control point in production of the active hormone. The skin of humans. but situations are also known in which vitamin D suppresses transcription. experiments using cultured cells have demonstrated that vitamin D has potent effects on the growth and differentiation of many types of cells. As a transcriptional regulator of bone matrix proteins. an intracellular protein that ferries calcium across the intestinal epithelial cell. The best-studied of these calcium transporters is calbindin. it induces the expression of osteocalcin and suppresses synthesis of type I collagen.The halflife of 25-hydroxycholecalciferol is several weeks. the vitamin D receptor has hormone-binding and DNA-binding domains.25-dihydroxycholecalciferol is roughly 1000 times that for 25-hydroxycholecalciferol. rats. although it also stimulates absorption of phosphate and magnesium ions. . Additionally.

You will also be more susceptible to stress-related syndromes like anxiety. Low vitamin D levels also cause continuous blood vessel constriction. Studies have proved the efficacy of this vitamin in reducing flu rates. and vitamin D deficiency is thereby averted by dietary intake. However. Multiple Sclerosis and HIV are examples of diseases. and provides a much-needed boost for the immune system. It also helps to improve the overall health of the skin. the symptoms of which and the disease progression are more severe in Vitamin D Deficient individuals. deficiency of this vitamin can cause tumor growth and increase your risk of breast. especially those with SPF ratings greater than 8.Sunscreens. I would like your thoughts on whether taking vitamin D3 cholecalciferol is okay for someone who is allergic to wool. ovarian. Higher level of circulating cholecalciferol strengthens your body’s defense against pathogen invasions. infection and cell mutation. hair and nails. schizophrenia and insomnia. growth and deaths. Vitamin D3 Deficiency has been linked to an increases susceptibility to developing roughly 2-1/2 dozen diseases and illness including everything from Cancer to Osteoporosis to Rickets to Parkinson's Disease. Since cholecalciferol also regulates cell proliferation. Fibromyalgia. people that use such sunscreens religiously live in industrial countries where many foods are supplemented with vitamin D. which increase your blood pressure and raise your risks of cardiovascular diseases and migraines. effectively block synthesis of vitamin D in the skin. D3 has been shown to help alleviate symptoms of depression and chronic fatigue.Cholecalciferol sufficiency is also important to prevent inflammation (this is true of arthritis sufferers as well as other forms of chronic pain). colon and pancreatic cancers. .

can decrease the absorption of vitamin D. 90 mg in ½ cup of vanilla ice cream and 300 mg in 8 ounces of calcium-fortified orange juice. and postmenopausal women also taking estrogen 1. mineral oil ( orlistat). 450 mg in 8 ounces of plain yogurt. chew the medication thoroughly before swallowing. Take your doses of these medications as far as possible from your doses of vitamin D (at least 2 hours apart. Vitamin D is best absorbed when taken after a meal but may be taken with or without food. 200 mg in 1 ounce of cheddar cheese.200 mg-1. with or without osteoporosis: 800 mg/day for children 1-10yrs of age 1. The following calcium intake has been recommended by the National Institutes of Health Consensus Conference on Osteoporosis for all people. premenopausal women.500 mg/day for pregnant and nursing mothers (breast milk usually has low levels of vitamin D) The total daily intake of calcium should not exceed 2. Certain medications (bile acid sequestrants such as cholestyramine/colestipol. . longer if possible). the average American diet contains approximately 250 mg of calcium. Alfacalcidol is usually taken with food.500 mg/day for postmenopausal women not taking estrogen 1. There is approximately 300 mg of calcium in an 8-ounce glass of milk.000 mg.Daily calcium intake can be calculated by the following method: Excluding dairy products.200 mg/day for teenagers and young adults 11-24yrs of age 1. If you are taking the chewable tablet. 130 mg in 1 cup of cottage cheese.000 mg/day for men.

it is important to review vitamin D content in dietary supplements before taking additional vitamin D. and children 400 IU/d for infants under 12 months But if a person already has osteoporosis. vitamin D can be obtained in combination with calcium in tablet forms. The calcium carbonate supplements are best taken in small divided doses with meals since the intestines may not be able to reliably absorb more than 500 mg of calcium all at once. Certain medications such as PPI can interfere with the absorption of calcium carbonate. Alternatively. Since various dietary supplements may also contain vitamin D. it is advisable to ensure 400 IU twice per day as the usual daily intake. Therefore. such as Caltrate 600 + D (600 mg of calcium and 200 IU of vitamin D) and others. men. Many "natural" calcium carbonate preparations. most commonly as a supplement alongside prescribed medications for osteoporosis. . may contain high levels of lead or other harmful elements and should be avoided.The Food and Nutrition Board of the Institute of Medicine has recommended the following as an adequate vitamin D intake: 800 IU/d for men and women over the age of 71 600 IU/d for women in other age groups. such as oyster shells or bone meal. one to two multivitamins a day should provide the recommended amount of vitamin D. An average multivitamin tablet contains 400 IU of vitamin D.

Alendronate (Fosamax). calcium. vitamins with minerals.So far. thereby resulting in loss of effectiveness. Food. and with at least 8 ounces (240 ml) of water (not juice). This improves the absorption of the biphosphonate. Patients should also remain upright for at least 30 minutes after taking the pill to avoid reflux of the pill into the esophagus. or aluminum can reduce the absorption of oral bisphosphonates. a regimen with risk of bone marrow suppression. Mycophenolate Mycophenolate is being increasingly utilized as a steroid sparing treatment in immune-mediated disorders including immunoglobulin A nephropathy. again in terms of response and side-effects. 30 minutes before breakfast. Also. small vessel vasculitides. oral bisphosphonates should be taken with plain water only in the morning before breakfast. no food or drink should be taken for at least 30 minutes afterward. iron supplements. bisphosphonates are the most well studied and effective category of prescription medication for treating postmenopausal osteoporosis. or zoledronate (Reclast) should be taken in the morning. or antacids containing calcium. where it can cause ulceration and scarring. magnesium. even propose that . on an empty stomach. Therefore. risedronate (Actonel). ibandronate (Boniva). Newer intravenous bisphosphonates. Its increasing application in treating lupus nephritis has demonstrated more frequent complete response and less frequent complications compared to cyclophosphamide bolus therapy. infertility. such as ibandronate (Boniva) and zoledronate (Reclast). and malignancy. bypass the potential esophagus and stomach problems. Taking the pill sitting or standing (as well as drinking adequate amounts of liquids) minimizes the chances of the pill being lodged in the esophagus. Walsh et al. and psoriasis. Further work addressing maintenance therapy demonstrated mycophenolate superior to cyclophosphamide.

and/or invasive cytomegalovirus (CMV) infection. fatigue. Infrequent adverse effects (0. Dual COX inhibitors act non-selectively on these two important human enzymes – COX-1 – known as the housekeeping enzyme. . systemic lupus erythematosus (SLE). headache. gastritis.1–1% of patients) include esophagitis.known as the inflammatory enzyme.More Potent Than Aspirin and Ibuprofen Lornoxicam is a member of the oxicam family of NSAIDs and has been described as a highly potent balanced dual inhibitor of the human cyclooxygenase (COX) -1 and COX-2 enzymes. In long-term immunosuppression. infections. it may be used to avoid calcineurin inhibitors or steroids.mycophenolate should be considered as a first-line induction therapy for treatment of lupus nephritis in patients without renal dysfunction. leukopenia. and COX-2 -. Mycophenolate mofetil is beginning to be used in the management of auto-immune disorders such as idiopathic thrombocytopenic purpura (ITP). and pemphigus vulgaris (PV) with success for some patients. nausea. and/or cough. Recently. fewer opportunistic infections and lower incidence of acute rejection. vomiting. Compared with azathioprine it is more lymphocyte-specific and is associated with less bone marrow suppression. Common adverse drug reactions (≥1% of patients) associated with mycophenolate therapy include diarrhea.and/or anemia. Lornoxicam Lornoxicam – A Dual Inhibitor of COX Enzymes -. gastrointestinal tract hemorrhage. suggesting that mycophenolate will be encountered more frequently in medical practice. drugs that cause highly selective and unbalanced inhibition of the COX-2 enzyme are believed responsible for excess numbers of cardiovascular events in patients using these highly-selective COX-2 inhibitor drugs.

Lornoxicam-QR and lornoxicam-IM did not differ with respect to AUC∞.d. People taking this medicine for longer than three months should have regular blood tests to monitor their blood count. People with liver diseases should have their liver function monitored regularly while taking this medicine. In laboratory tests. obese people. Cmax and tmax.Lornoxicam administered as a quick-release formulation was shown to be non-inferior to the equivalent formulation of diclofenac potassium in terms of onset of pain relief and more effective on most of the major standard efficacy outcomes. lornoxicam has been shown to be up to 3000 times more potent than aspirin in tests measuring inhibition of COX enzymes and is up to 400 times more potent than ibuprofen in these assays. in the stomach/duodenal bulb. .d. Lornoxicam 8 mg b. The drugs were equally well tolerated. but both lornoxicam-QR and lornoxicam-IM showed significantly shorter tmax and significantly higher Cmax values than lornoxicam-ST. caused significantly less mucosal injury than naproxen 500 mg b. high blood pressure or heart failure. kidney and liver functions. The analgesic and anti-inflammatory effects of lornoxicam are significantly superior to those of rofecoxib without inferiority in tolerability. those with impaired kidney function. those with stressed kidney function as a result of significant blood loss or severe dehydration and those who are to undergo major surgery. as well as in the mid/distal duodenum. Warning! Kidney function should be monitored in the following groups of people while taking this medicine: those over 65 years of age.

is a theophylline derivative which has shown interesting bronchodilating activity in patients responsive to the inhaled β2-agonist salbutamol. In the colon. Alpha glucosidase inhibitors Alpha-glucosidase inhibitors are competitive inhibitors of the digestive enzymes. They must be taken at the start of main meals (taken with first bite of meal) to have maximal effect. causing flatulence (78% of patients) and diarrhea (14% of patients). One . The culinary mushroom Maitake (Grifola frondosa) lowers blood sugar because the mushroom naturally contains an alpha glucosidase inhibitor. They may also be useful in patients with diabetes mellitus type 1. Another plant attracting a lot of attention is Salacia oblonga. Since Alpha-glucosidase inhibitors prevent the degradation of complex carbohydrates into glucose. This medicine should be taken before meals. Their effects on blood sugar levels following meals will depend on the amount of complex carbohydrates in the meal. and it appears to determine few adverse effects. this use has not been officially approved by the FDA. Doxophylline Doxophylline. however. some carbohydrate will remain in the intestine and be delivered to the colon. bacteria digest the complex carbohydrates.3-dioxolane.Elderly people over 65 years of age should have their kidney and liver function monitored regularly while taking this medicine. It is advised to start with a low dose and gradually increase the dose to the desired amount. or 2-(7'-theophyllinemethyl)1. People who are obese or who have high blood pressure should have their blood pressure monitored regularly while taking this medicine.

. liver enzymes should be checked before and during use of this medicine.I. Pneumatosis cystoides intestinalis is another reported side effect. safe and well tolerated in a large cohort of Asian patients with type 2 diabetes. Adults may take doses of 25 mg 3 times daily. Acarbose is significantly more effective in patients eating a relatively high carbohydrate Eastern diet. and disaccharides to glucose and other monosaccharides and ii) pancreatic alpha-amylase which hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Hepatitis has been reported with acarbose use. Since the drug will prevent the digestion of polysaccharides (or non-monosaccharides). non-monosaccharide foods may not effectively reverse a hypoglycemic episode in a patient taking an alpha-glucosidase inhibitor. of which voglibose is the newest. It is PPHG. It usually goes away when the medicine is stopped. Therefore. A recent large study concludes "acarbose is effective. increasing to 100 mg 3 times a day. not FPG. acarbose (Glucobay). trisaccharides. miglitol and voglibose (Voglib). Voglibose scores over both acarbose and miglitol in terms of side effect profile. and inhibits i) alpha glucosidase enzymes in the brush border of the small intestines. even on constant found that G. But acarbose has an edge over voglibose in terms of efficacy. side effects decreased significantly (from 50% to 15%) over 24 weeks. Alpha glucosidase inhibitors delay glucose absorption at the intestine level and thereby prevent sudden surge of glucose after a meal. they hydrolyze oligosaccharides. It is a starch blocker. Postprandial hyperglycemia (PPHG) is primarily due to first phase insulin secretion. which is the marker of cardiovascular disorders associated with diabetes. There are three drugs which belong to this class.

Deficiencies of arginine are rare. fish. preeclampsia. It's abundant in red meat. Arginine may help improve blood flow in the coronary arteries. They could interact with birth control medicines. A 2006 study showed that arginine was not helpful -. and chocolate. buckwheat. In the body. or L-arginine 1000 mg Tablets/capsules (20Rs/Tablet) Arginine is mostly present in protanines and histones. almonds. cereals. is involved in wound healing. certain heart medications and drugs such as Viagra. poultry. cashews. Miglitol is fairly well absorbed by the body.and may have been harmful -. hazelnuts. Arginine. Possible side effects include abdominal pain and bloating. whereas miglitol resembles a monosaccharide. however. gout and worsen asthma.for treating heart attacks in combination with standard treatment. Moreover. oats. It may also help migraines. Arginine does not seem to help with heart attack recovery. maintaining immune and hormone function. . and your body can also make it. hormone therapy drugs. or exercise tolerance in people with heart failure. a powerful neurotransmitter that helps blood vessels relax and also improves circulation. the amino acid arginine changes into NO. intermittent claudication and erectile dysfunction (but mostly when combined with other supplements such as yohimbine) and combats the symptoms of wasting caused by HIV. brown rice. L-arginine. and Brazil nuts). it is not metabolized and is excreted by the kidneys. grains. Arginine may interact with certain medications that lower blood pressure. helping the kidneys remove waste products from the body. acarbose inhibits pancreatic alpha-amylase in addition to alpha-glucosidase. changes to glucose and blood chemical levels. two proteins commonly associated with nucleic acids (like DNA and RNA). dairy products. wheat germ. diarrhea. pecans. nuts (walnuts. seeds (sesame and sunflower).Acarbose is an oligosaccharide. corn. peanuts. as opposed to acarbose.

While some bile acids are known to be colon tumor promoters (e. There is some thought that the ratio of lysine to arginine in the diet (or with supplements) can affect whether or not latent herpes viruses appear. Ursodeoxycholic acid has also been shown experimentally to suppress immune response such as immune cell phagocytosis. In double the recommended daily dose ursodeoxycholic acid reduces elevated liver enzyme levels in patients with primary sclerosing cholangitis.blood thinners. . There is no recommended daily amount established for arginine because the human body normally makes enough. and potassium. Ursodeoxycholic Acid 300mg (Udiliv) Ursodeoxycholic acid helps regulate cholesterol by reducing the rate at which the intestine absorbs cholesterol molecules while breaking up micelles containing cholesterol. perhaps by inducing cellular differentiation and/or cellular senescence in colon epithelial cells. It is believed to inhibit apoptosis. not just in the digestive system) ursodeoxycholic acid can be toxic (the development of cirrhosis. Some doctors recommend increasing lysine and decreasing arginine to help prevent the recurrence of symptoms associated with herpes simplex virus. death or liver transplantation). The safety of long-term arginine supplement use is not clear. others such as ursodeoxycholic acid are thought to be chemopreventive. varices. some painkillers. ginkgo biloba. deoxycholic acid). Prolonged exposure and/or increased quantities of systemic (throughout the body. One common dosage is 2 to 3 grams three times a day.g. garlic.

Although treatment with ursodeoxycholic acid showed a reduction in liver biochemistry. by using ursodiol to change the electrical properties of myofibroblast cells. it is likely that you will be asked to take 2-4 doses daily usually long-term unless you experience an adverse effect. . Some indigestion remedies stop ursodeoxycholic acid from working properly. both in patients who have suffered a heart attack and in foetuses. If you are taking ursodeoxycholic acid for primary biliary cirrhosis. Do not take antacid preparations containing aluminium salts at the same time as this medicine. and ascites. Myofibroblasts disrupt the transmission of electrical signals controlling heart rhythm. To dissolve gallstones. Take this medicine with or immediately after food. In absence of biochemical response to 13-15mg/kg/day ursodeoxycholic acid. jaundice. Try to avoid eating foods that are high in calories or cholesterol. its use is associated with an incidence of 20% hepatocellular carcinoma in patients with primary biliary cirrhosis in 15 years.Ursodiol may be used for biliary stasis in pregnant women to relieve the symptoms of itching and decrease bile absorption. Research by the Imperial College London has produced promising results in the treatment of arrhythmia. A method of contraception that contains less oestrogen may be more suitable for you. it did not decrease mortality or liver transplantation. it is usually taken once daily at bedtime up to two years and may continue your treatment for three to four months to ensure that they have completely cleared up.

The risk applies to all the DPP-4 inhibitors on the market (sitagliptin and saxagliptin). FDA . Itchy skin rash. DPP-4 enzyme is known to be involved in the suppression of certain malignancies. particularly in limiting the tissue invasion of these tumours. VILDAGLIPTINE (Eucreas : Vildagliptin + Metformin) Vildagliptine is a dipeptidyl peptidase-4 (DPP-4) inhibitorallowing GLP-1 and GIP to potentiate the secretion of insulin and suppress glucagon release.was approved by the FDA in 2006. such as non-small cell lung cancer (NSCLC).Common side-effects are Diarrhoea. etc. feeling sick. Sitagliptin .

alogliptin (Nesina. Kazano. Other possible adverse effects. liraglutide (Victoza).approval of Novartis' was delayed because of skin lesions with blistering observed in nonhuman primate toxicology studies. Jentadueto). sitagliptin (Januvia. Janumet. saxagliptin (Onglyza. a type of pancreatic cancer. Bydureon). Kombiglyze XR). The order referenced the March 2013 FDA study announcement that included the drugs exenatide (Byetta. Juvisync). Vildagliptine decreases gastric emptying. . include hypersensitivity reactions and pancreatitis and neuroendocrine tumor. Janumet XR. Oseni). and linagliptin (Tradjenta.