Gastrointestinal (Other)
Alosetron (lotronex®)
| Drug Category: Selective 5-HT3 Receptor Antagonist. Indication: Treatment of women with severe diarrhea-predominant irritable bowel syndrome (IBS) who have failed to respond to conventional therapy
Dosing (Adults) IBS: Female: Oral: Initial: 0.5 mg twice daily for 4 weeks, with or without food; if tolerated, but response is inadequate, may be increased after 4 weeks to 1 mg twice daily. If response is inadequate after 4 weeks of 1 mg twice-daily dosing, discontinue treatment. Note: Discontinue immediately if constipation or signs/symptoms of ischemic colitis occur. Do not reinitiate in patients who develop ischemic colitis. Renal Dosing: The need for dosage adjustment has not been defined (due to limited information on activity of metabolites). Supplied: Tablet: 0.5 mg, 1 mg |
Bezlotoxumab - zinplava™ injection
| Drug UPDATES: ZINPLAVA™ (bezlotoxumab) injection [Drug information / PDF] REVIEW PACKAGE INSERT FOR POSSIBLE UPDATES PACKAGE INSERT -Dosing: Click (+) next to Dosage and Administration section (drug info link) Initial U.S. Approval: 2016 Mechanism of Action: ZINPLAVA (bezlotoxumab) is a human monoclonal antibody that binds to C. difficile toxin B and neutralizes its effects INDICATIONS AND USAGE: Limitation of Use: DOSAGE AND ADMINISTRATION: HOW SUPPLIED: |
Infliximab (remicade ®)
| CLINICAL PHARMACOLOGY General Infliximab neutralizes the biological activity of TNFα by binding with high affinity to the soluble and transmembrane forms of TNFα and inhibits binding of TNFα with its receptors. Infliximab does not neutralize TNFβ (lymphotoxin α), a related cytokine that utilizes the same receptors as TNFα. Biological activities attributed to TNFα include: induction of pro-inflammatory cytokines such as interleukins (IL) 1 and 6, enhancement of leukocyte migration by increasing endothelial layer permeability and expression of adhesion molecules by endothelial cells and leukocytes, activation of neutrophil and eosinophil functional activity, induction of acute phase reactants and other liver proteins, as well as tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Cells expressing transmembrane TNFα bound by infliximab can be lysed in vitro or in vivo. Infliximab inhibits the functional activity of TNFα in a wide variety of in vitro bioassays utilizing human fibroblasts, endothelial cells, neutrophils, B and T lymphocytes and epithelial cells. The relationship of these biological response markers to the mechanism(s) by which REMICADE exerts its clinical effects is unknown. Anti-TNFα antibodies reduce disease activity in the cotton-top tamarin colitis model, and decrease synovitis and joint erosions in a murine model of collagen-induced arthritis. Infliximab prevents disease in transgenic mice that develop polyarthritis as a result of constitutive expression of human TNFα, and when administered after disease onset, allows eroded joints to heal. INDICATIONS AND USAGE Crohn's Disease REMICADE is indicated for reducing the number of draining enterocutaneous and rectovaginal fistulas and maintaining fistula closure in adult patients with fistulizing Crohn's disease. Ankylosing Spondylitis Psoriatic Arthritis Plaque Psoriasis Ulcerative Colitis Dosing (Adults): Crohn's disease: Induction regimen: 5 mg/kg IV over 2 hours. Repeat dose at 2 and 6 weeks, followed by 5 mg/kg every 8 weeks. Dose may be increased to 10 mg/kg in patients who respond but then lose their response. If no response by week 14, consider discontinuing therapy. Psoriatic arthritis (with or without methotrexate): 5 mg/kg IV at 0, 2, and 6 weeks, then every 8 weeks. Rheumatoid arthritis: (In combination with methotrexate therapy): 3 mg/kg IV at 0, 2, and 6 weeks then every 8 weeks thereafter. Doses have ranged from 3-10 mg/kg intravenous infusion repeated at 4 to 8 week intervals. Dosage adjustment with CHF: Weigh risk versus benefits for individual patient: |
Mesalamine (asacol ® , pentasa)
| CLINICAL PHARMACOLOGY Mesalamine is thought to be the major therapeutically active part of the sulfasalazine molecule in the treatment of ulcerative colitis. Sulfasalazine is converted to equimolar amounts of sulfapyridine and mesalamine by bacterial action in the colon. The usual oral dose of sulfasalazine for active ulcerative colitis is 3 to 4 grams daily in divided doses, which provides 1.2 to 1.6 grams of mesalamine to the colon. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs), is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. Adults (usual course of therapy is 3-8 weeks): Maintenance of remission of ulcerative colitis: Rectal: Rectal suppository (Canasa™): Note: Suppositories should be retained for at least 1-3 hours to achieve maximum benefit. Elderly: See adult dosing; use with caution Administration Supplied SELECTED INDIVIDUAL PRODUCT MONOGRAPHS (Mesalamine)APRISO™ (mesalamine) extended-release capsules: DOSAGE AND ADMINISTRATION DOSAGE FORMS AND STRENGTHS -------------------- The suppository should be retained for one to three hours or longer, if possible, to achieve the maximum benefit. While the effect of CANASA® suppositories may be seen within three to twenty-one days, the usual course of therapy would be from three to six weeks depending on symptoms and sigmoidoscopic findings. Studies have suggested that CANASA® suppositories will delay relapse after the six-week short-term treatment. -------------------- DOSAGE AND ADMINISTRATION: DOSAGE FORMS AND STRENGTHS Asacol® For the maintenance of remission of ulcerative colitis: The recommended dosage in adults is 1.6 grams daily, in divided doses. Treatment duration in the prospective, well-controlled trial was 6 months. Two Asacol 400 mg tablets have not been shown to be bioequivalent to one Asacol HD 800 mg tablet. DOSAGE AND ADMINISTRATION |
Misoprostol (cytotec ® )
| Pharmacodynamics Misoprostol has both antisecretory (inhibiting gastric acid secretion) and (in animals) mucosal protective properties. NSAIDs inhibit prostaglandin synthesis, and a deficiency of prostaglandins within the gastric mucosa may lead to diminishing bicarbonate and mucus secretion and may contribute to the mucosal damage caused by these agents. Misoprostol can increase bicarbonate and mucus production, but in man this has been shown at doses 200 mcg and above that are also antisecretory. It is therefore not possible to tell whether the ability of misoprostol to reduce the risk of gastric ulcer is the result of its antisecretory effect, its mucosal protective effect, or both. In vitro studies on canine parietal cells using tritiated misoprostol acid as the ligand have led to the identification and characterization of specific prostaglandin receptors. Receptor binding is saturable, reversible, and stereospecific. The sites have a high affinity for misoprostol, for its acid metabolite, and for other E type prostaglandins, but not for F or I prostaglandins and other unrelated compounds, such as histamine or cimetidine. Receptor-site affinity for misoprostol correlates well with an indirect index of antisecretory activity. It is likely that these specific receptors allow misoprostol taken with food to be effective topically, despite the lower serum concentrations attained. Misoprostol produces a moderate decrease in pepsin concentration during basal conditions, but not during histamine stimulation. It has no significant effect on fasting or postprandial gastrin nor on intrinsic factor output. ---------------------- Uterine effects Other pharmacologic effects Dosage - Oral: Medical termination of pregnancy: Refer to Mifepristone monograph. Intravaginal: Adults: Labor induction or cervical ripening (unlabeled use): 25 mcg ( 1 /4 of 100 mcg tablet); may repeat at intervals no more frequent than every 3-6 hours. Do not use in patients with previous cesarean delivery or prior major uterine surgery. Administration Supplied |
Neomycin
| INDICATIONS Orally to prepare GI tract for surgery; topically to treat minor skin infections; treatment of diarrhea caused by E. coli ; adjunct in the treatment of hepatic encephalopathy; bladder irrigation Dosage Hepatic encephalopathy: 50-100 mg/kg/day in divided doses every 6-8 hours or 2.5-7 g/m 2 /day divided every 4-6 hours for 5-6 days not to exceed 12 g/day Children and Adults: Topical: Topical solutions containing 0.1% to 1% neomycin have been used for irrigation Preoperative intestinal antisepsis: 1 g each hour for 4 doses then 1 g every 4 hours for 5 doses; or 1 g at 1 PM, 2 PM, and 11 PM on day preceding surgery as an adjunct to mechanical cleansing of the bowel and oral erythromycin; or 6 g/day divided every 4 hours for 2-3 days Hepatic encephalopathy: 500-2000 mg every 6-8 hours or 4-12 g/day divided every 4-6 hours for 5-6 days Chronic hepatic insufficiency: 4 g/day for an indefinite period |
Octreotide (sandostatin ®)
| CLINICAL PHARMACOLOGY Octreotide acetate exerts pharmacologic actions similar to the natural hormone, somatostatin. It is an even more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Like somatostatin, it also suppresses LH response to GnRH, decreases splanchnic blood flow, and inhibits release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide. By virtue of these pharmacological actions, octreotide acetate has been used to treat the symptoms associated with metastatic carcinoid tumors (flushing and diarrhea), and Vasoactive Intestinal Peptide (VIP) secreting adenomas (watery diarrhea). Octreotide acetate substantially reduces growth hormone and/or IGF-I (somatomedin C) levels in patients with acromegaly. Single doses of octreotide acetate have been shown to inhibit gallbladder contractility and to decrease bile secretion in normal volunteers. In controlled clinical trials the incidence of gallstone or biliary sludge formation was markedly increased. Octreotide acetate suppresses secretion of thyroid stimulating hormone (TSH). Adults: SubQ: Initial: 50 mcg 1-2 times/day and titrate dose based on patient tolerance and response Carcinoid: 100-600 mcg/day in 2-4 divided doses VIPomas: 200-300 mcg/day in 2-4 divided doses Diarrhea: Initial: I.V.: 50-100 mcg every 8 hours; increase by 100 mcg/dose at 48-hour intervals; maximum dose: 500 mcg every 8 hours Esophageal varices bleeding: I.V. bolus: 25-50 mcg followed by continuous I.V. infusion of 25-50 mcg/hour Acromegaly: Initial: SubQ: 50 mcg 3 times/day; titrate to achieve growth hormone levels <5 ng/mL or IGF-I (somatomedin C) levels <1.9 U/mL in males and <2.2 U/mL in females; usual effective dose 100 mcg 3 times/day; range 300-1500 mcg/day Note: Should be withdrawn yearly for a 4-week interval in patients who have received irradiation. Resume if levels increase and signs/symptoms recur. =================== GH >2.5 ng/mL, IGF-1 is elevated, and/or symptoms uncontrolled: Increase octreotide LAR® to 30 mg I.M. every 4 weeks GH </= 1 ng/mL, IGF-1 is normal, symptoms controlled: Reduce octreotide LAR® to 10 mg I.M. every 4 weeks Dosage adjustment for carcinoid tumors and VIPomas: After 2 months of depot injections the dosage may be continued or modified as follows: =================== Supplied Injection, solution, as acetate (Sandostatin®): 0.05 mg/mL (1 mL); 0.1 mg/mL (1 mL); 0.2 mg/mL (5 mL); 0.5 mg/mL (1 mL); 1 mg/mL (5 mL) |
Olsalazine (dipentum ® )
| CLINICAL PHARMACOLOGY After oral administration, olsalazine has limited systemic bioavailability. Based on oral and intravenous dosing studies, approximately 2.4% of a single 1.0 g oral dose is absorbed. Less than 1% of olsalazine is recovered in the urine. The remaining 98 to 99% of an oral dose will reach the colon, where each molecule is rapidly converted into two molecules of 5-aminosalicylic acid (5-ASA) by colonic bacteria and the low prevailing redox potential found in this environment. The liberated 5-ASA is absorbed slowly resulting in very high local concentrations in the colon. The conversion of olsalazine to mesalamine (5-ASA) in the colon is similar to that of sulfasalazine, which is converted into sulfapyridine and mesalamine. It is thought that the mesalamine component is therapeutically active in ulcerative colitis (A.K. Azad-Kahn et al, LANCET, 2: 892-895, 1977). The usual dose of sulfasalazine for maintenance of remission in patients with ulcerative colitis is 2 grams daily, which would provide approximately 0.8 grams of mesalamine to the colon. More than 0.9 grams of mesalamine would usually be made available in the colon from 1 gram of olsalazine. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways (i.e., prostanoids) and through the lipoxygenase pathways (i.e., leukotrienes [LTs] and hydroxyeicosatetraenoic acids [HETEs]) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. INDICATIONS AND USAGE CONTRAINDICATIONS Dosing (Adults): Ulcerative colitis: 500mg orally bid. Administration |
Orlistat (xenical ®)
| Mechanism of Action Orlistat is a reversible inhibitor of lipases. It exerts its therapeutic activity in the lumen of the stomach and small intestine by forming a covalent bond with the active serine residue site of gastric and pancreatic lipases. The inactivated enzymes are thus unavailable to hydrolyze dietary fat in the form of triglycerides into absorbable free fatty acids and monoglycerides. As undigested triglycerides are not absorbed, the resulting caloric deficit may have a positive effect on weight control. Systemic absorption of the drug is therefore not needed for activity. At the recommended therapeutic dose of 120 mg three times a day, orlistat inhibits dietary fat absorption by approximately 30%. Dosing (Adults): Weight loss: Supplied |
Sucralfate (carafate ® )
| CLINICAL PHARMACOLOGY Sucralfate is only minimally absorbed from the gastrointestinal tract. The small amounts of the sulfated disaccharide that are absorbed are excreted primarily in the urine. Although the mechanism of sucralfate’s ability to accelerate healing of duodenal ulcers remains to be fully defined, it is known that it exerts its effect through a local, rather than systemic, action. The following observations also appear pertinent: 1]Studies in human subjects and with animal models of ulcer disease have shown that sucralfate forms an ulcer-adherent complex with proteinaceous exudate at the ulcer site. These observations suggest that sucralfate’s antiulcer activity is the result of formation of an ulcer-adherent complex that covers the ulcer site and protects it against further attack by acid, pepsin, and bile salts. There are approximately 14-16 mEq of acid-neutralizing capacity per 1 g dose of sucralfate Dosing Stress ulcer prophylaxis: 1 g 4 times/day Duodenal ulcer: Maintenance: Prophylaxis: 1 g twice daily Stomatitis (unlabeled use): 1 g/10 mL suspension, swish and spit or swish and swallow 4 times/day Dosage comment in renal impairment: Aluminum salt is minimally absorbed (<5%), however, may accumulate in renal failure Administration |
Sulfasalazine (azulfadine ®)
| CLINICAL PHARMACOLOGY Pharmacodynamics The mode of action of sulfasalazine (SSZ) or its metabolites, 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), is still under investigation, but may be related to the anti-inflammatory and/or immunomodulatory properties that have been observed in animal and in vitro models, to its affinity for connective tissue, and/or to the relatively high concentration it reaches in serous fluids, the liver and intestinal walls, as demonstrated in autoradiographic studies in animals. In ulcerative colitis, clinical studies utilizing rectal administration of SSZ, SP, and 5-ASA have indicated that the major therapeutic action may reside in the 5-ASA moiety. INDICATIONS AND USAGE a. in the treatment of mild to moderate ulcerative colitis, and as adjunctive therapy in severe ulcerative colitis; and CONTRAINDICATIONS Patients with intestinal or urinary obstruction, Adults: Rheumatoid arthritis: Enteric coated tablet: Initial: 0.5-1 g/day; increase weekly to maintenance dose of 2 g/day in 2 divided doses; maximum: 3 g/day (if response to 2 g/day is inadequate after 12 weeks of treatment) Dosing interval in renal impairment: Supplied |
Ursodiol (actigall ®)
| Gallstone dissolution: Oral: 8-10 mg/kg/day in 2-3 divided doses; use beyond 24 months is not established; obtain ultrasound images at 6-month intervals for the first year of therapy; 30% of patients have stone recurrence after dissolution. Gallstone prevention: Oral: 300 mg twice daily. Primary biliary cirrhosis: Oral: 13-15 mg/kg/day in 2-4 divided doses (with food). Supplied: [Supplied: 300 capsule] |
Vasopressin (pitressin ®)
| CLINICAL PHARMACOLOGY The antidiuretic action of vasopressin is ascribed to increasing reabsorption of water by the renal tubules. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules with less effect on the smooth musculature of the large veins. The direct effect on the contractile elements is neither antagonized by adrenergic blocking agents nor prevented by vascular denervation. Following subcutaneous or intramuscular administration of vasopressin injection, the duration of antidiuretic activity is variable but effects are usually maintained for 2-8 hours. The majority of a dose of vasopressin is metabolized and rapidly destroyed in the liver and kidneys. Vasopressin has a plasma half-life of about 10 to 20 minutes. Approximately 5% of a subcutaneous dose of vasopressin is excreted in urine unchanged after four hours. INDICATIONS DOSING I.M., SubQ: Continuous I.V. infusion: Children and Adults: 0.5 milliunit/kg/hour (0.0005 unit/kg/hour); double dosage as needed every 30 minutes to a maximum of 0.01 unit/kg/hour. Intranasal: Administer on cotton pledget, as nasal spray, or by dropper. Abdominal distention: Adults: I.M.: 5 units stat, 10 units every 3-4 hours ====================== Children: Initial: 0.002-0.005 units/kg/minute; titrate dose as needed; maximum: 0.01 unit/kg/minute; continue at same dosage (if bleeding stops) for 12 hours, then taper off over 24-48 hours AdAdults: Initial: 0.2-0.4 unit/minute, then titrate dose as needed, if bleeding stops; continue at same dose for 12 hours, taper off over 24-48 hours Out-of-hospital asystole (unlabeled use): Adults: I.V.: 40 units; if spontaneous circulation is not restored in 3 minutes, then repeat dose Pulseless VT/VF (ACLS protocol): I.V.: 40 units (as a single dose only); if no I.V. access, administer 40 units diluted with NS (to a total volume of 10 mL) endotracheally Vasodilatory shock/septic shock (unlabeled use): Adults: I.V.: Vasopressin has been used in doses of 0.01-0.1 units/minute for the treatment of septic shock. Doses >0.05 units/minute may have more cardiovascular side effects. Most case reports have used 0.04 units/minute continuous infusion as a fixed dose. Administration GIGI hemorrhage: Administration requires the use of an infusion pump and should be administered in a peripheral line. Vasodilatory shock: Administration through a central catheter is recommended. |
Reference(s)
National Institutes of Health, U.S. National Library of Medicine, DailyMed Database.
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