Ulcer healing

The mechanism by which sucralfate accelerates healing of duodenal ulcers has not been determined. It does not have significant antisecretory, acid neutralizing activity or direct stimulation of ulcer healing. It is known that the mechanism is local rather than systemic. Binding of pepsin or bile salts may contribute to its effect. It is indicated for the short-term therapy of active duodenal ulcers and for maintenance at reduced dosage. 

FIGURE 8.20 Drugs as subsets of clinical profiles. While burimamide, cimetidine, and metiamide are all active histamine H2 antagonists with ulcer healing activity burimamide lacks a suitable toxicity and pharmacokinetic profile and cimetidine is adequately absorbed but still toxic. Only metiamide fulfills the requirements of a clinically useful drug. 

Gastric outlet obstruction occurs in approximately 2% of patients with PUD and is usually caused by ulcer-related inflammation or scar formation near the peripyloric region. Signs and symptoms of outlet obstruction include early satiety after meals, nausea, vomiting, abdominal pain, and weight loss. Ulcer healing with conventional acid-suppressive therapy is the primary treatment, but if this is unsuccessful then an endoscopic procedure (e.g., balloon dilation) is required. 

BSS 525 mg four times a day + metronidazole 250 mg four times a day + tetracycline 500 mg four times a day + H2RA (conventional ulcer-healing dose)c... 

TABLE 15-4. Oral Drug Regimens to Heal Peptic Ulcers or Maintain Ulcer Healing... 

Drug Duodenal Ulcer or Gastric Ulcer Healing (mg/day) Maintenance of DU or GU Healing (mg/day)... 

Conventional Treatment of Active Duodenal and Gastric Ulcers and Long-Term Maintenance of Ulcer Healing... 

Epidemiologic evidence links cigarette smoking to PUD, impaired ulcer healing, and ulcer-related GI complications. The risk is proportional to the amount smoked per day. 

For treatment of NSAID-induced ulcers, nonselective NSAIDs should be discontinued (when possible) if an active ulcer is confirmed. Most uncomplicated NSAID-induced ulcers heal with standard regimens of an H2RA, PPI, or sucralfate (see Table 29-2) if the NSAID is discontinued. If the NSAID must be continued, consideration should be given to reducing the... 

The persistence or recurrence of symptoms within 14 days after the end of treatment suggests failure of ulcer healing or HP eradication, or an alternative diagnosis such as gastroesophageal reflux disease. 

Most patients with uncomplicated HP-positive ulcers do not require confirmation of ulcer healing or HP eradication. 

RD.C. Smith, From skin disorders to venous leg ulcers pathophysiology and efficacy of Daflon 500 mg in ulcer healing. Angiology 54 (Suppl. 1) (2003) S45-S51. 

Skin crusts were reported on mice exposed repeatedly to 5 mg phenol as a 5% (w/v) solution for 32 weeks, whereas skin ulceration was observed in mice exposed to 5 mg phenol as a 20% (w/v) solution (Salaman and Glendenning 1957). The skin ulceration healed in 4 weeks after the end of the exposure. 

Q19 Wh ich of the following products is NOT indicated as an agent to be used in gastrointestinal ulcer healing ... 

Pla. Parke, D. V., and Lindup, W. E., Quantitative and qualitative aspects of the plasma protein binding of carbenoxolone, an ulcer-healing drug. Ann. N.Y. Acad. Sci. (1973), in press. 

Apply 4 times/day beginning as soon as symptoms occur. Use after oral hygiene. With gentle pressure, dab paste onto each ulcer in mouth. Use until ulcer heals. If significant healing or pain reduction has not occurred in 10 days, consult a dentist or physician. 

Clarithromycin/Omeprazole/Amoxicillin- 500 mg clarithromycin, 20 mg omeprazole, and 1 g amoxicillin every 12 hours for 10 days. In patients with an ulcer present at the time of initiation of therapy, an additional 18 days of omeprazole 20 mg once daily is recommended for ulcer healing and symptom relief. 

Clarithromycin/Omeprazole - 500 mg clarithromycin 3 times/day (every 8 hours), and 40 mg omeprazole once daily (every morning) for 14 days. An additional 14 days of 20 mg omeprazole once daily is recommended for ulcer healing and symptom relief. 

Carbenoxolone is a derivative of glycyrrhizic acid and both carbenoxolone and liquorice have ulcer healing properties. However, carbenoxolone has considerable mineralocorticoid activity, frequently producing Na+ and fluid retention, hypertension and hypokalemia. It is therefore not generally recommended for routine use. 

A. If the precipitant can be withdrawn then an-tisecretory treatment with a histamine H2 antagonist or proton pump inhibitor, or misoprostol (an antisecretory and mucosally protective prostaglandin) for a month may be enough to induce ulcer healing. 

Answer Peptic ulcer disease is most frequently secondary to either Helicobacter pylori infection or use of NSAIDs. The patient does admit to NSAID use (naproxen), but should also be checked for concomitant H. pylori infection at time of endoscopy or by a serology test. If the patient was found to have H. pylori, an appropriate eradication regimen should be prescribed. The patient should also be counseled to avoid NSAIDs. The patient should be prescribed a proton pump inhibitor for 8 weeks to heal the ulcer. A repeat endoscopy should be done at that time to document ulcer healing and rule out gastric cancer. In addition, the patient should be counseled to stop smoking, which is a risk factor for more severe peptic ulcer disease. 

Ulcer healing inhibition. Cigarette smoke or smoke extract, administered to ulcerated rats once daily for 3 days, produced concomitant and dose-dependent reduction of angiogenesis and constitutive NOS activity. The same treatments also delayed ulcer healing. Results indicated that cigarette... 

Cho. Cigarette smoke and its extract delays ulcer healing and reduces nitric oxide synthase activity and angiogenesis in rat stomach. Clin Exp Pharmacol Physiol 1999 26(10) 828-829. 

Gastrointestinal system Carbenoxolone Cimetidine Amiloride, spironolactone Antacids Inhibition of ulcer healing. Reduced absorption if taken simultaneously. 

Selective muscarinic receptor blocker. It inhibits gastric secretion. Thus is effective in peptic ulcer patients and promotes ulcer healing. It does not produce atropinic side effect (due to blockade of and M3 receptors). 

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