At least half an hour should pass after intake of alendronate before eating dairy products or taking the supplement or drug. Highly active vitamin D analogues or fluorides: no data is available. Concomitant treatment should be avoided. The additional beneficial effect of HRT (hormone replacement therapy) with estrogens/progestins or raloxifene in postmenopausal women with osteoporosis remains to be elucidated, but no interactions have been seen. The combination is therefore possible, but controversial. Intravenous ranitidine increases the oral bioavailability of alendronate. No clinical consequences are known. The combination of NSAIDs and alendronate may increase the risk of gastric ulcers. Both these drugs have the potential to irritate the upper gastro-intestinal mucosa. Pharmacology
Mechanism of action
Alendronate inhibits osteoclast-mediated bone-resorption. Like all bisphosphonates, it is chemically related to inorganic pyrophosphate, the endogenous regulator of bone turnover. But while pyrophosphate inhibits both osteoclastic bone resorption and the mineralization of the bone newly formed by osteoblasts, alendronate specifically inhibits bone resorption without any effect on mineralization at pharmacologically achievable doses. Its inhibition of bone-resorption is dose-dependent and approximately 1,000 times stronger than the equimolar effect of the first bisphosphonate drug, etidronate. Under therapy, normal bone tissue develops, and alendronate is deposited in the bone-matrix in a pharmacologically inactive form. For optimal action, enough calcium and vitamin D are needed in the body in order to promote normal bone development. Hypocalcemia should, therefore, be corrected before starting therapy. Etidronate has the same disadvantage as pyrophosphate in inhibiting mineralization, but all of the potent N-containing bisphosphonates, including alendronate, risedronate, ibandronate, and zoledronate, do not.
Esophageal webs are thin membranes occurring anywhere along the esophagus. Presentation
Its main symptoms are pain and difficulty in swallowing (dysphagia).Esophageal webs are thin 2–3 mm (0.08–0.12 in) membranes of normal esophageal tissue consisting of mucosa and submucosa that can partially protrude/obstruct the esophagus. They can be congenital or acquired. Congenital webs commonly appear in the middle and inferior third of the esophagus, and they are more likely to be circumferential with a central or eccentric orifice. Acquired webs are much more common than congenital webs and typically appear in the cervical area (postcricoid).Clinical symptoms of this condition are selective (solid more than liquids) dysphagia, thoracic pain, nasopharyngeal reflux, aspiration, perforation and food impaction (the last two are very rare). Causes
They are mainly observed in the Plummer–Vinson syndrome, which is associated with chronic iron deficiency anemia. One in 10 patients with Plummer-Vinson syndrome will eventually develop squamous cell carcinoma of the esophagus, but it is unclear if esophageal webs in and of themselves are a risk factor. Esophageal webs are associated with bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), with graft versus host disease involving the esophagus, and with celiac disease.Esophageal webs are more common in white individuals and in women (with a ratio of 2:1). The literature describes relations between these webs and Plummer-Vinson Syndrome, bullous dermatologic disorders, inlet patch, graft-versus-host disease and celiac disease. The postulated mechanisms are sideropenic anemia (mechanism unknown) or some interference of the immune system. Esophageal webs can be ruptured during upper endoscopy.