Drug – bio-affecting and body treating compositions – Plant material or plant extract of undetermined constitution...
Reexamination Certificate
2001-01-28
2002-04-02
Witz, Jean C. (Department: 1651)
Drug, bio-affecting and body treating compositions
Plant material or plant extract of undetermined constitution...
Reexamination Certificate
active
06365198
ABSTRACT:
BACKGROUND OF INVENTION
This invention relates to a pharmaceutical preparation mainly for treating gastrointestinal wounds, ulcers and rectal inflammation conditions such as hemorrhoids. An alcoholic extract of natural ingredients in dried powdered state consisting of Huangqin (baikal skullcap), Huanglian (rhizome of Chinese goldthread or rhizoma Coptidis), Huangbo (cortex phellodendri), Pheretima (dilong) and Cactus (opuntia ficus indica) is used in an oily medium such that the quantity of each ingredient in its dried form represents less than 2% of the final amount of preparation. In the foregoing assertion, efforts have been made to find a suitable palliative and/or curative agent for the treatment of gastrointestinal ulcer conditions and hemorrhoids from medicinal plants and other natural ingredients.
Peptic ulcer is defined as a benign lesion of gastric or duodenal mucosa occurring at a site where the mucosal epithelium is exposed to acid and pepsin. It is a gastrointestinal problem that has been prevalent throughout the world population. It is estimated that approximately 10% of most populations globally will develop severe peptic ulcer conditions at some time during their lifetime. The lesions occur at all ages and affect both sexes. It is estimated that at least five million people suffer from active peptic ulcers each year, and approximately 350,000 to 500,000 new cases are diagnosed annually in the U.S. alone. More than 600,000 patients are hospitalized in the U.S. each year for severe episodes. In approximately one-third of these cases serious complications occur, including intestinal obstruction, upper gastrointestinal hemorrhage and perforation. Furthermore, each year, over 6,000 deaths in the U.S. are directly caused by ulcer disorders. In addition, peptic ulcer conditions have been implicated as an indirect contributing factor in an additional 11,000 deaths each year.
The occurrence of the disease has been associated with over-indulgence, inappropriate habits, anxiety and stress. Considerable energy and resources have been expended towards relieving symptoms of peptic ulcer, which usually manifests as an excruciating pain, especially in the upper abdomen. Peptic ulceration reflects an imbalance between the aggressive action of acid peptic secretions and the defensive forces that protect the mucosa. Gastric ulcers result from lowered defensive mechanisms and duodenal ulcers are the consequence of the destructive action of increased acid-peptic secretions.
Duodenal ulcers occur when gastric mucosa secretes substantial amounts of acid. Although some patients with duodenal ulcers have normal levels of acid secretion, on the average they are hyperchlorhydric. Gastric acid has two phases: a cephalic phase (vagally mediated) in which direct cholinergic stimulation of parietal cells induces gastrin release from the antrum, and a less powerful antral phase when food enters the stomach, causing liberation of more gastrin from the antral mucosa. Evidence that patients with duodenal ulcers have increased parietal cell mass also suggests a genetic predisposition even though experimental data indicate that parental cell hyperplasia can be acquired.
Gastric ulceration results from lowering of the gastric mucosal resistance. Principal among the defensive influences is mucous secretion. The increased frequency of gastric ulcers with advancing age might be compatible with progressive inability to secrete a protective layer of mucous. Chronic gastritis is a frequent concomitant of gastric ulcer, is associated with impaired mucous secretion and is also age-related. In experimental animals, it has been demonstrated that protein depletion, avitaminoses and general malnutrition increase the susceptibility to gastric ulceration.
The symptoms evoked by peptic ulcers are exceedingly variable; some ulcers being virtually asymptomatic. Nausea and vomiting may be produced by either duodenal or gastric ulcers, but particularly by the latter. The most consistent manifestation is epigastric pain described variably as burning, gnawing or boring. Classically, the duodenal ulcer pain becomes most severe two or three hours after the last meal and persists until food or antacids relieve it. For this reason, the pain recurs in the middle of the night and requires a glass of milk or antacid for its relief. Such episodic pain may last for weeks or months only to abate, usually with regulated dietary regimen and therapy. Recurrence is often triggered by dietary indiscretions or stress and is usually very rapid and sometimes dramatic, presenting with hemorrhage or perforation. Death from peptic ulcer is usually due to bleeding or perforation. In addition, a high proportion of patients who die or whose ulcers bleed or perforate have no warning signals.
In the past, chronic gastritis with prolonged dyspeptic symptoms in the upper stomach, the peptic ulcer, duodenal ulcer and ventral ulcer with pain in the upper stomach after meals or epigastric pain on empty stomach were a syndrome with unclear etiology. Its pathogenesis had not been clarified in detail. Generally, it can still be said today that there is no peptic ulcer without proteolytic gastric acid. Differential-diagnostic measures usually succeed in differentiating the peptic formation of ulcers from psychogenic gastrointestinal malfunctions. The final diagnosis depends on X-ray results.
For a long time, neutralization of gastric acid secretion with antacids and H2-receptor antagonists, have provided the only relief from the pains of peptic ulcer. The treatment modalities have historically included treatment based on administering antacids, such as magnesium or aluminum compounds, calcium carbonates, alkaline bismuth salts, e.g. bismuth aluminate, colloidal bismuth salts. A high relapse rate of over 80% and side effects, such as the rebound effect of acid secretion, deposits of aluminum and bismuth salts in the tissue to bismuth nephropathy, and bismuth encephalopathy forced the medical field to pursue new paths. The selective proximal vagotomy with surgical exclusion of the appropriate vagus branches or the acid-producing stomach sections in the case of relapsing stomach duodenal ulcers was another medical path that usually went nowhere. The relapse rate usually did not change with this serious surgical procedure. In acid secretion, H
2
-receptors are involved. The introduction of the H
2
-receptor antagonists cimetidine (Tagamet®) in 1977, and then ranitidine (Zantac®, Zostril®) represented a milestone in medicinal ulcer therapy. This led to rapid pain elimination with the healing of duodenal and ventral ulcers. Side effects of long-term therapy, such as infectious diarrhea, persistent hypergastrinemia with germ settlements on the antacid stomach lumen and nitrosamine formation, had to be accepted. Despite progress in acute therapy and the short-term prophylaxis of peptic lesions, the course of ulcers and the relapse rate has not been influenced by the H
2
-receptor antagonists. The currently most potent molecule in the stemming of gastric acid is omeprazol and the newer generation pentaprazol. This category of proton pump inhibitors specifically blocks the H
+
/K
30
adenosinetriphosphatases (ATP) of the mucosa of the stomach and thus hinders acid secretion. A suspected disadvantage is that, under permanent hypergastrinemia during Omeprazol therapy, a hyperplasia of neuroendocrine cells occurs and can lead to carcinoid tumors. The high effectiveness compared to the H
2
-receptor antagonists, however, led to shorter treatment times at lower dosage (20 mg/day). The relapse rate remained unchanged.
Marshall et al. succeeded in 1983-1985 to prove the connection between the infection and gastritis through the rediscovery and ability to cultivate the germ
Campylobacter pylori
and through an oral infection in a self-test. This way the actual pathogenic factor of the ulcer was recognized. Initially, the germ was gained from biopsies of the antrum and corpus mucous membrane. In vitro cultivation did not succeed until later. According to examinatio
Gulf Pharmaceutical Industries
Ozga Brett
Witz Jean C.
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