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Helicobacter Pylori and Gastritis
This unusual name identifies a specific bacteria that can cause infection of the stomach. This infection can contribute to the development of diseases, such as dyspepsia (heartburn, bloating and nausea), gastritis (inflammation of the stomach), and ulcers in the stomach and duodenum. It will be useful to know some things about the upper digestive tract to understand how and where Helicobacter pylori infection can occur.
When food is swallowed it passes through the esophagus (the tube that connects the throat to the stomach) It then enters the larger upper part of the stomach. A strong acid that helps to break down the food is secreted in the stomach. The narrower, lower part of the stomach is called the antrum. The antrum contracts frequently and vigorously, grinding up the food and squirting it into the small intestine. The duodenum is the first part of the small intestine, just beyond the stomach. The stomach, including the antrum, is covered by a layer of mucous that protects it from the strong stomach acid.
It is known that alcohol, aspirin, and arthritis drugs such as ibuprofen, can disrupt the protective mucous layer. This allows the strong stomach acid to injure underlying stomach cells. In some people, corticosteroids, smoking, and stress appear to contribute in some way. Until the mid 1980s, it was felt that one or more of these factors working together led to the development of gastritis and ulcers. Since that time, evidence has been mounting that Helicobacter pylori (H. pylori) has a major role in causing these diseases.
The Infection
H. pylori is a fragile bacteria that has found an ideal home in the protective mucous layer of the stomach. These bacteria have long threads protruding from them that attach to the underlying stomach cells. The mucous layer that protects the stomach cells from acid also protects H. pylori. These bacteria do not actually invade the stomach cells as certain other bacteria can. The infection, however, is very real and it does cause the body to react. Infection-fighting white blood cells move into the area, and the body develops H. pylori antibodies in the blood.
H. pylori infection probably occurs when an individual swallows the bacteria in food, fluid, or perhaps from contaminated utensils. The infection is likely one of the most common worldwide. The rate of infection increases with age, so it occurs more often in older people. It also occurs frequently in young people in the developing countries of the world, since the infection tends to be common where sanitation is poor or living quarters are cramped. In many cases it does not produce symptoms. In other words, the infection can occur without the person knowing it. The infection remains localized to the gastric area, and probably persists unless specific treatment is given.
How is H. pylori Infection Diagnosed?
There are currently three ways to diagnose H. pylori infection. During endoscopy (a visual exam of the stomach through a thin, lighted, flexible tube), the physician can remove small bits of tissue through the tube. The tissue is then tested for the bacteria. A breath test is now available. In this test a substance called urea is given by mouth. A strong enzyme in the bacteria breaks down the urea into carbon dioxide, which is then exhaled and can be measured. And finally, there is a blood test that measures the protein antibodies against these bacteria that are present in the blood. This antibody can mean the infection is present, or that it was present in the past and is now cleared.
Gastritis and Dyspepsia
The symptoms are discomfort, bloating, nausea and perhaps vomiting. The person may also have symptoms that suggest ulcers - burning or pain in the upper abdomen, usually occurring about an hour or so after meals or even during the night. The symptoms are often relieved temporarily by antacids, milk, or medications that reduce stomach acidity. Yet, the physician does not find an ulcer when the patient is tested by x-ray or endoscopy. When H. pylori is found in the stomach, it is tempting to believe that it is the cause of the symptoms, although this connection is not yet clear cut. The physician will usually prescribe antibiotic therapy to see if clearing the infection relieves symptoms.
Ulcers
Stomach Ulcers: With stomach ulcers, H. pylori infection is found in 60 to 80 percent of the cases. Again, it is still uncertain how the infection acts to cause the ulcer. It probably weakens the protective mucous layer of the stomach. This allows acid to seep in and injure the underlying stomach cells. However, there is still a great deal of research to be done to unravel this relationship.
Duodenal Ulcers: In times past, physicians were taught "no acid, no ulcer." The medical profession felt the single most important factor causing duodenal ulcers to form was strong stomach acid. Research has now shown that over 90% of all patients who develop duodenal ulcers have H. pylori infection in the stomach as well. Medical studies are under way to determine the relationship between the two and how an infection in the stomach can be related to a duodenal ulcer. Acid is still important; patients without acid in the stomach never get duodenal ulcers. However, physicians now accept the fact that the infection is directly related to the development of duodenal ulcers. It is now rather easy to clear duodenal ulcers with the strong acid-reducing medicines available. But, the ulcers will usually recur unless the H. pylori infection is also cleared from the stomach.
Stomach Cancer and Lymphoma
These two types of cancer are now known to be related to H. pylori bacteria. This does not mean that all people with H. pylori infection will develop cancer; in fact, very few do. However, it is likely that if the infection is present for a long time, perhaps from childhood, these cancers may then develop. This is another reason why it is important to treat H. pylori infection.
When is Treatment Necessary?
Since the infection is so common, it is sometimes recommended that no treatment be given when there are no symptoms. However, these recommendations may change as more research develops. Increasingly, physicians are treating the acute ulcer with acid-reducing medicines and treating the infection with antibiotics. Interestingly, one of these antibiotics is a bismuth compound that is available over-the-counter as Pepto-Bismol. It is also available as a generic drug called bismuth subsalicylate. The bismuth part of the medicine actually kills the bacteria. However, do not go to the drugstore and purchase a bottle of Pepto-Bismol, expecting this alone to cure the infection. H. pylori is buried deep in the stomach mucous, so it is difficult to get rid of this infection. Several antibiotic drugs are always used together to prevent the bacteria from developing resistance to any one of them. Current medical studies are being done to develop earlier treatment programs for this difficult infection
Helicobacter pylori infection causes chronic gastritis, which can lead to atrophic gastritis, itself a precursor of gastric cancer. Raising the gastric pH can alter or worsen chronic gastritis in patients infected with H. pylori, and can also raise gastrin levels, both of which favor atrophic gastritis. This study was designed to look at the interaction between H. pylori infection, omeprazole therapy and the development of atrophic gastritis.
Methods
The study compared gastric biopsies in two cohorts of patients with reflux esophagitis, one treated with omeprazole and one treated surgically with fundoplication.
The authors conclude that patients receiving prolonged acid-suppressive therapy with omeprazole who are also infected with H. pylori are at risk for developing atrophic gastritis. They imply that omeprazole-treated patients who are H. pylori negative, however, are not at increased risk for atrophic gastritis. They note that there are some differences between the two cohorts (the omeprazole group was 9 years older, on average). Nevertheless, they believe that these differences are not sufficient to explain the results of their study.
The data from the fundoplication cohort are incomplete (53 out of 137 were not analyzed because of an incomplete series of biopsy specimens). Because of the small numbers, we cannot conclude that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression.
The data from the omeprazole group are more complete, and the results do suggest that, in this group, patients infected with H. pylori are at significantly higher risk for developing atrophic gastritis than those who are not infected.
Because of the problems with comparing the two cohorts, I do not believe the data show that patients receiving omeprazole therapy who are not infected are not at increased risk for atrophic gastritis. Furthermore, it is not possible to extrapolate these results to therapeutic efficacy -- we don't know if antibiotic treatment will decrease the incidence of atrophic gastritis in these patients and thus make omeprazole therapy "safer".
This study is another one that adds to the growing number of reports indicating a significant pathogenetic role for H. pylori. Given its high prevalence in the upper age groups, treatment in order to prevent atrophic gastritis and gastric cancer would be an enormously expensive proposition. Targeted treatment of high risk groups (such as the acid-suppressed group examined here) needs to be investigated by randomized trials.
June 24, 1996
The authors of this paper reply:We appreciate the attention and comments of Dr. Jacobson made as contribution to this journalclub on our recent paper in the NEJM. We would like to use the opportunity to address the issues raised by Dr. Jacobson in his comments.
Dr. Jacobson states that we can not conclude from our data that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression. That is a valid statement, which however, with all due respect, is besides the point of our paper. The introduction of our paper actually starts with giving an overview of the strong association between H. pylori and atrophic gastritis, ending with the sentence that 'the development of atrophic gastritis induced by persistent H. pylori infection is an essential step in the cascade of events leading to gastric cancer' (NEJM 1996; 334: 1018*).
H. pylori causes chronic gastritis in virtually all infected individuals. In many of them, this persistent inflammation leads to ultimate development of multifocal atrophic gastritis. However, this is generally a very slow process. As pointed out in our discussion, various cohort follow-up studies described an annual increase in the prevalence of atrophy of approximately 1 - 3% annually. These studies were done both in developed countries (Finland, the Netherlands) and developing countries (Estonia, Colombia), but nevertheless had very concordant results. The first study that differentiated between H. pylori positive and negative subjects in its cohort, was our study from Amsterdam, showing an annual 0.3% increase of atrophy prevalence in uninfected compared to a significantly higher 1.8% in infected subjects (Lancet 1995; 345: 1525-8*). The point thus is that H. pylori is a very important factor in the process of development of atrophic gastritis, but that this process is slow. After 20 years of follow-up, approximately 1 out of 3 infected adults will have signs of atrophy.
The chance to develop atrophy is however dependent upon the severity of gastritis, which is determined by characteristics of the bacterial strain and of the infected host. We have recently shown that within the population of H. pylori infected subjects, those that are infected with a cagA positive strain have more active gastritis and a 2-fold higher chance to develop atrophy than those that are infected with a cagA negative strain (J Natl Cancer Inst 1995; 87: 1777-80*). This sheds new light on the observation that acid suppression also increases the severity of gastritis, in particular in the gastric body. This effect has consistently been observed by various research groups, including Dr. Logan from the UK (Gut 1995; 36: 12-6), Dr. Solcia from Italy (Scand J Gastroenterol 1994; 201: 28-34) and ourselves (Am J Gastroenterol 1995; 90: 1401-6*). In the past, the same effect had also been observed in DU patients treated with a vagotomy. This led to our hypothesis that acid suppressive maintenance therapy may increase the risk for atrophic gastritis (see Am J Gastroenterol 1995; 90: 1401-6, or Aliment Pharmacol Ther 1995; 9: 331-40*). For that purpose, we evaluated the development of atrophy in our cohort of GERD patients treated with omeprazole. As pointed out in our NEJM paper, the H. pylori negative GERD patients had an annual rate of atrophy development (0.8%) that was very low and not significantly differed from our Amsterdam volunteer population of the same age not treated with omeprazole (0.3% ; Lancet 1995; see above). However, the H. pylori positive omeprazole treated GERD patients had indeed a high rate of atrophy development (6.1%), which significantly differed from the 1.8% found in our Amsterdam volunteer population of the same age not treated with omeprazole (Lancet 1995; see above). At this rate, it did not take 20 years, but only 5 years for atrophy to develop in 1 out of every 3 infected subjects! We presented these data on the 1995 AGA meeting in San Diego and submitted them to the NEJM, including the comparison with the Lancet - Amsterdam cohort of subjects without specific disease or treatment. The main comment we received, was that, although both cohorts were from the same city and had comparable mean ages, we could not exclude the possibility that GERD by itself increased the chance for atrophy development. For that reason, we then made another comparison with the Swedish fundoplication cohort, again showing that H. pylori negatives did not differ whether treated with omeprazole, fundoplication, or nothing at all (Amsterdam - Lancet cohort), whereas in H. pylori positives the acid suppressive therapy significantly increased the rate of atrophy. This hypothesis receives further strong support from a comparison with all data from other histological cohort follow-ups. I refer for this comparison to the graphical display of these data as presented in the Am J Gastroenterol 1995; 90: 1401-6*. The new data published in the NEJM fit very well the data presented in this graph.
Thus, the point of our paper is that H. pylori causes gastritis, which can lead to atrophy. The chance to develop atrophy is dependent upon the severity of gastritis. More than ten different short-term studies have now consistently shown that profound acid suppression increases gastritis activity and our NEJM study is the first long-term study on this topic. The data from this study strongly suggest that the permanently increased gastritis activity has important long-term implications. These data are supported by the other limited available cohort follow-up data as extensively discussed in the discussion of our paper.
This brings me to the specific points raised by Dr. Jacobson. First of all, this is indeed not a randomized study, although I do not see why this automatically without any specific arguments makes the comparison of dubious validity. As I already pointed out, the data do fit with those of other available cohort studies and they also do fit a plausible explanation for the effect of an increased development of atrophy. Therefore, the comparison may actually be very valid. The two populations are indeed from two countries (Sweden and the Netherlands), but it would serve the American reader to know that the distance between the two cities is about the same as the distance between San Francisco and San Diego within one state of the USA. Furthermore, both countries contain a largely caucasian population and are very similar with respect to socio-economic status, dietary, drinking and smoking habits, medication use, life expectancy and incidence of atrophic gastritis and gastric cancer. Baseline data of both cohorts are not incomplete, they are given in both the NEJM paper and in the two other papers that we refer to. Dr. Jacobson raises the need for randomized controlled studies. Although we agree with this need, the chance that they will ever be performed on this topic is close to nil, as no ethical committee will allow the randomization of GERD patients to medication or surgery.
A total of 137 Swedish patients was treated with a fundoplication cohort, yet only in one hospital were the biopsy specimens taken according to the same protocol as in our omeprazole treated patients. Therefore, we had to use only 72 of the 137 fundoplication patients. These did not significantly differ from the excluded patients.
The discussion then comes back to the comparison between the two cohorts. Dr. Jacobson states that he believes that H. pylori uninfected patients receiving omeprazole may still be at increased risk to develop atrophy. What can we say? We observed an approximately 10-fold higher chance for omeprazole treated GERD patients to develop atrophy in the presence of H. pylori compared to those who were not infected, and an even 35-fold higher chance to develop argyrophil cell hyperplasia. Furthermore, the rate of atrophy development was as low in the non-infected omeprazole treated GERD patients as it was in a non-treated non-GERD volunteer population (see Lancet publication). This is strong evidence against the belief of Dr. Jacobson and in favour of the safety of omeprazole maintenance treatment. Finally, we fully agree with Dr. Jacobson that the results can not be extrapolated to therapeutic efficacy. This is actually the last sentence of our paper, saying that 'it remains to be seen whether eradication therapy can prevent atrophy and argyrophil-cell hyperplasia'. This needs to be determined in future studies. Therefore, we suggest in our paper that at this time we should consider H. pylori eradication in H. pylori infected GERD patients requiring profound acid suppressive maintenance therapy.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
* Please submit any reprint requests to: Ms. Sylvia Band, e-mail address: gastrol@azvu.nl
Certainly, my statement that since this wasn't a randomized trial, any comparisons between the groups are of "dubious validity" was cavalier. My apologies.
The actual reason for using a surgically treated cohort in this study wasn't clear to me until I read your explanation of the previous objections to using a non-GERD group as controls. I am still concerned that comparing a surgically treated group from one country with a medically treated group from another country leaves room for significant differences which could affect the results. Although the demographics of Sweden and the Netherlands may be similar, can the same be said for the two cohorts studied here? I would have been more confident in the comparability of the two groups if I knew a little more about them -- say, number of diabetics, alcohol consumption, number of smokers and why the surgical group was referred for surgery. Were baseline vitamin B12 levels similar in both groups?
That acid suppression enhances susceptibility to H-Pylori associated atrophic gastritis is plausible, based on this study. I'm just not sure to what extent the degree of enhancement can be deduced without more evidence of the comparability of the two groups.
Date: Mon, 01 Jul 1996
From: Howard Homler MD <76212.32@compuserve.com>
Prilosec seemed too good to be true! Once the fear of inducing gastric carcinoid tumors quieted down, we really thought we had a wonder drug. The study reviewed here is a timely warning to avoid the cavalier use of proton pump inhibitors in our GERD patients. I would suspect that the incidence of chronic atrophic gastritis in H pylori infected individuals treated with H-2 blockers would be intermediate between the control group and the group treated with Prilosec...seem reasonable?
Dr. Kuipers (author of the paper) responds:
Date: Tue, 02 Jul 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
I fully agree that the hypothesis brought forward makes much sense. The data to support or refute it are however still very scarce. I am aware of two studies that claimed some increase of H. pylori associated body gastritis during H2-blocker and also during antacid therapy (Stolte et al. Ir J Med Science 1992; proceedings of the IVth (?) International meeting on H. pylori, respectively Lanza et al. Am J Gastroenterol 1994). However, there have been no cohort follow-up data published yet to show whether or not this effect would make any difference with respect to the development of atrophy. There has been one cross-sectional study (Penston et al. Aliment Pharmacol Therap 1990) that focused on long-term effectivity of 150-300 mg ranitidin maintenance treatment in DU patients and did not find atrophic gastritis at a single observation after five years of therapy. However, there is obviously a clear need for additional data, to address this issue.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
What about lansoprazole (prevacid)? In vitro, it is more active against H. pylori than omeprazole, but costs a bit more. For formulary consideration, I would keep omeprazole.
Dr. Kuipers' response:
Date: Tue, 13 Aug 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
With respect to lansoprazole, my reply is twofold:
1/ The effects of proton pump inhibitors on H.pylori are not exerted by the inactive prodrug that we prescribe, but by the activated sulphenamide form of the drug. This means that the PPI's first have to bind a proton before they have any effect on Hp. Such binding of a proton in the lab is obviously performed by acidifying the solution. In vivo however, this occurs predominantly within the vesicles of the parietal cell, where it is then immediately and irreversibly bound to the proton-pump. It is therefore on theoretical grounds very questionable whether PPI's have any significant anti-Hp effect in vivo. There are to my knowledge no data that prove otherwise. Patients can be treated with high dose PPI's for years and will not become Hp negative (in our recent NEJM study, we did not observe any patient to become Hp negative during 3-8 years omeprazole therapy for GERD). The important contribution of PPI's in Hp eradication therapies is particularly due to the acid suppressive effect. This is true for omeprazole, but also for lansoprazole and pantoprazole. Even though lansoprazole may have a greater in vitro antibacterial effect on Hp, the mechanism is still the same and we have to assume that the clinical importance of this antibacterial effect is minimal .
2/ Hp positive patients treated with lansoprazole do get exactly the same increase in corpus gastritis as observed during omeprazole therapy. With maintenance therapy, this does place them at risk for the development of atrophic gastritis and argyrophil cell hyperplasia just as with omeprazole therapy (see for instance Eissele et al. Gastroenterology 1996; 110 (4): A101 (abstract). As mentioned in our NEJM paper, the effect is associated with the level of acid suppression and not with the method by which the acid suppression is being achieved (e.g. it also occurs after vagotomy). Therefore, the same advice is to treat these patients with Hp eradication at the start of lansoprazole maintenance therapy.
With kind regards,
Sincerely,
Ernst Kuipers
Dr. Ernst Kuipers
kuipere@ctrvax.vanderbilt.edu
Vanderbilt University Medical Center
Department of Infectious Diseases
Letters to the Editor about this article from the NEJM site.
Helicobacter pylori infection causes chronic gastritis, which can lead to atrophic gastritis, itself a precursor of gastric cancer. Raising the gastric pH can alter or worsen chronic gastritis in patients infected with H. pylori, and can also raise gastrin levels, both of which favor atrophic gastritis. This study was designed to look at the interaction between H. pylori infection, omeprazole therapy and the development of atrophic gastritis.
Methods
The study compared gastric biopsies in two cohorts of patients with reflux esophagitis, one treated with omeprazole and one treated surgically with fundoplication.
The authors conclude that patients receiving prolonged acid-suppressive therapy with omeprazole who are also infected with H. pylori are at risk for developing atrophic gastritis. They imply that omeprazole-treated patients who are H. pylori negative, however, are not at increased risk for atrophic gastritis. They note that there are some differences between the two cohorts (the omeprazole group was 9 years older, on average). Nevertheless, they believe that these differences are not sufficient to explain the results of their study.
The data from the fundoplication cohort are incomplete (53 out of 137 were not analyzed because of an incomplete series of biopsy specimens). Because of the small numbers, we cannot conclude that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression.
The data from the omeprazole group are more complete, and the results do suggest that, in this group, patients infected with H. pylori are at significantly higher risk for developing atrophic gastritis than those who are not infected.
Because of the problems with comparing the two cohorts, I do not believe the data show that patients receiving omeprazole therapy who are not infected are not at increased risk for atrophic gastritis. Furthermore, it is not possible to extrapolate these results to therapeutic efficacy -- we don't know if antibiotic treatment will decrease the incidence of atrophic gastritis in these patients and thus make omeprazole therapy "safer".
This study is another one that adds to the growing number of reports indicating a significant pathogenetic role for H. pylori. Given its high prevalence in the upper age groups, treatment in order to prevent atrophic gastritis and gastric cancer would be an enormously expensive proposition. Targeted treatment of high risk groups (such as the acid-suppressed group examined here) needs to be investigated by randomized trials.
June 24, 1996
The authors of this paper reply:We appreciate the attention and comments of Dr. Jacobson made as contribution to this journalclub on our recent paper in the NEJM. We would like to use the opportunity to address the issues raised by Dr. Jacobson in his comments.
Dr. Jacobson states that we can not conclude from our data that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression. That is a valid statement, which however, with all due respect, is besides the point of our paper. The introduction of our paper actually starts with giving an overview of the strong association between H. pylori and atrophic gastritis, ending with the sentence that 'the development of atrophic gastritis induced by persistent H. pylori infection is an essential step in the cascade of events leading to gastric cancer' (NEJM 1996; 334: 1018*).
H. pylori causes chronic gastritis in virtually all infected individuals. In many of them, this persistent inflammation leads to ultimate development of multifocal atrophic gastritis. However, this is generally a very slow process. As pointed out in our discussion, various cohort follow-up studies described an annual increase in the prevalence of atrophy of approximately 1 - 3% annually. These studies were done both in developed countries (Finland, the Netherlands) and developing countries (Estonia, Colombia), but nevertheless had very concordant results. The first study that differentiated between H. pylori positive and negative subjects in its cohort, was our study from Amsterdam, showing an annual 0.3% increase of atrophy prevalence in uninfected compared to a significantly higher 1.8% in infected subjects (Lancet 1995; 345: 1525-8*). The point thus is that H. pylori is a very important factor in the process of development of atrophic gastritis, but that this process is slow. After 20 years of follow-up, approximately 1 out of 3 infected adults will have signs of atrophy.
The chance to develop atrophy is however dependent upon the severity of gastritis, which is determined by characteristics of the bacterial strain and of the infected host. We have recently shown that within the population of H. pylori infected subjects, those that are infected with a cagA positive strain have more active gastritis and a 2-fold higher chance to develop atrophy than those that are infected with a cagA negative strain (J Natl Cancer Inst 1995; 87: 1777-80*). This sheds new light on the observation that acid suppression also increases the severity of gastritis, in particular in the gastric body. This effect has consistently been observed by various research groups, including Dr. Logan from the UK (Gut 1995; 36: 12-6), Dr. Solcia from Italy (Scand J Gastroenterol 1994; 201: 28-34) and ourselves (Am J Gastroenterol 1995; 90: 1401-6*). In the past, the same effect had also been observed in DU patients treated with a vagotomy. This led to our hypothesis that acid suppressive maintenance therapy may increase the risk for atrophic gastritis (see Am J Gastroenterol 1995; 90: 1401-6, or Aliment Pharmacol Ther 1995; 9: 331-40*). For that purpose, we evaluated the development of atrophy in our cohort of GERD patients treated with omeprazole. As pointed out in our NEJM paper, the H. pylori negative GERD patients had an annual rate of atrophy development (0.8%) that was very low and not significantly differed from our Amsterdam volunteer population of the same age not treated with omeprazole (0.3% ; Lancet 1995; see above). However, the H. pylori positive omeprazole treated GERD patients had indeed a high rate of atrophy development (6.1%), which significantly differed from the 1.8% found in our Amsterdam volunteer population of the same age not treated with omeprazole (Lancet 1995; see above). At this rate, it did not take 20 years, but only 5 years for atrophy to develop in 1 out of every 3 infected subjects! We presented these data on the 1995 AGA meeting in San Diego and submitted them to the NEJM, including the comparison with the Lancet - Amsterdam cohort of subjects without specific disease or treatment. The main comment we received, was that, although both cohorts were from the same city and had comparable mean ages, we could not exclude the possibility that GERD by itself increased the chance for atrophy development. For that reason, we then made another comparison with the Swedish fundoplication cohort, again showing that H. pylori negatives did not differ whether treated with omeprazole, fundoplication, or nothing at all (Amsterdam - Lancet cohort), whereas in H. pylori positives the acid suppressive therapy significantly increased the rate of atrophy. This hypothesis receives further strong support from a comparison with all data from other histological cohort follow-ups. I refer for this comparison to the graphical display of these data as presented in the Am J Gastroenterol 1995; 90: 1401-6*. The new data published in the NEJM fit very well the data presented in this graph.
Thus, the point of our paper is that H. pylori causes gastritis, which can lead to atrophy. The chance to develop atrophy is dependent upon the severity of gastritis. More than ten different short-term studies have now consistently shown that profound acid suppression increases gastritis activity and our NEJM study is the first long-term study on this topic. The data from this study strongly suggest that the permanently increased gastritis activity has important long-term implications. These data are supported by the other limited available cohort follow-up data as extensively discussed in the discussion of our paper.
This brings me to the specific points raised by Dr. Jacobson. First of all, this is indeed not a randomized study, although I do not see why this automatically without any specific arguments makes the comparison of dubious validity. As I already pointed out, the data do fit with those of other available cohort studies and they also do fit a plausible explanation for the effect of an increased development of atrophy. Therefore, the comparison may actually be very valid. The two populations are indeed from two countries (Sweden and the Netherlands), but it would serve the American reader to know that the distance between the two cities is about the same as the distance between San Francisco and San Diego within one state of the USA. Furthermore, both countries contain a largely caucasian population and are very similar with respect to socio-economic status, dietary, drinking and smoking habits, medication use, life expectancy and incidence of atrophic gastritis and gastric cancer. Baseline data of both cohorts are not incomplete, they are given in both the NEJM paper and in the two other papers that we refer to. Dr. Jacobson raises the need for randomized controlled studies. Although we agree with this need, the chance that they will ever be performed on this topic is close to nil, as no ethical committee will allow the randomization of GERD patients to medication or surgery.
A total of 137 Swedish patients was treated with a fundoplication cohort, yet only in one hospital were the biopsy specimens taken according to the same protocol as in our omeprazole treated patients. Therefore, we had to use only 72 of the 137 fundoplication patients. These did not significantly differ from the excluded patients.
The discussion then comes back to the comparison between the two cohorts. Dr. Jacobson states that he believes that H. pylori uninfected patients receiving omeprazole may still be at increased risk to develop atrophy. What can we say? We observed an approximately 10-fold higher chance for omeprazole treated GERD patients to develop atrophy in the presence of H. pylori compared to those who were not infected, and an even 35-fold higher chance to develop argyrophil cell hyperplasia. Furthermore, the rate of atrophy development was as low in the non-infected omeprazole treated GERD patients as it was in a non-treated non-GERD volunteer population (see Lancet publication). This is strong evidence against the belief of Dr. Jacobson and in favour of the safety of omeprazole maintenance treatment. Finally, we fully agree with Dr. Jacobson that the results can not be extrapolated to therapeutic efficacy. This is actually the last sentence of our paper, saying that 'it remains to be seen whether eradication therapy can prevent atrophy and argyrophil-cell hyperplasia'. This needs to be determined in future studies. Therefore, we suggest in our paper that at this time we should consider H. pylori eradication in H. pylori infected GERD patients requiring profound acid suppressive maintenance therapy.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
* Please submit any reprint requests to: Ms. Sylvia Band, e-mail address: gastrol@azvu.nl
Certainly, my statement that since this wasn't a randomized trial, any comparisons between the groups are of "dubious validity" was cavalier. My apologies.
The actual reason for using a surgically treated cohort in this study wasn't clear to me until I read your explanation of the previous objections to using a non-GERD group as controls. I am still concerned that comparing a surgically treated group from one country with a medically treated group from another country leaves room for significant differences which could affect the results. Although the demographics of Sweden and the Netherlands may be similar, can the same be said for the two cohorts studied here? I would have been more confident in the comparability of the two groups if I knew a little more about them -- say, number of diabetics, alcohol consumption, number of smokers and why the surgical group was referred for surgery. Were baseline vitamin B12 levels similar in both groups?
That acid suppression enhances susceptibility to H-Pylori associated atrophic gastritis is plausible, based on this study. I'm just not sure to what extent the degree of enhancement can be deduced without more evidence of the comparability of the two groups.
Date: Mon, 01 Jul 1996
From: Howard Homler MD <76212.32@compuserve.com>
Prilosec seemed too good to be true! Once the fear of inducing gastric carcinoid tumors quieted down, we really thought we had a wonder drug. The study reviewed here is a timely warning to avoid the cavalier use of proton pump inhibitors in our GERD patients. I would suspect that the incidence of chronic atrophic gastritis in H pylori infected individuals treated with H-2 blockers would be intermediate between the control group and the group treated with Prilosec...seem reasonable?
Dr. Kuipers (author of the paper) responds:
Date: Tue, 02 Jul 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
I fully agree that the hypothesis brought forward makes much sense. The data to support or refute it are however still very scarce. I am aware of two studies that claimed some increase of H. pylori associated body gastritis during H2-blocker and also during antacid therapy (Stolte et al. Ir J Med Science 1992; proceedings of the IVth (?) International meeting on H. pylori, respectively Lanza et al. Am J Gastroenterol 1994). However, there have been no cohort follow-up data published yet to show whether or not this effect would make any difference with respect to the development of atrophy. There has been one cross-sectional study (Penston et al. Aliment Pharmacol Therap 1990) that focused on long-term effectivity of 150-300 mg ranitidin maintenance treatment in DU patients and did not find atrophic gastritis at a single observation after five years of therapy. However, there is obviously a clear need for additional data, to address this issue.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
What about lansoprazole (prevacid)? In vitro, it is more active against H. pylori than omeprazole, but costs a bit more. For formulary consideration, I would keep omeprazole.
Dr. Kuipers' response:
Date: Tue, 13 Aug 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
With respect to lansoprazole, my reply is twofold:
1/ The effects of proton pump inhibitors on H.pylori are not exerted by the inactive prodrug that we prescribe, but by the activated sulphenamide form of the drug. This means that the PPI's first have to bind a proton before they have any effect on Hp. Such binding of a proton in the lab is obviously performed by acidifying the solution. In vivo however, this occurs predominantly within the vesicles of the parietal cell, where it is then immediately and irreversibly bound to the proton-pump. It is therefore on theoretical grounds very questionable whether PPI's have any significant anti-Hp effect in vivo. There are to my knowledge no data that prove otherwise. Patients can be treated with high dose PPI's for years and will not become Hp negative (in our recent NEJM study, we did not observe any patient to become Hp negative during 3-8 years omeprazole therapy for GERD). The important contribution of PPI's in Hp eradication therapies is particularly due to the acid suppressive effect. This is true for omeprazole, but also for lansoprazole and pantoprazole. Even though lansoprazole may have a greater in vitro antibacterial effect on Hp, the mechanism is still the same and we have to assume that the clinical importance of this antibacterial effect is minimal .
2/ Hp positive patients treated with lansoprazole do get exactly the same increase in corpus gastritis as observed during omeprazole therapy. With maintenance therapy, this does place them at risk for the development of atrophic gastritis and argyrophil cell hyperplasia just as with omeprazole therapy (see for instance Eissele et al. Gastroenterology 1996; 110 (4): A101 (abstract). As mentioned in our NEJM paper, the effect is associated with the level of acid suppression and not with the method by which the acid suppression is being achieved (e.g. it also occurs after vagotomy). Therefore, the same advice is to treat these patients with Hp eradication at the start of lansoprazole maintenance therapy.
With kind regards,
Sincerely,
Ernst Kuipers
Dr. Ernst Kuipers
kuipere@ctrvax.vanderbilt.edu
Vanderbilt University Medical Center
Department of Infectious Diseases
Letters to the Editor about this article from the NEJM site.
Helicobacter pylori infection causes chronic gastritis, which can lead to atrophic gastritis, itself a precursor of gastric cancer. Raising the gastric pH can alter or worsen chronic gastritis in patients infected with H. pylori, and can also raise gastrin levels, both of which favor atrophic gastritis. This study was designed to look at the interaction between H. pylori infection, omeprazole therapy and the development of atrophic gastritis.
Methods
The study compared gastric biopsies in two cohorts of patients with reflux esophagitis, one treated with omeprazole and one treated surgically with fundoplication.
The authors conclude that patients receiving prolonged acid-suppressive therapy with omeprazole who are also infected with H. pylori are at risk for developing atrophic gastritis. They imply that omeprazole-treated patients who are H. pylori negative, however, are not at increased risk for atrophic gastritis. They note that there are some differences between the two cohorts (the omeprazole group was 9 years older, on average). Nevertheless, they believe that these differences are not sufficient to explain the results of their study.
The data from the fundoplication cohort are incomplete (53 out of 137 were not analyzed because of an incomplete series of biopsy specimens). Because of the small numbers, we cannot conclude that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression.
The data from the omeprazole group are more complete, and the results do suggest that, in this group, patients infected with H. pylori are at significantly higher risk for developing atrophic gastritis than those who are not infected.
Because of the problems with comparing the two cohorts, I do not believe the data show that patients receiving omeprazole therapy who are not infected are not at increased risk for atrophic gastritis. Furthermore, it is not possible to extrapolate these results to therapeutic efficacy -- we don't know if antibiotic treatment will decrease the incidence of atrophic gastritis in these patients and thus make omeprazole therapy "safer".
This study is another one that adds to the growing number of reports indicating a significant pathogenetic role for H. pylori. Given its high prevalence in the upper age groups, treatment in order to prevent atrophic gastritis and gastric cancer would be an enormously expensive proposition. Targeted treatment of high risk groups (such as the acid-suppressed group examined here) needs to be investigated by randomized trials.
June 24, 1996
The authors of this paper reply:We appreciate the attention and comments of Dr. Jacobson made as contribution to this journalclub on our recent paper in the NEJM. We would like to use the opportunity to address the issues raised by Dr. Jacobson in his comments.
Dr. Jacobson states that we can not conclude from our data that H. pylori infection is not associated with atrophic gastritis in the absence of acid-suppression. That is a valid statement, which however, with all due respect, is besides the point of our paper. The introduction of our paper actually starts with giving an overview of the strong association between H. pylori and atrophic gastritis, ending with the sentence that 'the development of atrophic gastritis induced by persistent H. pylori infection is an essential step in the cascade of events leading to gastric cancer' (NEJM 1996; 334: 1018*).
H. pylori causes chronic gastritis in virtually all infected individuals. In many of them, this persistent inflammation leads to ultimate development of multifocal atrophic gastritis. However, this is generally a very slow process. As pointed out in our discussion, various cohort follow-up studies described an annual increase in the prevalence of atrophy of approximately 1 - 3% annually. These studies were done both in developed countries (Finland, the Netherlands) and developing countries (Estonia, Colombia), but nevertheless had very concordant results. The first study that differentiated between H. pylori positive and negative subjects in its cohort, was our study from Amsterdam, showing an annual 0.3% increase of atrophy prevalence in uninfected compared to a significantly higher 1.8% in infected subjects (Lancet 1995; 345: 1525-8*). The point thus is that H. pylori is a very important factor in the process of development of atrophic gastritis, but that this process is slow. After 20 years of follow-up, approximately 1 out of 3 infected adults will have signs of atrophy.
The chance to develop atrophy is however dependent upon the severity of gastritis, which is determined by characteristics of the bacterial strain and of the infected host. We have recently shown that within the population of H. pylori infected subjects, those that are infected with a cagA positive strain have more active gastritis and a 2-fold higher chance to develop atrophy than those that are infected with a cagA negative strain (J Natl Cancer Inst 1995; 87: 1777-80*). This sheds new light on the observation that acid suppression also increases the severity of gastritis, in particular in the gastric body. This effect has consistently been observed by various research groups, including Dr. Logan from the UK (Gut 1995; 36: 12-6), Dr. Solcia from Italy (Scand J Gastroenterol 1994; 201: 28-34) and ourselves (Am J Gastroenterol 1995; 90: 1401-6*). In the past, the same effect had also been observed in DU patients treated with a vagotomy. This led to our hypothesis that acid suppressive maintenance therapy may increase the risk for atrophic gastritis (see Am J Gastroenterol 1995; 90: 1401-6, or Aliment Pharmacol Ther 1995; 9: 331-40*). For that purpose, we evaluated the development of atrophy in our cohort of GERD patients treated with omeprazole. As pointed out in our NEJM paper, the H. pylori negative GERD patients had an annual rate of atrophy development (0.8%) that was very low and not significantly differed from our Amsterdam volunteer population of the same age not treated with omeprazole (0.3% ; Lancet 1995; see above). However, the H. pylori positive omeprazole treated GERD patients had indeed a high rate of atrophy development (6.1%), which significantly differed from the 1.8% found in our Amsterdam volunteer population of the same age not treated with omeprazole (Lancet 1995; see above). At this rate, it did not take 20 years, but only 5 years for atrophy to develop in 1 out of every 3 infected subjects! We presented these data on the 1995 AGA meeting in San Diego and submitted them to the NEJM, including the comparison with the Lancet - Amsterdam cohort of subjects without specific disease or treatment. The main comment we received, was that, although both cohorts were from the same city and had comparable mean ages, we could not exclude the possibility that GERD by itself increased the chance for atrophy development. For that reason, we then made another comparison with the Swedish fundoplication cohort, again showing that H. pylori negatives did not differ whether treated with omeprazole, fundoplication, or nothing at all (Amsterdam - Lancet cohort), whereas in H. pylori positives the acid suppressive therapy significantly increased the rate of atrophy. This hypothesis receives further strong support from a comparison with all data from other histological cohort follow-ups. I refer for this comparison to the graphical display of these data as presented in the Am J Gastroenterol 1995; 90: 1401-6*. The new data published in the NEJM fit very well the data presented in this graph.
Thus, the point of our paper is that H. pylori causes gastritis, which can lead to atrophy. The chance to develop atrophy is dependent upon the severity of gastritis. More than ten different short-term studies have now consistently shown that profound acid suppression increases gastritis activity and our NEJM study is the first long-term study on this topic. The data from this study strongly suggest that the permanently increased gastritis activity has important long-term implications. These data are supported by the other limited available cohort follow-up data as extensively discussed in the discussion of our paper.
This brings me to the specific points raised by Dr. Jacobson. First of all, this is indeed not a randomized study, although I do not see why this automatically without any specific arguments makes the comparison of dubious validity. As I already pointed out, the data do fit with those of other available cohort studies and they also do fit a plausible explanation for the effect of an increased development of atrophy. Therefore, the comparison may actually be very valid. The two populations are indeed from two countries (Sweden and the Netherlands), but it would serve the American reader to know that the distance between the two cities is about the same as the distance between San Francisco and San Diego within one state of the USA. Furthermore, both countries contain a largely caucasian population and are very similar with respect to socio-economic status, dietary, drinking and smoking habits, medication use, life expectancy and incidence of atrophic gastritis and gastric cancer. Baseline data of both cohorts are not incomplete, they are given in both the NEJM paper and in the two other papers that we refer to. Dr. Jacobson raises the need for randomized controlled studies. Although we agree with this need, the chance that they will ever be performed on this topic is close to nil, as no ethical committee will allow the randomization of GERD patients to medication or surgery.
A total of 137 Swedish patients was treated with a fundoplication cohort, yet only in one hospital were the biopsy specimens taken according to the same protocol as in our omeprazole treated patients. Therefore, we had to use only 72 of the 137 fundoplication patients. These did not significantly differ from the excluded patients.
The discussion then comes back to the comparison between the two cohorts. Dr. Jacobson states that he believes that H. pylori uninfected patients receiving omeprazole may still be at increased risk to develop atrophy. What can we say? We observed an approximately 10-fold higher chance for omeprazole treated GERD patients to develop atrophy in the presence of H. pylori compared to those who were not infected, and an even 35-fold higher chance to develop argyrophil cell hyperplasia. Furthermore, the rate of atrophy development was as low in the non-infected omeprazole treated GERD patients as it was in a non-treated non-GERD volunteer population (see Lancet publication). This is strong evidence against the belief of Dr. Jacobson and in favour of the safety of omeprazole maintenance treatment. Finally, we fully agree with Dr. Jacobson that the results can not be extrapolated to therapeutic efficacy. This is actually the last sentence of our paper, saying that 'it remains to be seen whether eradication therapy can prevent atrophy and argyrophil-cell hyperplasia'. This needs to be determined in future studies. Therefore, we suggest in our paper that at this time we should consider H. pylori eradication in H. pylori infected GERD patients requiring profound acid suppressive maintenance therapy.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
* Please submit any reprint requests to: Ms. Sylvia Band, e-mail address: gastrol@azvu.nl
Certainly, my statement that since this wasn't a randomized trial, any comparisons between the groups are of "dubious validity" was cavalier. My apologies.
The actual reason for using a surgically treated cohort in this study wasn't clear to me until I read your explanation of the previous objections to using a non-GERD group as controls. I am still concerned that comparing a surgically treated group from one country with a medically treated group from another country leaves room for significant differences which could affect the results. Although the demographics of Sweden and the Netherlands may be similar, can the same be said for the two cohorts studied here? I would have been more confident in the comparability of the two groups if I knew a little more about them -- say, number of diabetics, alcohol consumption, number of smokers and why the surgical group was referred for surgery. Were baseline vitamin B12 levels similar in both groups?
That acid suppression enhances susceptibility to H-Pylori associated atrophic gastritis is plausible, based on this study. I'm just not sure to what extent the degree of enhancement can be deduced without more evidence of the comparability of the two groups.
Date: Mon, 01 Jul 1996
From: Howard Homler MD <76212.32@compuserve.com>
Prilosec seemed too good to be true! Once the fear of inducing gastric carcinoid tumors quieted down, we really thought we had a wonder drug. The study reviewed here is a timely warning to avoid the cavalier use of proton pump inhibitors in our GERD patients. I would suspect that the incidence of chronic atrophic gastritis in H pylori infected individuals treated with H-2 blockers would be intermediate between the control group and the group treated with Prilosec...seem reasonable?
Dr. Kuipers (author of the paper) responds:
Date: Tue, 02 Jul 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
I fully agree that the hypothesis brought forward makes much sense. The data to support or refute it are however still very scarce. I am aware of two studies that claimed some increase of H. pylori associated body gastritis during H2-blocker and also during antacid therapy (Stolte et al. Ir J Med Science 1992; proceedings of the IVth (?) International meeting on H. pylori, respectively Lanza et al. Am J Gastroenterol 1994). However, there have been no cohort follow-up data published yet to show whether or not this effect would make any difference with respect to the development of atrophy. There has been one cross-sectional study (Penston et al. Aliment Pharmacol Therap 1990) that focused on long-term effectivity of 150-300 mg ranitidin maintenance treatment in DU patients and did not find atrophic gastritis at a single observation after five years of therapy. However, there is obviously a clear need for additional data, to address this issue.
Ernst J. Kuipers, M.D., Ph.D.
Dept. of Gastroenterology, Free University Hospital, Amsterdam, The Netherlands
Vanderbilt University School of Medicine, Nashville, TN
E-mail: kuipere@ctrvax.vanderbilt.edu
What about lansoprazole (prevacid)? In vitro, it is more active against H. pylori than omeprazole, but costs a bit more. For formulary consideration, I would keep omeprazole.
Dr. Kuipers' response:
Date: Tue, 13 Aug 1996
From: kuipere@ctrvax.Vanderbilt.Edu (Ernst Kuipers)
With respect to lansoprazole, my reply is twofold:
1/ The effects of proton pump inhibitors on H.pylori are not exerted by the inactive prodrug that we prescribe, but by the activated sulphenamide form of the drug. This means that the PPI's first have to bind a proton before they have any effect on Hp. Such binding of a proton in the lab is obviously performed by acidifying the solution. In vivo however, this occurs predominantly within the vesicles of the parietal cell, where it is then immediately and irreversibly bound to the proton-pump. It is therefore on theoretical grounds very questionable whether PPI's have any significant anti-Hp effect in vivo. There are to my knowledge no data that prove otherwise. Patients can be treated with high dose PPI's for years and will not become Hp negative (in our recent NEJM study, we did not observe any patient to become Hp negative during 3-8 years omeprazole therapy for GERD). The important contribution of PPI's in Hp eradication therapies is particularly due to the acid suppressive effect. This is true for omeprazole, but also for lansoprazole and pantoprazole. Even though lansoprazole may have a greater in vitro antibacterial effect on Hp, the mechanism is still the same and we have to assume that the clinical importance of this antibacterial effect is minimal .
2/ Hp positive patients treated with lansoprazole do get exactly the same increase in corpus gastritis as observed during omeprazole therapy. With maintenance therapy, this does place them at risk for the development of atrophic gastritis and argyrophil cell hyperplasia just as with omeprazole therapy (see for instance Eissele et al. Gastroenterology 1996; 110 (4): A101 (abstract). As mentioned in our NEJM paper, the effect is associated with the level of acid suppression and not with the method by which the acid suppression is being achieved (e.g. it also occurs after vagotomy). Therefore, the same advice is to treat these patients with Hp eradication at the start of lansoprazole maintenance therapy.
With kind regards,
Sincerely,
Ernst Kuipers
Dr. Ernst Kuipers
kuipere@ctrvax.vanderbilt.edu
Vanderbilt University Medical Center
Department of Infectious Diseases
Letters to the Editor about this article from the NEJM site.
نقش تغذيه در بيماريها عفوني را مجموعا به چهار گروه مي توان تقسيم نمود:
1- تغذيه در رابطه با ايجاد بيماريهاي عفوني، شامل بيماريهاي گوارشي و مسوميت هاي غذايي ( بوتوليسم)، بيماريهاي روده اي مثل اسهال هاي ميکروبي و بيماريهاي عفوني سيستميک ( بروسلوز و تيفوئيد)
2- تغذيه در بيماران عفوني ( محدوديتها و ممنوعيتها)
3- درمان سوء تغذيه به عنوان عارضه بيماريهاي عفوني
4- تغذيه در بيماران با نقص دفاعي شديد
تغذيه در رابطه با ايجاد بيماريهاي عفوني
قبل از اينکه وارد اين بحث شويم مقدمتا به مسئله مقاومت بدن در رابطه با غذا اشاره مي کنم که شايد در عامه مردم هم اين مسئله شناخته شده باشد که اگر غذاي کافي باشد، بيماري کمتر است يا به اصطلاح « دوايش ته ديگ است.»
در عصر قبل از آنتي بيوتيک ها، يکي از بيماريهاي کشنده بشر، سل بود که متاسفانه هنور هم هست، وقتي کسي مسلول مي شد او را به يک باشد.وش آب و هوا منتقل مي کردند و غذاهاي مقوي مي دادند درمان تقريبا به همين صورت انجام مي شد. شايد به همين جهت بيمارستان مسلولين و استراحتگاه آنها را جايي مي ساختند که فضاي کافي، هواي کافي، نور کافي و غذاي کافي داشته باشد. در کشورهاي فقير يکي از علل شايع مرگ و مير کودکان بيماريهاي روده اي و اسهال است فقر دانش، فقر اقتصادي و فقر بهداشتي در اين کشورها از عوامل مهم بيماريهاي جسماني، رواني و اجتماعي است. يعني فقر اقتصادي و غذايي و جهل ايجاد مي کند که پايه و اساس خيلي از بيماريهاي عفوني و واگير دار در اين کشورها هستند و مرگ و مير زيادي را به خصوص در اطفال به دنبال دارد.
اثر غذا در تکوين سيستم دفاعي انسان از دوره جنيني آغاز مي شود. يعني خانمي که حامله مي شود در واقع همان موقع تغذيه جنين او بايد جامع، کافي و حساب شده باشد. اگر در اين دوره به مادر پروتئين کافي، ويتامني کافي، املاح کافي از جمله آهن برسد بچه در همين دوره تکويني که معولا سه ماهه اول حيات است رشد لازم را پيدا مي کند. و اگر جنين رشد کافي کرده و جنين سالمي باشد وزن و اندازه طبيعي خواهد داشت. وزن طبيعي جنين معيار مهمي براي سلامتي اوست. و بعد از تولد تغذيه نوزاد با شير مادر شروع مي شود که هم ويتامين کافي و هم املاح کافي دارد و مي تواند ضامن رشد کودک باشد.
بنابراين سوء تغذيه از دوره تکامل جنيني نسل بشر نقش خودش را براي تمام عمر ابقا مي کند. اگر سيستم دفاعي کودکي در اين دوره رشد نکرده باشد. در تمام مراحل بعدي رشد نمي تواند در مقابل عوامل بيماري زا نقش دفاعي کافي داشته باشد. به خصوص ياد آوري مي کنم که دوره شير خوارگي دومين مرحله مهم است. تغذيه مناسب با شير مادر که داراي ويتامين و املاح کافي است رشد دفاعي کودک را تداوم مي بخشد. کودکي که سوء تغذيه دارد و پروتئين و ويتامين کافي به او نمي رسد مستعد بيماريهاي عفوني است و به واکسيناسيون ها هم جواب خوبي نمي دهد. بنابراين تغذيه مبناي مقاومت بشر در مقابل عوامل بيماري زاي محيطي است که اين عوامل محدود به بيماريهاي عفوني نيست و مي شود به ساير بيماريها هم تعميم داده شود. گر چه در حال حاضر بشريت مرفه از سوي تغذيه به گونه پر خوري و مصرف بيش از حد لازم رنج مي برد. بخش وسيع انسانهاي محرومي هم هستند که از کمبود تغذيه مورد نياز خود رنج مي برند. در مورد نقش تغذيه در ايجاد مقاومت در مقابله با بيماريهاي عفوني بررسي هاي زيادي انجام گرفته است مثلا ديده شده اگر به يک گروه غذاي کافي برسانيم و به گروه ديگري واکسن سل بزنيم آنهايي که تغذيه کافي مي شوند کمتر از آنهايي که واکسن زده اند به سل مبتلا مي شوند.
احتمال بروز سل در آنها که تغذيه کافي داشته اند و واکسن سل هم زده اند بسيار کمتر مي شود.
- نقش تغذيه در ايجاد بيماريها
غذا به عنوان منبع انرژي زاي بدن اگر دچار آلودگي هاي ميکروبي باشد مي تواند منشاء بيماريهاي مختلف و در راس آنها بيماريهاي گوارشي و مسموميت هاي غذايي باشد. ما در فصول مختلف در معرض مسموميت هاي مختلف غذايي هستيم. به خصوص زماني که هوا گرم مي شود ما شاهد بيماريهاي روده اي بيشتري هستيم که خطرناک ترين آنها « وبا» است. چنانچه در همين تهران، زهدان و در خيلي از کشورهاي جهان، به خصوص کشورهاي مرسوم به جهان سوم به طور موضعي شاهد بروز بيماري « وبا» هستيم.
مسموميت هاي غذايي هم در رابطه با غذاهاي مانده و آلوده بروز مي کنند. به دليل آنکه غذاها به طور بهداشتي تهيه نمي شوند و ما در مراکز توليد غذا و رستوران ها کنترل واقعي نداريم. يعني هر کس که بيکار مانده در زمينه تغذيه کار مي کند و خيلي ها از اصول بهداشت غذا آگاهي ندارند و برخي از آنها که از جنبه بيماريهاي انگلي که بررسي مي شوند بيش از يک انگل دارند و مي توانند آلودگي و بيماريهاي انگلي را از طريق دست به ديگران انتقال دهند. به عبارت ديگر هم در توليد مواد غذايي و هم در توزيع آن رعايت نکات بهداشتي را نمي کنيم. بسياري موارد مواد غذايي کنسور شده که خراب مي شوند از رده خارج نمي شوند که بسيار خطرناکند. همين طور کشک هايي که در ظرفهاي مخصوص نگهداري مي شوند اگر دچار فساد و آلودگي شوند مي توانند باعث بيماريهاي مهلکي مثل بوتوليسم که يک بيماري خطرناک و کشنده است، بشوند. تب روده يا تيفوييد يا حصبه هم يکي از بيماريهاي خطرناک است که از طريق آب و غذاي آلوده انتقال مي يابد و با توجه به مقاومت نسبت به آنتي بيوتيک که طي سالهاي اخير تکوين يافته است مشکلات زيادي را براي مبتلايان به همراه دارد. که از طريق آب و غذا انتقال مي يابد به ويژه نزد کودکان مي توانند سبب ايجاد اسال هاي شديد و بيماريهاي عفوني خطرناک شوند.
لازم به ذکر است حصبه به وسيله آب آلوده ايجاد مي شود و معمولا از بيمار به فرد ديگر انتقال پيدا مي کند و اگر چنين اتفاقي بيفتد مطلقا به دليل رعايت بهداشت است. نکته ديگر اينکه ديده شده به دليل باورهاي غلط مردم و حتي برخي از پزشکان و پرستاران بيماران تيفوييدي را چنان از خوردن غذا محروم مي کنند که منجر به سوء تغذيه شديد و مرگ آنها مي شود. مثلا مي گويند بيمار حصبه اي نبايد نان بخورد.
يکي از بيماريهاي مهمي که از طريق تغذيه مواد آلوده در ايران شيوع دارد تب مالت است. همان طور که مس دانيد تب مالت يک بيماري مشترک بين انسان و دام است. ميکرب تب مالت در گوسفند، بز، گاو، و در حيوانات ديگري مثل خوک و سگ مي توان ايجاد بيماري کند و انسان به طور اتفاقي در تماس با اين حيوانات و با مصرف مواد آلوده عمدتا غذايي که از شير نجوشيده تهيه شده باشد. ( مثلا پنير از شير نجوشيده به عمل مي آيد.) مبتلا مي شود.
معمولا پنير را بايد سه ماه در آب نمک نگه دارند و بعد توزيع کننده که اين اصل رعايت نمي شود به هر حال مصرف پنير آلوده سبب بيماري تب مالت در انسان مي شود. يکي از بيماريهاي مهمي که از طريق آب و مصرف غذاي آلوده براي انسان ايجاد شود اسهال هاي آميبي است که آن هم در تمام فصول وجود دارد و در غالب شهرها شيوع دارد. ولي در فصل تابستان شايع تر است. همين طور مصرف جگر نيم پز گوسفند منجر به بيماري « توکسوپلاسموز» مي شود که کيست انگل وارد معده انسان مي شود تحت تاثير اسيد معده باز مي شود و انگل آزاد مي شود و از طريق مخاط روده جذب و وارد کبد مي شود و وارد غدد لنفاوي مي شود. اگر خانم حامله اي فرضا دچار اين بيماري شود اين انگل خودش را به جنين مي رساند و در جنين ايجاد بيماري مغز و اعصاب مي کند و مي تواند منجر به گرفتاري مرکز عصبي حساس چشم و مغز شود که يکي از بيماريهاي ايجاد کننده سقط در زمان حاملگي است.
بيماري انگلي ديگري که از طريق تغذيه منتقل مي شوند کرمک است که در تمام کشورهاي متمدن و عقب مانده شيوع بسيار دارد و در بچه ها بيشتر از بالغين است.
بيماريهاي انگلي از نوع کرمهاي کدو و قلاب دار و نيز در رابطه با تغذيه ايجاد مي شود.
نقش تغذيه در بيماريهاي عفوني
جاي تاسف است که بگويم نه تنها عامه مردم دچار سوء برداشتهائي در مورد بيماريهاي تب دار مي باشند که خيلي از پزشکان و پرستاران هم تحت تاثير بد آموزيهاي سنتي ما قرار دارند. يعني مي شود يک چيز کلي را در مورد بيماران تب دار مطرح کرد. آن، اينکه بيمار تب دار به علت سوزاندن بيشتر انرژي نياز بيشتري به تامين انرژي دارد.
بيماري که تب دارد ممکن است به علت دردهاي گلو و دستگاه گوارش نتواند تغذيه مناسب داشته باشد و يا ممکن است به علت اختلال در هوشياري بيمار ما نتوانيم از راه دهان تغذيه مناسبي داشته باشيم.
متاسفانه يکي از نکاتي که هميشه فراموش مي شود در درجه اول تغذيه اين بيماران است. در حالي که از همان آب و الکتروليت که شروع مي کنيم، بايد فکر کنيم بيمار چقدر کالري احتياج دارد و اين کالري را محاسبه و تامين کنيم. و بعد به ازاء هر درجه تب حساب کنيم چقدر کالري و آب نياز دارد.
آنچه در عامه مردم مطرح است و بايستي بدانند اين است تفکرات غلط و نادرست گذشته درباره بيماريهاي تب دار به خصوص در حصبه را ياد آوري کنيم. اين طور رايج است که به بيمار حصبه اي نان نبايد داد. در حالي که اگر مي خواهيم بيمار بر بيماري غلبه کند بايد او را تقويت کنيم که گار اين کار را بکنيم حتي اگر دارو ندهيم بيمار بعد از يکي دو هفته خوب خواهد شد. پس مي توان گفت که چيزي که بيمار حصبه اي را از بين مي برد سوء تغذيه است يعني محروم کردن او از خوردن گوشت، نان وميوه که ممنوع کردن آن اصلا کار درستي نيست. بلکه بايد هر چه اشتهاي بيمار طلب مي کند در اختيارش بگذاريم. در سرماخوردگي ها هم يک چيز غير عملي رايج است و متاسفانه اگر ما پزشکان بگوييم هر چه بيمار دوست دارد بخورد و خدايي نخواسته اتفاقي بيفتد مي گويند طبيب مسئول است.
البته ما مي دانيم بعضي از مواد غذايي و ميوه هاي مثل خربزه و انگور محرک هستند و اگر بيماري حساسيت نشان بدهد و احيانا گلويش ناراحت بشود بهتر است نخورد. ولي به طور عام و از نظر علمي محدوديتي نداريم بيماري که سرماخورده بايد سبزي بخورد. مواد پروتئيني بخورد و موادغذايي و هيدروکربن هم مصرف کند . مگر اينکه بيماري خاصي مثل ديابت و يا اوره داشته باشد که توصيه مي کنيم مواد قندي و مواد گوشتي کمتر مصرف کند. يا در کودکان يا حتي بزرگسالان وقتي دچار اسهال مي شوند شايسته است شير مصرف نکنند. البته شير مادر در کودکان در زمان اسهال هم بلامانع است.
در رابطه با بيماران مزمن عفوني، مثلا مسلولين و بيماراني که دچار بيماري مزمن هستند و عفونت يک عارضه ثانويه در آنها است. مثلا بيماران سرطاني يا بيماراني که فلج هستند. کاهش قدرت عضلاني و لاغري آنها قبل از آن که مربوط به بيماري آنها باشد. مربوط به سوء تغذيه است. يعني بايد در هر شرايط غذاي کافي به آنها برسانيم.
درمان سوء تغذيه به عنوان بيماريهاي عفوني
در بيماريهاي عفوني دستگاههاي مختلف بدن انسان ويا در نتيجه توکسين ( سم) توليد شده توسط ميکروب در بدن و تاثير آن بر سيستم مغز و اعصاب و مرکز اشتها بيمار دچار کم اشتهايي و در نتيجه سوء تغذيه مي شود و يا عضو مبتلا به ويژه اگر دستگاه گوارش باشد منجر به سوء تغذيه مي شود به علاوه در بيماريهاي تب دار به علت مصرف بيش از حد کالري، ضعف و لاغري ايجاد مي شود. براي درمان اينها هر چه هست وظيفه ما جبران انرژي تحليل رفته و يا جبران کاهش وزن است. به همين منظور براي همه بيماران تغذيه را اصل قرار مي دهيم خيلي از مردم فکر مي کنند عامل بروز لاغري مصرف انواع آنتي بيوتيک هاست که کاملا نادرست است. آنتي بيوتيک براي درمان بيماري است. اگر فرضا براي ذات الريه آتني بيوتيک مصرف نشود احتمالا به مرگ او مي انجامد. واقعيت اين است که هر بيماري عفوني کاهش وزن ميدهد کاهش وزن باعث نقصان فعاليت سيستم دفاعي بيمار مي شود و يکي از علل شايع مرگ بيماران بروز عفونتهاي ثانويه ايست که در زمينه سوء تغذيه و کاهش مقاومت ايجاد مي شود.
مثلا در درمان کزاز گاهي شايد بيمار ار ده روز زير دستگاه تنفي مصنوعي بگذاريم تا فلج او از بين مي رود. و هوشيار مي شود به علت زير دستگاه بودن عفونت هاي ريوي مي کند که آن را هم درمان مي کنيم در نتيجه بيمار حدود دو ماه در اين شرايط زندگي مي کند و در اين مدت قوايش تحليل رفته و غذاي مناسب به او نرسيده اگر عفونت کند به علت سوء تغذيه شديد است و ممکن است نتوانيم کاري کنيم.
در بيماريهاي مزمن تغذيه کليد درمان است و با يد به اين شاه کليد توجه داشته باشيم و پروتئين راس همه غذاها است و بعد ويتامين کافي، املاح کافي، هيدروکربن کافي، براي اينکه بيمار مبتلا به بيماري مزمن را زودتر حرکت دهيم بايد از نظر غذايي کمک کنيم و شايد لازم باشد به جاي سه وعده غذا هر سه ساعت يکبار غذا بدهيم.
وقتي صحبت از نقص دفاعي شديد مي کنيم. بيشتر عفونت پذيري مورد نظرمان است. ممکن است در حال عادي غذايي سمي کنسرو ( نيمه کنسرو) را بخوريم و دچار بيماري عفوني نشويم ولي در شرايطي که دچار نقص دفاعي شديدي باشيم اگر از همين غذا بخوريم ممکن است دچار بيماري شويم. در بيماران با نقص دفاعي شديد به خصوص آنها که گلبول هاي سفيدشان زير 1000 يا کمتر از آن است تاکيد مي کنيم از غذاي خام استفاده نکنند و ميوه جات را با آنکه ويتامين دارند به دليل آنکه پخته نيستند و مي توانند ميکروب را انتقال بدهند توصيه مي کنيم به صورت کمپوت مصرف کنند. و در دوراني که گلبول هاي سفيد زير 1000 است از مصرف خشکبار خودداري کنند. مصرف آب آشاميدني هم در اين موارد مهم است. البته به محض آنکه گلبولهاي آنها به بالاي 2000 و 3000 رسيد مي توانند از مواد خام هم به طور طبيعي استفاه کنند.
در پايان جا دارد که از بالانس مثبت انرژي، يعني پرخوري هم که الآن يک بيماري شايع در جوامع بشري به خصوص در جوامع مرفه تمام کشورهاي جهان است صحبتي داشته باشيم. متاسفانه چيزي که امروز به آن توجه نمي شود زيان هاي پرخوري و مصرف بيش از حد انرژي است.
واقعيت اين است تمام افراد چاق بالقوه ديابتيک هستند و تمام افراد ديابتيک بالقوه عفونت پذيرند. بنابراين عفونت نزد افراد چاق خطرناک است يک ذات الريه نزديک آدم چاق بيشتر باعث مرگ مي شود تا يک آدم با وزن مناسب بنابراين تاکيد مي کنم پرخوري مازاد بر انرژي لازم و چاقي يکي از بلاهاي مهمي است که بشر را تهديد مي کند. در بيماريهاي قلبي و عروقي نقش مهمي دارد.
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مرور سینوزیت
سینوزیت
آیا تا بحال به سرماخوردگی یا حساسیت شدیدی دچار شده اید که به مدت زیادی طول کشیده و بهبود نمی یابد؟ اگر چنین بوده احتمالاً دچار سینوزیت شده اید.
این بیماری از بیماریهای شایع است و از آنجا که تعدادی از موارد بیماری با سرماخوردگی یا حساسیت اشتباه گرفته می شود و فرد به پزشک مراجعه نمی کند، شیوع آن بیشتر از مواردی است که تشخیص داده می شود.
برای اینکه شما در مراحل اولیه بیماری متوجه ابتلای خود به سینوزیت شوید باید به سؤالات زیر پاسخ دهید. اگر به ۳ مورد سؤالات پاسخ « بله » دارید، احتمالاً مبتلا به سینوزیت شده اید و باید به پزشک مراجعه کنید. علت سینوزیت می تواند از عفوت با باکتری، قارچ و یا التهاب در نتیجه حساسیت باشد ولی در هر صورت مراجعه به پزشک ضروری است.
۱- آیا با فشار بر روی گونه های خود دچار درد می شوید؟
۲- آیا از سر درد رنج می برید ؟
۳- آیا دچار گرفتگی و احتقان بینی شده اید؟
۴- آیا ترشحات بینی شما غلیظ و برنگ زرد – سبز می باشد ؟
۵- آیا مبتلا به تب خفیف ( ۸/۳۷-۲/۳۷ ) می باشید ؟
۶- آیا تنفس شما بد بو شده است ؟
۷- آیا در دندانهای بالائی خود احساس درد می کنید ؟
همانطور که گفته شد اگر به ۳ مورد جواب مثبت بود باید به پزشک مراجعه کرد تا احتمال ابتلا به سینوزیت بررسی شود .
سینوزیت چیست ؟
سینوزیت حاد باکتریائی، عفونت حفرات سینوس است که به باکتری آلوده شده اند. این بیماری معمولاً در پی یک سرماخوردگی ، حملات حساسیت و با تحریک توسط آلوده کننده های محیطی ایجاد می شود و بر خلاف سرماخوردگی و یا حساسیت ، تشخیص و درمان سینوزیت با پزشک بوده و به آنتی بیوتیک نیاز دارد. تا هم عفونت درمان شده و هم از ایجاد عوارض بعدی جلوگیری شود.
در حالت عادی ترشحات داخل سینوسها به درون فضای بینی تخلیه می شود و در هنگام ابتلا به سرماخوردگی و یا حساسیت ، سینوسها ملتهب شده و در تخلیه ترشحات خود دچار مشکل می شوند که این قضیه می تواند باعث احتقان و سپس عفونت سینوس شود. تشخیص سینوزیت حاد پس از معاینه و پرسشهای پزشک در مورد علائم شما داده می شود ممکن است از عکس رادیولوژیک سینوسها و گاهی نمونه ترشحات سینوس شما برای آزمایش وجود باکتری در آن استفاده شود.
چه موقع سینوزیت حاد تبدیل به سینوزیت مزمن می شود ؟
اگر فرد بطور مکرر مبتلا به سینوزیت حاد شود و یا عفونت سینوس او برای مدت ۳ ماه یا بیشتر باقی بماند ممکن است به سینوزیت مزمن تبدیل شود. علائم سینوزیت مزمن ممکن است خفیف تر از نوع حاد باشد ولی عدم درمان سینوزیت مزمن می تواند باعث آسیب و تخریب سینوسها و استخوان گونه شود که گاهی ترمیم آن نیاز به جراحی خواهد داشت.
سيـنوزيت(sinusitis) بـه عـفـونـت، التـهـاب و تـورم مـخـاط يـك يـا تـمام سينوسهاي مجاور بيني اطلاق ميگردد.
سينوسهاي مجاوربيني(paranasal sinuses):
حفره هاي توخالي و پـر از هـوايي هستـنـد كـه در مـيان استخوانهاي صورت و جمجمه قرار گرفته و با حفره بيني در ارتباط مي بـاشنـد.
در هـر طــرف صورت ۴ عدد سينوس وجود دارد كه عبارتند از:
۱- سينوسهاي فكي (maxillary sinuses):در زير چشمها و در استخوان گونه واقع ميباشند.
۲- سينوسهاي پيشاني(frontal sinuses):در بالاي چشمها و در استخوان پيشاني واقع ميباشند.
۳-سينوسهاي اتموئيد و يا پرويزني(ethmoid sinuses):بين چشمها و بيني و در استخوان پرويزني واقع ميباشند.
۴- سينوسهاي شب پره اي(sphenoid sinuses):در پشت سينوس پرويزني و چشمها و در مركز استخوان جمجمه زير غده هيپوفيز واقع ميباشند.
پيدايش و رشد سينوسها:
۱-سينوسهاي پيشاني تا سن ۵-۱۰ سالگي وجود ندارند. اين سينوسها از سن ۷ سالگي به بعد پديد مي آيند.
۲-سينوسهاي فكي و پرويزني از بدو تولد وجود داشته و تا ۱۸ سالگي به رشد خود ادامه مي دهند.
۳-سينوسهاي شب پره اي در سنين بلوغ ظاهر مي گردند.
وظايف سينوسها:
۱-سبك شدن استخوان جمجمه و استخوانهاي صورت.
۲-افزايش رزونانس (تشديد) صداي انسان.
۳-ايجاد يك بافر (ضربه گير) در برابر ضربات وارده به سر و صورت.
۴-مرطوب و گرم كردن هواي تنفسي.
۵-تصفيه هواي تنفسي.
۶-عايق بندي ساختارهاي حساس از قبيل ريشه دندانها و چشمها در برابر نوسانات سريع دمايي حفره بيني.
نكته:سينوسهاي مجاور بيني توسط سوراخهاي ريزي بنام(ostium/ostia) به حفره بيني مرتبط مي باشند. توسط اين روزنه ها(مجاري) تبادل هوايي صورت گرفته و ترشحات سينوسها تخليه ميگردد.
نكته:موكوس(mucus) يك ترشح لغزنده مخاطي است. موكوس يك كلوئيد چسبناك و غليظ كه حاوي آنزيمهاي آنتي باكتريال نظير ليزوزيم و پادتنها (ايمنوگلوبينها) است. موكوس بطور طبيعي سفيد و يا بي رنگ است.
وظايف موكوس در سيستم تنفسي عبارت است از:
مقابله با عوامل ميكروبي و محافظت از ششها با به دام انداختن ذرات خارجي كه همراه با هواي تنفسي وارد بيني ميگردند.
نكته:بطور طبيعي مخاط سينوسها و بيني از مژكهاي ميكروسكوپي موسوم به سيليا (cilia) پوشيده شده است. اين مژكهاي ضرباندار با حركات ريتميك به سمت عقب و جلو به مانند يك جاروب ميكروسكوپي موكوس، ميكروبها، ذرات محرك، گردو غبار و مواد حساسيت زا را به دام انداخته و به سمت سوراخهاي بيني و يا پشت حلق و معده مي رانند.
نكته: آب و هواي سرد باعث ميگردد فعاليت مژك هاي مخاط بيني و سينوسها كاهش يافته و يا كاملا متوقف گردند. اين امر باعث آبريزش بيني ميشود. همچنين موكوس در هواي سرد غليظ ترميشود، از اينرو هنگامي كه شما از هواي آزاد به داخل منزل مي آييد، موكوس رقيق تر شده و مجددا دچار آبريزش بيني ميگرديد.
نكته:استعمال سيگار و آلودگي هوا ميتوانند حركات مژكها را مختل و يا متوقف سازند.
نكته: به هر علت كه مخاط سينوسها ملتهب شود، سبب مسدود شدن منافذ (راه هاي ارتباطي) ميان سينوسها و بيني ميگردد. احتباس هوا، موكوس و چرك باعث ايجاد فشار به ديواره سينوسها ميگردد.
همچنين وقتي هوا نميتواند وارد سينوسها شود، خلاء ايجاد شده ايجاد درد خواهد كرد. انسداد راههاي ارتباطي موكوس (ترشحات سينوسها) را به يك محيط مستعد براي رشد ميكروبها تبديل ميكند.
انواع سينوزيت:
۱-سينوزيت فكي:باعث ايجاد درد و احساس فشار در گونه ها ميشود (دندان درد و سردرد)
۲-سينوزيت پيشاني: باعث ايجاد درد و احساس فشار در بالاي چشمها ميشود(سردرد)
۳-سينوزيت پرويزني: باعث ايجاد درد و احساس فشار بين بيني و چشمها ميشود(سردرد)
۴-سينوزيت شب پره اي: باعث ايجاد درد و احساس فشار پشت چشمها ميشود.
سينوزيت حاد:
سينوزيت حاد بين ۲ تا ۴ هفته بطول مي انجامد. سينوزيت حاد عمدتاً در پي سرما خوردگي و آنفلوآنرا بروز ميكند.
عفونت اوليه به مخاط سينوسها هجوم آورده و ايجاد التهاب در آنها مي كند. بدن شما با توليد بيشتر موكوس به اين هجوم ويروسها پاسخ مي دهد.
افزايش موكوس سبب ميگردد كه دهانه سينوسها تنگ و يا مسدود شود. در نتيجه احتباس ترشحات و ميكروبها روي ميدهد. تجمع اين ترشحات محيط مساعدي براي رشد و تكثير ميكروبها فراهم مي آورد (چراكه با جريان طبيعي تخليه نشده اند).
در مجاري فوقاني تنفسي باكتريهاي بي ضرري وجود دارند، اما هنگامي كه سيستم ايمني بدن تضعيف ميگردد، و يا تخليه سينوسهاي مسدود شده (در پي سرماخوردگي و يا عفونتهاي ويروسي) مختل مي شود ،اين باكتريها بسرعت تكثير يافته و به سينوسها هجوم مي آورند.
گاه عفونتهاي قارچي نيز ميتوانند ايجاد سينوزيت حاد كنند. چنانچه علايم سرماخوردگي بيش از يك هفته باقي بماند ممكن است به سينوزيت تبديل شده باشد.
سينوزيت مزمن:
سينوزيت وقتي بيش از ۴ هفته تداوم مي يابد مزمن شده است. سينوزيت مزمن ممكن است تا سالها گريبانگير بيمار شود. عموماً توسط عوامل آلرژي زا و عفونتهاي باكتريايي ايجاد ميشود. آسم و اختلالات آلرژيك مزمن عموماً باعث ايجاد سينوزيت مزمن ميگردند. ۲۰ درصد از بيماران مبتلا به سينوزيت مزمن به پوليپ بيني نيز مبتلا ميشوند.
سينوزيت عود كننده:
بيمار چندين حمله سينوزيتي را در طي سال تجربه ميكند. حملات بر اثر واكنش آلرژيك، تغييرات دمايي شديد (هواي خيلي سرد و خشك و يا خيلي گرم)، مو و شوره سر حيوانات، گرده گياهان، مايت ها، دود سيگار و گرد و غبار ايجاد ميگردند.
عوامل ايجاد كننده سينوزيت:
۱-آلرژي ها: با متورم و مسدود ساختن راههاي ارتباطي و دهانه سينوسها و جلوگيري از تخليه سينوسها. حساسيت ميتواند به گرده گياهان، مايت ها، شوره سر حيوانات، كپك ها، گرد و غبار و يا غذاها باشد.
۲-عفونتهاي ويروسي:آنفلوآنزا و سرماخوردگي باعث التهاب مخاط سينوسها و تورم آنها شده و با افزايش ترشح موكوس موجب انسداد روزنه ها مي شوند. در ۳ درصد بالغين و ۲۰ درصد كودكان، سرماخوردگي به عفونت باكتريايي ثانويه و سينوزيت خواهد انجاميد.
۳-عفونت هاي باكتريايي: باكتريهايي كه بطور طبيعي در مجاري تنفسي فوقاني بسر ميبرند وقني سيستم ايمني بدن تضعيف شده و يا تخليه سينوسها بدرستي صورت نميگيرد، باكتريهاي محبوس شده تكثير يافته و ايجاد عفونت ميكنند.
۴-پوليپ هاي بيني: پوليپ رشد خوش خيم بافت مخاطي بيني است. پوليپ بيني در افراد مبتلا به آلرژي و آسم شايع ميباشد. پوليپ ها ميتوانند دهانه سينوسها را مسدود سازند.
۵-عفونتهاي قارچي:عمدتاً به علت تضعيف سيستم ايمني بدن پديد مي آيند. عفونتهاي قارچي بيشتر در افراد مبتلا به آسم مشاهده شده و بيشتر سينوسهاي فكي را درگير مي كنند.
۶-ناهنجاريهاي ساختار بيني: انحراف تيغه بيني و بزرگ بودن شاخك هاي بيني ميتوانند منافذ سينوسها را مسدود سازد.
۷-آلودگي هوا: هواي آلوده معمولاً از ذرات مولكولي بزرگ تشكيل يافته اند كه در مخاط گير افتاده و ممكن است واكنش آلرژيك و التهاب مخاط را سبب گردند.
۸-شنا كردن:شنا كردن در آب حاوي كلر باعث ميشود مژك هاي مخاط بيني و سينوسها تضعيف شده و تخليه ترشحات به خوبي صورت نگيرد. همچنين كلر باعث التهاب مخاط بيني ميشود و فرد را مستعد عفونت باكتريايي ميكند.
۹-سيگار كشيدن: دود سيگار حركت طبيعي مژك ها را كند و يا متوقف ميسازد.تجمع موكوس نيز ايجاد عفونت و ترشح پشت حلق ميكند.
۱۰-اختلالات ضعف ايمني بدن نظير بيماريهاي ايدز و فيبروز سيستيك.
۱۱-عفونت دندانها: انتشار عفونت دندانهاي آسياي فك بالا نيز ميتواند باعث سينوزيت فكي گردد.
علايم سينوزيت:
۱-احساس درد و يا فشار در پيشاني، گيجگاه ها، گونه ها، بيني، پشت و يا دور چشم ها.
۲-تنفس از راه بيني دشوار ميشود.
۳-تخليه ترشحات غليظ، زرد و يا سبز رنگ از بيني و يا پشت حلق.
۴-كاهش حس بويايي و چشايي.
۵-گرفتگي و احتقان بيني، آبريزش بيني.
۶-درد در فك فوقاني و يا دندانهاي آرواره بالا.
۷-سر درد هنگام برخاستن از خواب كه با خم شدن به طرف جلو بدتر ميشود.
۸-بوي بد دهان.
۹-گوش درد-احساس گرفتگي گوشها.
۱۰-خستگي.
۱۱-سرفه (در هنگام شب تشديد ميشود)، گلو درد.
۱۲-حالت تهوع و استفراغ.
۱۳-علايم سرماخوردگي اي كه به درمان پاسخ نميدهند.
۱۴-درد و تورم در ناحيه صورت.
۱۵-احساس سنگين بودن سر.
علايم سينوزيت هاي خاص:
۱-سينوزيت فكي: درد در فك بالا و دندانهاي فك فوقاني-گونه ها حساس به لمس مي شوند.
۲-سينوزيت پيشاني: لمس و فشار اندك به پيشاني ايجاد درد ميكند.چشم ها حساس به نور ميشوند.
۳-سينوزيت شب پره اي: گوش درد، گردن درد، درد در عمق سر.
۴-سينوزيت پرويزني: تورم پلك ها و درد در ناحيه بين بيني و چشمها-حساسيت به لمس در دو طرف بيني-از دست رفتن حس بويايي .
موارد زير ريسك ابتلا به سينوزيت را در شما افزايش مي دهد:
۱-آلرژي ها.
۲-علايم سرماخوردگي و آنفلوآنزاي عود كننده.
۳-استرس.
۴-عفونتهاي باكتريايي و ويروسي مجاري تنفسي فوقاني.
۵-شنا كردن در استخر، شيرجه رفتن.
۶-استعمال سيگار و استنشاق دود سيگار.
۷-قرار گيري در معرض آلودگي هوا.
۸-هواي سرد و خشك.
۹-مصرف مشروبات الكلي.
۱۰-استفاده مكرر و طولاني مدت از قطره هاي ضد احتقان بيني.
۱۱-تغييرات سريع فشار هوا.
۱۲-ناهنجاريهاي ساختاري بيني-پوليپ بيني.
۱۳-كم آبي بدن.
۱۴-نگهداري از حيوانات خانگي.
اقدامات تشخيصي:
۱-معاينات بيني (آندوسكوپي بيني)
۲-سي تي اسكن و ام آر آي.
۳-تستهاي آلرژي.
۴-بيوپسي مخاط حفره بيني و سينوسها بمنظور شناسايي عوامل بيماريزاي باكتريايي.
درمان سينوزيت:
۱-داروهاي ضد درد از جمله آسپرين، استامينوفن، پاراستامول، ايبوپروفين براي تخفيف درد.
۲-آنتي بيوتيك ها: چنانچه علت سينوزيت عفونت باكتريايي باشد آنتي بيوتيك تجويز ميگردد. مدت درمان با آنتي بيوتيك ۳ تا ۱۲ هفته بطول مي انجامد. ( و يا تا يك هفته پس از ناپديد شدن علايم)
۳-كورتيكواستروئيدها: براي كاهش التهاب سينوسها تجويز ميشود. (بصورت اسپري و يا خوراكي)
۴-ضد احتقان ها و آنتي هيستامين ها: به اشكال خوراكي و يا افشانه تجويز ميگردند. آنتي هيستامينها ميزان ترشح موكوس را كاهش و يا متوقف ميكند. ضد احتقان ها نيز گرفتگي بيني را برطرف ميكنند. توجه داشته باشيد كه نبايد از ضد احتقان ها بيش از ۳ روز متوالي استفاده شود. چراكه پس از قطع آنها التهاب و تورم بيني افزايش خواهد يافت.
۵-رطوبت: استفاده از دستگاه بخور و رطوبت سازها روند تخليه سينوسها را تسهيل ميكند.
۶-شستشوي بيني: شستشوي بيني با سرم نمكي باعث رقيق شدن موكوس ميشود.
۷-درمان سرماخوردگي و آلرژي ها.
۸-مصرف فراوان مايعات. به ويژه مايعات گرم مانند چاي و سوپ. مايعات باعث رقيق شدن موكوس ميشود.
۹-استفاده از اسپري هاي ضد قارچ (به ندرت)
۱۰-قرار دادن كمپرس گرم و مرطوب بروي موضع درد به مدت ۵ تا ۱۰ دقيقه.
۱۱-استحمام و دوش آب گرم باعث شل شدن و رقيق شدن موكوس ميشود.
۱۲-عمل جراحي: چنانچه درمان دارويي موثر واقع نشود در موارد نادر بايستي عمل جراحي صورت گيرد.
اهداف عمل جراحي به قرار زير است:
- برداشتن بافت عفوني، متورم و آسيب ديده.
- برداشتن استخوان و يا غضروف اضافي بمنظور گشاد كردن منافذ سينوسها. (اصلاح ساختار تيغه و شاخك هاي بيني)
- برداشتن پوليپ.
- خارج كردن اجسام خارجي اي كه مجاري بيني و سينوسها را مسدود ساخته اند (در كودكان)
انواع جراحي سينوسها:
۱-جراحي سينوس به كمك آندوسكوپي (Endoscopic Sinus Surgery):
اين جراحي توسط آندوسكوپ صورت ميگيرد. بنابراين شكافي بروي بيني ايجاد نميگردد و تمام فرايند جراحي از طريق سوراخهاي بيني انجام ميگيرد.
۲-ساينوپلاستي (ballon sinuplasty):
ساينوپلاستي روش نويني است كه مشابه آنژيوپلاستي عروق ميباشد. قرار دادن يك بادكنك (بالن) و سپس باد كردن آن در حفره سينوس ها كه كمتر تهاجمي است، باعث گشاد شدن مجاري تنگ ميگردد.
نكته:از خم شدن به سمت جلو پرهيز كنيد، چراكه درد و احساس فشار تشديد ميشود.
نكته:هنگام فين كردن به آرامي اين كار را انجام دهيد.
نكته:تا ميتوانيد استراحت كنيد.
پيشگيري از سينوزيت:
۱-رعايت بهداشت: دست هاي خود را بطور منظم بشوييد. به ويژه قبل از غذا و پس از دست دادن با ديگران.
۲-عوامل آغازگر آلرژي را از محيط زندگي خود حذف كنيد. آلرژي را تحت كنترل در آوريد.
۳-علايم سرماخودرگي را فورا درمان كنيد.
۴-از استعمال سيگار، استنشاق دود سيگار و از هواي آلوده پرهيز كنيد.
۵-از دستگاه بخور و رطوبت ساز در خانه استفاده كنيد.
۶-حملات آسم را با حذف آغازگر هاي آن كنترل كنيد.
۷-از نوشيدن مايعات خيلي سرد پرهيز كنيد.
۸-بطور منظم ورزش كرده و فعاليت بدني داشته باشيد.
۹-از تماس با افرادي كه مبتلا به سرماخوردگي و يا عفونت ويروسي مجاري تنفسي فوقاني ميباشند ،اجتناب كنيد.
۱۰-از تغييرات دمايي شديد اجتناب كنيد. از هواهاي خيلي گرم و يا خيلي سرد نيز دوري كنيد.
۱۱-در منزل از دستگاه هاي تصفيه هوا استفاده كنيد.
۱۲-از مصرف مشروبات الكلي اجتناب ورزيد. الكل باعث تورم مخاط بيني و سينوسها ميشود.
۱۳-از شنا كردن و شيرجه رفتن پرهيز كنيد.
۱۴-از مصرف زياد لبنيات خودداري كنيد. مصرف بيش از حد لبنيات باعث غليظ شدن موكوس ميشود.
۱۵-از سفرهاي هوايي پرهيز كنيد. حداقل پيش از سفرهاي هوايي از قطره ضد احتقان استفاده كنيد.
۱۶-رطوبت منزل خود را كنترل كنيد. هواي خيلي خشك و يا خيلي مرطوب سينوزيت را تشديد ميكند.
۱۷-عطر و اودكلن نيز ميتوانند باعث تورم مخاط بيني گردند، بنابراين از آنها اجتناب كنيد.
۱۸-استرس خود را كنترل كنيد.
۱۹-حداقل روزي ۷ ليوان آب بنوشيد.
۲۰-هنگام خروج از منزل در فصول سرد سال، بوسيله شال و كلاه سينوسهاي خود را گرم نگه داريد.
۲۱-بمنظور برخورداري از سيستم ايمني قوي بايستي تغذيه مناسبي داشته باشيد.
عوارض سينوزيت:
نادر است اما ميتواند خطرناك باشد.
۱-عفونت استخوانهاي صورت(osteomyelitis)
۲-عفونت پرده هاي مغز، مننژيت(meningitis)
۳-انتشار عفونت به خارج سينوس و ايجاد آبسه در كاسه چشم، سر و يا نسوج صورت .
درمان سینوزیت
درمان سینوزیت باکتریائی باید با آنتی بیوتیک مناسب صورت گیرد. علاوه بر آنتی بیوتیک گاهی اسپرهای دهان و یا بینی . یا قطره های ضد احتقان ممکن است برای رفع احتقان تجویز شود، گرچه باید از مصرف اسپری بینی و قطره بدون تجویز پزشک به مدت طولانی خودداری کرد. همچنین تنفس در هوای مرطوب و شستشوی بینی با محلولهای استریل نیز می تواند مفید باشد.
گاهی بیمار به یک آنتی بیوتیک جواب نمی دهد.این بعلت مقاومت باکتری به این آنتی بیوتیک است که این پدیده درمان سینوزیت را مشکل می کند . بیماران می توانند با توجه به توصیه های پزشک از بروز این حالت جلوگیری کنند. اگر به هر دلیل برای شما توسط پزشک آنتی بیوتیکی تجویز شد، توجه داشته باشید که در تمام طول مدت تعیین شده باید آنتی بیوتیک را مصرف کنید و اگر پس از چند روز احساس بهبودی کردید، هرگز درمان خود را قطع نکنید چون این کار باعث ایجاد باکتریهای مقاوم می شود.
اما درمان سینوزیت مزمن کمی متفاوت است. گرچه گاهی آنتی بیوتیک درمانی شدید، برای آن انجام می شود ولی گاهی برای درمان نیاز به جراحی است تا انسداد ایجاد شده در مسیر سینوس رفع شود. علاوه بر جراحی باز، امروزه جراحی سینوس با کمک اندوسکوپ نیز میسر شده است. با این وسیله جراح می تواند مستقیماً داخل سینوس را مشاهده کند و همزمان هر عاملی که غیر طبیعی بنظر می رسد مثل بافت بیمار و یا پولیپ را برداشته و یا کانالهای باریک بین سینوسها را پاک کند.
پیشگیری
برای اینکه در هنگام ابتلا به سرماخوردگی و یا حملات حساسیت به سینوزیت دچار نشوید باید سینوسهای خود را در این مواقع مرتب پاک کنید و برای اینکار :
۱- از داروهای ضد احتقان خوراکی و یا قطره یا اسپری ضد احتقان بینی ( برای دوره کوتاه) استفاده کنید.
۲- مرتب فین کنید و بینی خود را از ترشحات پاکیزه کنید.
۳- مقادیر زیادی آب بنوشید تا ترشحات بینی شما رقیق بماند.
۴- از مسافرتهای هوائی در مواقع ابتلا به سرماخوردگی و حساسیت پرهیز کنید و اگر مجبور به این کار هستید از اسپری های ضد احتقان قبل از بلند شدن هواپیما استفاده کنید تا از انسداد سینوس و عدم تخلیه ترشحات آن جلوگیری شود.
۵- اگر مبتلا به حساسیت هستید از چیزهائی که باعث تحریک شما و شروع حساسیت و علائم آن
می شود اجتناب کنید و در صورت ابتلا به حساسیت از آنتی هیستامین و اسپری بینی برای کنترل آن استفاده کنید.
سینوزیت در کودکان
در کودکان تکامل سینوسها تا حدود ۲۰ سالگی ادامه دارد ولی کودکان نیز می توانند به سینوزیت مبتلا شوند. تشخیص سینوزیت در کودکان مشکل است زیرا عفونتهای تنفسی در آنها بسیار شایعتر بوده و همچنین علائم در کودکان می توانند خفیف بوده و تشخیص را مشکل کنند. علائم زیر در کودکان می تواند ناشی از سینوزیت بوده و باید در صورت مشاهده آنها به پزشک مراجعه کرد :
- سرماخوردگی که بیش از ۱۴-۱۰ روز طول کشیده و گاهی با تب خفیف همراه است
- ترشحات بینی غلیظ برنگ زرد – سبز
- ترشحات پشت حلق که گاهی باعث گلو درد ، تنفس بدبو،سرفه ، تهوع و یا استفراغ می شود.
- سردرد ( معمولاً زیر ۶ سال وجود ندارد )
- تحریک پذیری یا خستگی
- تورم اطراف چشم
اگر علیرغم درمان مناسب طبی این علائم پا برجا ماند، باید بدنبال پیدا کردن یک عامل
زمینه ای که باعث سینوزیت می شود، بود که در این میان باید حتماً حساسیت و عفونتهای مکرر تنفسی بعنوان عوامل زمینه ای در نظر گرفته شوند.
