![[Thumbnail]](lsfig1.gif)
Click to
view 12k gif of WCC
This case arose when Mr. Schoenman and his physician noticed a fall in the white cell count after he was treated for his H.pylori. Mr Schoenman's case is somewhat imperfect in that proof of cure of H.pylori has not yet been done.
We realize that there is a tendency for under-reporting of negative case reports, therefore, we suggest the following rules for new cases of CLL who might wish to investigate their H.pylori status and report to this service;
When 10 cases have been reported here we will make a preliminary judgement as to the relevance of this possible association. In the meantime patients may correspond with Mr. Schoenman if he allows.
The editor (BJM) requests that Mr. Schoenman and others are especially sensitive in reporting or responding to this information. Remember that we are dealing with potentially fatal conditions and patients may be very disappointed if they do not have H.pylori, do not respond to antibiotics, or continue to gradually deteriorate from their CLL. Remember also that mere changes in the white cell count will not always reflect the status of the patient i.e. whether he/she is getting better or worse. Other aspects of the disease might be more important to the physician.
There is good evidence that some B-cell malignancies are caused by Helicobacter pylori (HP). Mucosa associated lymphoid tissue (MALT) lymphoma localized to the stomach is cured in 50% of patients after eradication of the associated HP infection (Isaacson 1993, Bayerdorffer et al 1994). CLL is a B-cell leukemia, usually low grade, associated with abnormal antibody production at times and with a presentation in some patients similar to lymphoma. This report describes partial remission of CLL in a patient with peptic ulcer who was treated with antibiotics for HP.
The CLL patient is a 59 year old Caucasian male, in otherwise good health, with only casual (normal) exposure to "toxic" materials. An extended period of treatment by injection for allergic rhinitis-post nasal drip was of limited benefit and terminated at the onset of CLL in 1990 (editor's note - many patients with CLL have lowered immunity and are susceptible to bacterial infections).
A peptic ulcer condition had been initially diagnosed by X-ray in 1984. The condition was periodic, possibly seasonable, and satisfactory controlled with Zantac over a 4 to 6 week period. On the average this repeated two to three times each year with the onset coinciding with periods of particularly severe post nasal drip. The combination of Zantac and antihistamine was the most effective.
CLL was first diagnosed during a routine physical in 1991 and confirmed by monoclonal blood tests, bone marrow biopsy and CAT scan. Only minor lymph node involvement was noted.
During the period between 1991 and 1995, the WBC, monitored from 4 to 8 times each year, rose from a pre 1989, 20 year mean of 5400, to a peak of 60,000. The trend was continuously up with four exceptions, three of which are noted as points A, B, and C on the attached chart ( Figure 1 ).
Each of the declines followed antibiotic treatments for unrelated illnesses of various types. Only some antibiotics were effective. Penicillin types produced no WBC reductions. During this entire period the patient recieved no treatment for the CLL.
The stomach ulcer condition became dormant in 1993 and has not been treated since. The WBC was in the 20,000 to 30,000 range at the time. The May 1995 test for the H.pylori was at the patient's request. The request was triggered by the published articles cited above, a family history of ulcers and G-I related cancer. The two prior temporary remission points, ("A" and "B"), followed administration of antibiotics that are commonly used in combinations, at much higher dosages, for the treatment of an HP infection.
The HP titer taken at point "C" on the chart was >10, which is off the measurement scale.
The HP was treated with metronidazole, tetracycline and bismuth for 14 days.
The WBC has been in exponential decay since the start of the HP treatment.
The slope closely follows the decay from point "B" which was a 5 day course of Zithromax (azithromycin).
Although too soon to make any firm conclusions, one HP titer (point D) taken 6 weeks after the treatment was complete, followed the direction of the WBC and is back within measurement standards [8.4]. This patient will continue to be monitored via CBC'S and for the presence of H.pylori. The results reported as new information is developed.
Possibilities This observation raises the possibility that in addition to MALT lymphoma CLL may also develop as a result of the extended durations of imune system stimulation by chronic bacteria induced infection.
Multiple confirmation of this observation is required
The authors recommend that other patients with CLL have their HP status evaluated as part of the blood work and that the response (good or bad) be posted on the HP forum. To be published*, we must be notified of the case before the diagnostic tests for HP are done. Patients treated for HP must be followed up to confirm cure with either breath test or biopsy (breath testsshould be widely available in 6 months).
This is the first of our cases of CLL. I hope that the patient can confirm cure of the HP infection with a breath test or show continuing downward trend in HP antibody level. I also hope that he continues to improve, perhaps to a cure. Regardless of the outcome, at least we may eventually be able to rule in or rule out CLL as a disease linked to HP.
For persons interested in the HP-CLL link suspected by this patient, remember that CLL usually occurs in persons over the age of 60 years and about 40% of these people could have HP, regardless of symptoms. We should observe the prevalence of HP in this condition but recognize that a control group will be difficult to collect. If we carry outtreatment trials then each patient can be his own control.
This case has several interesting aspects. The history of bacterial sinus infection (or allergy) associated with peptic ulcer relapse is not new to me and it is well known that ulcer patients are more susceptible to bronchitis and similar mucosal infections. They are also more likely to be blood group "O" and non-secretors of blood group antigens in mucus. Blood group "O" is more common in ulcer patients with HP (weak association) and it has been found that HP particularly likes to stick to blood group "O" red cells. The link with ulcers could be the defective mucosal immunity. predisposing to more active HP infections.
In any case, since CLL patients have problems with mucosal bacterial infections in general, it makes sense that they should have eradication of HP if there are any G.I. symptoms.
Return to Helicobacter Foundation Cancer Pages
Return to Dr. Marshall's Home Page