Introduction: Clozapine has several major side-effects for example agranulocytosis. There are however several severe cardiac side-effects associated with the use of clozapine. We present two psychotic patients, who were treated with clozapine. One patient developed myocarditis and the other patient developed cardiomyopathy. These findings raised questions about the frequency of cardiac side-effects due to clozapine treatment. Objectives: Awareness of cardiotoxic side-effects of clozapine; Creation of a clinical guideline for myocarditis and cardiomyopathy in clozapine treatment Methods: Two case reports, one male 57 years, suffering from paranoid schizophrenia developing myocarditis, the other a female of 62 years also suffering from paranoid schizophrenia, developing cardiomyopathy during clozapine treatment are presented. Secondly, an extensive literature search with keywords: Myocarditis; cardiomyopathy, heartfaillure and clozapine has been performed. Results: The incidence of myocarditis and cardiomyopathy associated with clozapine use are possibly around 1 percent, 10-100 times higher than previously assumed. Conclusion: Myocarditis and cardiomyopathy are cardiac side-effects of clozapine use which are severe and have a possible fatal outcome. Diagnosis of namely myocarditis can be difficult. Research suggests that these side-effects might be less rare as thought of until recently. A clinical guideline for monitoring of these side-effects didn't really exist to this moment. A proposition for a clinical guideline has been made in this presentation consisting of namely: anamnestic findings laboratory tests and ECG controls. Awareness for myocarditis is especially necessary during the first 4 weeks of clozapine treatment.
The morphological changes of gastric mucosa taken from different areas has been studied in patients of approximately the same age with achlorhydria, extreme hypochlorhydria and normochlorhydria. The serum gastrin level and parietal cell antibodies were determined in the achlorhydric parietal cell antibodies were determined in the achlorhydric patients. In the latter the diffuse gastritis was localized in the corpus-fundic area, while the changes in the antral region were few and occurred mostly in the superficial zone. In normochlorhydric patients however, the diffuse gastritis was localized in the antral region, with only few changes at the corpus-fundic area. In patients with extreme hypochlorhydira either the fundic or the antral region was involved. Besides the diffuse gastritis intestinal metaplasia, pseudopyloric metaplasia, and atrophy of mucosa were also observed, although much less commonly. The increase of gastrin level could not be related to a definite morphological pattern in the gastric mucosa. It can be assumed that each of the two types of gastritis has a different natural history; the antral site of gastrititis cannot be transformed into the fundic site, nor can the fundic site be transformed into the antral site.
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