olanzapine has been researched along with Anemia* in 2 studies
2 other study(ies) available for olanzapine and Anemia
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Can atypical dysgeusia in depression be related to a deafferentation syndrome?
Atypical dysgeusia such as having the sensation of a sweet tooth is an uncommon clinical presentation in severe depression. First, we present the case of a 67 year-old-man admitted to the psychiatric ward for depression after a suicide attempt by drug ingestion. The patient manifested a sweet taste sensation in the upper and lower gums that increased with mood swings and notably with severe depressive symptoms. Blood tests showed an elevated serum creatinine level (115 μmol/L), a normocytic anemia (hemoglobin 6.5 mmol/L; MCV 96 fL) and a deficit in vitamin B12 (122.4 pmol/L). The patient received vitamin B12 supplementation and was treated with clomipramine, lithium, mirtazapine, modafinil, and olanzapine. He was discharged after improvement of his depressive symptoms and decrease in the sweet taste. On follow-up, the patient's dysgeusia had subsided. Second, we hypothesize that the atypical dysgeusia may have been induced by vitamin B12 deficiency and medical comorbidities, leading to deafferentation (development of erroneous mouth mucosae sensations felt by the patient). This could have been increased by depression. Dysgeusia in elederly patients with depression should be extensively investigated in order to elucidate somatic contributing factors but it may not resolve until improvement of the depressive symptoms. Topics: Aged; Anemia; Depression; Dysgeusia; Humans; Male; Olanzapine; Vitamin B 12 | 2020 |
Using histamine (H1) antagonists, in particular atypical antipsychotics, to treat anemia of chronic disease via interleukin-6 suppression.
Anemia of chronic disease (ACD) is a condition of decreased red cell mass secondary to some other chronic inflammatory condition. In ACD total body iron stores are normal, though serum iron is typically low secondary to iron sequestration by macrophages, and often iron supplementation is not an effective treatment for ACD for the same reason. The pathogenesis of ACD had been poorly understood, but recently there has been important progress: upregulation of interleukin-6 (Il-6) secondary to the underlying chronic inflammatory disease upregulates expression of the protein hepcidin. Upregulation of hepcidin causes anemia by a number of mechanisms: decreased intestinal absorption of iron from the duodenum, increased sequestration of iron by macrophages. Thus, downregulation of Il-6 may represent a most important treatment avenue for ACD. Anti-Il-6 antibodies might be a way to lower Il-6 levels, but such antibodies besides being expensive would have to be given intravenously or intramuscularly, and such large immunogenic molecules may not be appropriate in patients already with a chronic inflammatory condition. Here, we note that an immediately available and potentially effective treatment for ACD is to decrease Il-6 levels by histamine (H1) receptor antagonism, given that histamine acting through the H1 receptor is known to be a potent positive regulator of Il-6. Among the classes of medications that are H1 antagonists we point out that atypical antipsychotic medications such as olanzapine and quetiapine are among the most potent H1 antagonists, and can have simple daily dosing schedules and thus may be particularly useful in ACD. Topics: Anemia; Antimicrobial Cationic Peptides; Antipsychotic Agents; Benzodiazepines; Chronic Disease; Dibenzothiazepines; Down-Regulation; Gene Expression Regulation; Hepcidins; Histamine Antagonists; Humans; Interleukin-6; Iron; Models, Biological; Olanzapine; Quetiapine Fumarate; Receptors, Histamine H1; Up-Regulation | 2005 |