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The aim of this study was to determine if the problem-solving therapy (PST) helps control metabolic variables in patients with type 2 diabetes mellitus (T2DM) who show depressive and anxiety symptoms.
T2DM is a chronic-degenerative multifactorial disease. It is considered one of the main public health problems in the world, and it represents an important social and economic burden. It is frequently associated with major depression and anxiety disorders, which are related with high glycated hemoglobin (HbA1c) concentrations and poor metabolic control.
We initially included 123 patients diagnosed with T2DM from five primary care centers (PCC) in Mexico City. HbA1c, central glucose, and lipid profile were measured in each patient. In addition, the Kessler psychological distress scale (K-10), the Beck Depression Inventory, and the Beck Anxiety Inventory were applied at the beginning and, to those who continued, at the end of the PST, as well as four months later.
In total, 36 patients completed the PST and the follow-up. There was a significant decrease in depressive and anxiety symptoms (P<0.001), as well as in total cholesterol (P=0.002), HbA1c (P=0.05), and low-density lipoprotein (LDL) (P=0.022). The PST helps reduce depressive and anxiety symptoms and may help stabilize glucose and cholesterol up to four months. Further studies on this area are recommended. If our findings are confirmed, the PST could help improve the quality of life of thousands of individuals with psychiatric-metabolic co-morbidity who only visit PCC.
Elias Jabbour, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Hagop M. Kantarjian, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA,
Jorge E. Cortés, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Chronic myeloid leukemia (CML) is a relatively rare disease but is one of the most extensively studied and best understood neoplasms, and one for which a direct gene link has been found. CML is characterized by a balanced genetic translocation, t(9;22)(q34;q11.2), involving a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is known as the Philadelphia chromosome (Ph). The molecular consequence of this translocation is the generation of a BCR-ABL fusion oncogene, which in turn translates into a Bcr-Abl oncoprotein. Bcr-Abl displays transforming activity owing to its constitutive kinase activity, which results in multiple signal transduction pathways leading to uncontrolled cell proliferation and reduced apoptosis and resulting in the malignant expansion of pluripotent stem cells in bone marrow. CML is usually diagnosed in the chronic phase (CP) and, if not treated, progresses through an accelerated phase (AP) to a terminal blastic phase (BP).
Incidence, epidemiology, and etiology
CML accounts for 15% to 20% of cases of leukemia in the United States. There is a slight male preponderance. Its annual incidence is about 1 to 2 cases per 100,000 individuals. About 5000 to 6000 cases of CML are diagnosed annually. This incidence has not changed over the past few decades, and increases with age. The median age at CML diagnosis is 55 to 60 years; it is uncommon in children and adolescents. Before imatinib therapy, the prevalence of CML was about 25,000 cases in the United States.
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