Breastfeeding and depression: a systematic review of the literature

Background: Research has separately indicated associations between pregnancy depression and breastfeeding, breastfeeding and postpartum depression, and pregnancy and postpartum depression. This paper aimed to provide a systematic literature review on breastfeeding and depression, considering both pregnancy and postpartum depression. Methods: An electronic search in three databases was performed using the keywords: “breast feeding”, “bottle feeding”, “depression”, “pregnancy”, and “postpartum”. Two investigators independently evaluated the titles and abstracts in a first stage and the full-text in a second stage review. Papers not addressing the association among breastfeeding and pregnancy or postpartum depression, non-original research and research focused on the effect of antidepressants were excluded. 48 studies were selected and included. Data were independently extracted. Results: Pregnancy depression predicts a shorter breastfeeding duration, but not breastfeeding intention or initiation. Breastfeeding duration is associated with postpartum depression in almost all studies. Postpartum depression predicts and is predicted by breastfeeding cessation in several studies. Pregnancy and postpartum depression are associated with shorter breastfeeding duration. Breastfeeding may mediate the association between pregnancy and postpartum depression. Pregnancy depression predicts shorter breastfeeding duration and that may increase depressive symptoms during postpartum. Limitations: The selected keywords may have led to the exclusion of relevant references. Conclusions: Although strong empirical evidence regarding the associations among breastfeeding and pregnancy or postpartum depression was separately provided, further research, such as prospective studies, is needed to clarify the association among these three variables. Help for depressed pregnant women should be delivered to enhance both breastfeeding and postpartum psychological adjustment.

Friedreich's Ataxia: Cardiac Evaluation of 25 Patients with Clinical Diagnosis and Literature Review

OBJECTIVE - Cardiac evaluation (clinical, electrocardiographic and echocardiographic) of 25 Brazilian patients with clinical diagnosis of Friedreich's ataxia (FA) related to the frequency and the size of GAA repeats (unstable expansion of trinucleotide repeats that results in the disease). METHODS - Clinical and cardiac study including electrocardiogram and echocardiogram of all patients and molecular analysis to detect the frequency and the size of GAA expansion, by polymerase chain reaction analysis. RESULTS - Homozygous GAA expansion was detected in 17 patients (68%) -- all typical cases. In 8 (32%) cases (6 atypical and 2 typical), no GAA expansion was observed, therefore it was not considered Friedreich's ataxia. All patients with GAA expansion (100%) had electrocardiographic abnormalities, and only 25% of the cases without GAA expansion had some abnormality on this exam. However, only 6% of all patients revealed some signals/symptoms suggestive of cardiac involvement. CONCLUSION - A molecular analysis is essential to confirm the diagnosis of Friedreich's ataxia; however, an adequate cardiac evaluation, including an electrocardiogram, was extremely useful to better screening the patients which should perform these molecular analysis.

Cardiac Damage from Chronic Use of Chloroquine: A Case Report and Review of the Literature

Chloroquine has been widely used in rheumatological treatment, but potential severe side effects require careful follow-up. Cardiac damage is not a common consequence, but its clinical relevance has not yet been described. We report the case of a 58-year-old woman with rheumatoid arthritis, in whom chronic chloroquine use resulted in major irreversible cardiac damage. She presented with syncopal episodes due to complete atrioventricular block confirmed by electrophysiological study whose changes were concluded to be irreversible and a permanent pacemaker was indicated. Endomyocardial biopsy was also performed to search for histopathological and ultrastructural cardiac damage. We also reviewed the 22 cases of chloroquine-induced cardiopathy described to date as well as its pathophysiology.

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

2 (New Series)

Investigación de defectos genéticos en el sistema de la fosforilasa hepática en pacientes argentinos. Definición nosológica mediante una estrategia de análisis molecular. Investigation of genetic defects in the hepatic phosphorylase system in Argentinean patients. Nosological definition by molecular analysis strategy.

Las Enfermedades de Atesoramiento de Glucógeno (EAGs) también llamadas Glucogenosis comprenden un grupo de entidades causadas por una deficiencia enzimática específica relacionada con la vía de síntesis o degradación de esta macromolécula. La heterogeneidad fenotípica de los pacientes afectados dificulta la identificación de las diferentes variantes de EAG y por ende la correcta definición nosológica. En el Centro de Estudio de las Metabolopatías Congénitas, CEMECO, se fueron definiendo los diferentes tipos de Glucogenosis a través de una estrategia multidisciplinaria que integra distintos niveles de investigación clínica y complementaria, laboratorio metabólico especializado, enzimático, histomorfológico y de análisis molecular. Sin embargo, en algunos enfermos, entre los que se encuentran aquellos con defectos en el sistema de la fosforilasa hepática (EAG-VI y EAG-IX), la exacta definición nosológica aún no está resulta. La EAG-VI se refiere a un defecto en la fosforilasa hepática, enzima codificada por el gen PYGL, mientras que la EAG-IX es causada por un defecto genético en una de las subunidades de la fosforilasa b quinasa hepática codicadas por los genes PHKA2, PHKB y PHKG2, respectivamente. El objetivo del presente trabajo es propender a la definición nosológica de pacientes con defectos en el sistema de la fosforilasa mediante una estrategia de análisis molecular investigando los genes PYGL, PHKA2, PHKB y PHKG2. Los pacientes incluidos en este estudio deberán ser compatibles de padecer una EAG-VI o EAG-IX sobre la base de síntomas clínicos y hallazgos bioquímicos. La metodología incluirá la determinación de la enzima fosforilasa b quinasa en glóbulos rojos y dentro del análisis molecular la extracción de DNA genómico a partir de sangre entera para la amplificación por PCR de los exones más las uniones exon/intron de los genes PHKG2 y PYGL y la extracción de RNA total y obtención de cDNA para posterior amplificación de los cDNA PHKA2 y PHKB. Todos los fragmentos amplificados serán sometidos a análisis de secuencia de nucleótidos. Resultados esperados. Este trabajo, primero en Argentina, permitirá establecer las bases moleculares de los defectos del sistema de la fosforilasa hepática (EAG-VI y EAG-IX). El poder lograr este nivel de investigación traerá aparejado, una oferta integrativa en el vasto capítulo de las glucogenosis hepáticas, con extraordinaria significación en la práctica asistencial para el manejo, pronóstico y correspondiente asesoramiento genético. Hepatic glycogen storage diseases (GSDs) are a group of disorders produced by a deficiency in a specific protein involved in the metabolism of glycogen causing different types of GSDs. Phenotypic heterogeneity of affected patients difficult to identify the different GSD variants and therefore the correct definition of the disease. In the “Centro de Estudio de las Metabolopatías Congénitas”, CEMECO, were defined the different GSD types by a protocol which included complex gradual levels of clinical, biochemical, enzymatic and morphological investigation. However, in some patients, like those one with defects in the hepatic phosphorylase system (GSD-VI and GSD-IX) the exact definition of the disease has not yet been resolved. The GSD-VI is produced by a defect in the PYGL gen that encode the liver phosphorylase, while the GSD-IX is caused by a genetic defect in one of the Phosphorylase b kinase subunits, encoded by the PHKA2, PHKB and PHKG2 genes, respectively. The aim of the present study is to define the phosphorylase system defects in argentinian patients through a molecular strategy that involve the investigation of PYGL, PHKA2, PHKB and PHKG2 genes. Patients included in the present study must be compatible with a GSD-VI or GSD-IX on the bases of clinical symptoms and biochemical findings. The phosphorylase b kinase activity will be assay on in blood red cells. The molecular study will include genomic DNA extraction for the amplification of PHKG2 and PYGL genes and the total RNA extraction for amplification of the PHKA2 and PHKB cDNA by PCR. All PCR-amplified fragments will be subjected to direct nucleotide sequencing. This work, first in Argentina, will make possible to establish the molecular basis of the defects on the hepatic phosphorylase system (GSD-VI and GSD IX). To achieve this level of research will entail advance in the study of the hepatic glycogen storage disease, with extraordinary significance in the treatment, prognosis and the genetic counselling.

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

14 (New Series)

Quarterly Journal of Science, Literature and the Arts.

20

Quarterly Journal of Science, Literature and the Arts.

1827 (July - Dec.)

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

4 (New Series)

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

13 (New Series)

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

15 (New Series)

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

18 (New Series)

Monthly Magazine or British Register (of Politics, Literature and the Belles Lettres)

10 (New Series)