No increased risk of psychological/behavioral disorders in siblings of women with hyperemesis gravidarum (HG) unless their mother had HG

2012 ◽  
Vol 3 (5) ◽  
pp. 375-379 ◽  
Author(s):  
P. M. Mullin ◽  
A. Bray ◽  
V. Vu ◽  
F. Schoenberg-Paik ◽  
K. MacGibbon ◽  
...  

Hyperemesis gravidarum (HG), severe nausea and vomiting of pregnancy, is characterized by prolonged maternal stress, undernutrition and dehydration. Maternal stress and malnutrition of pregnancy are linked to poor neonatal outcome and associated with poor adult health, and we recently showed that in utero exposure to HG may lead to increased risks of psychological and behavioral disorders in the offspring. In addition, we have shown familial aggregation of HG, which is strong evidence for a genetic component to the disease. In this study, we compare the rates of psychological and behavioral disorders in 172 adults with and 101 adults without a sibling with HG. The rate of emotional/behavioral disorders is identical (15%) in both groups. The results suggest that the etiology of HG is not likely to include genetic factors associated with emotional and behavioral disorders. In addition, this study provides evidence that the increased incidence of psychological/behavioral disorders among offspring of women with HG is attributable to the HG pregnancy itself, rather than to confounding genetic factors linked to HG.

2011 ◽  
Vol 2 (4) ◽  
pp. 200-204 ◽  
Author(s):  
P. M. Mullin ◽  
A. Bray ◽  
F. Schoenberg ◽  
K. W. MacGibbon ◽  
R. Romero ◽  
...  

Hyperemesis gravidarum (HG), severe nausea and vomiting of pregnancy, is characterized by long-term maternal stress, undernutrition and dehydration. While maternal stress and malnutrition of pregnancy are linked to poor neonatal outcome and associated with poor adult health, long-term outcome of fetal exposure to HG has never been explored. The purpose of this study is to determine whether long-term emotional and behavioral diagnoses may be associated with fetal exposure to HG. Emotional and behavioral diagnoses of adults born of a pregnancy complicated by HG were compared to diagnoses from non-exposed controls. Offspring exposed to HG in utero were significantly more likely to have a psychological and behavioral disorder (OR = 3.6, P < 0.0001) with diagnoses primarily of depression, bipolar disorder and anxiety. In utero exposure to HG may lead to increased risks of psychological and behavioral disorders in the offspring.


2019 ◽  
Vol 79 (04) ◽  
pp. 382-388 ◽  
Author(s):  
Marlena Fejzo ◽  
Peter Fasching ◽  
Michael Schneider ◽  
Judith Schwitulla ◽  
Matthias Beckmann ◽  
...  

Abstract Objective Hyperemesis gravidarum, severe nausea and vomiting in pregnancy, occurs in up to 2% of pregnancies and leads to significant weight loss, dehydration, electrolyte imbalance, and ketonuria. It is associated with both maternal and fetal morbidity. Familial aggregation studies and twin studies suggest a genetic component. In a recent GWAS, we showed that placentation, appetite, and cachexia genes GDF15 and IGFBP7 are linked to hyperemesis gravidarum (HG). The purpose of this study is to determine whether GDF15 and IGFBP7 are upregulated in HG patients. Methods We compared serum levels of GDF15 and IGFBP7 at 12 and 24 weeksʼ gestation in women hospitalized for HG, and two control groups, women with nausea and vomiting of pregnancy (NVP), and women with no NVP. Results We show GDF15 and IGFBP7 serum levels are significantly increased in women with HG at 12 weeksʼ gestation. Serum levels of hCG are not significantly different between cases and controls. At 24 weeks gestation, when symptoms have largely resolved, there is no difference in GDF15 and IGFBP7 serum levels between cases and controls. Conclusion This study supports GDF15 and IGFBP7 in the pathogenesis of HG and may be useful for prediction and diagnosis. The GDF15-GFRAL brainstem-activated pathway was recently identified and therapies to treat conditions of abnormal appetite are under intense investigation. Based on our findings, HG should be included.


Diagnostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 599
Author(s):  
Gloria Pérez-Rubio ◽  
Ramcés Falfán-Valencia ◽  
Juan Carlos Fernández-López ◽  
Alejandra Ramírez-Venegas ◽  
Rafael de Jesús Hernández-Zenteno ◽  
...  

Genetic variability influences the susceptibility to and severity of complex diseases; there is a lower risk of COPD in Hispanics than in non-Hispanic Caucasians. In this study, we included 830 Mexican-Mestizo subjects; 299 were patients with COPD secondary to tobacco smoking, and 531 were smokers without COPD. We employed a customized genotyping array of single nucleotide polymorphisms (SNPs). The population structure was evaluated by principal component analysis and allele association through a logistic regression model and haplotype identification. In this study, 118 individuals were identified with a high Caucasian component and 712 with a high Amerindian component. Independent of the ancestral contribution, two SNPs were associated with a reduced risk (p ≤ 0.01) of developing COPD in the CYP2A6 (rs4105144) and CYP2B6 (rs10426235) genes; however, a haplotype was associated with an increased risk of COPD (p = 0.007, OR = 2.47) in the CHRNA5-CHRNA3 loci among smokers with a high Caucasian component. In Mexican-Mestizo smokers, there are SNPs in genes that encode proteins responsible for the metabolism of nicotine associated with a lower risk of COPD; individuals with a high Caucasian component harboring a haplotype in the CHRNA5-CHRNA3 loci have a higher risk of suffering from COPD.


Author(s):  
Nitao Cheng ◽  
Xinran Cui ◽  
Chen Chen ◽  
Changsheng Li ◽  
Jingyu Huang

Lung carcinoma is one of the most deadly malignant tumors in mankind. With the rising incidence of lung cancer, searching for the high effective cures become more and more imperative. There has been sufficient research evidence that living habits and situations such as smoking and air pollution are associated with an increased risk of lung cancer. Simultaneously, the influence of individual genetic susceptibility on lung carcinoma morbidity has been confirmed, and a growing body of evidence has been accumulated on the relationship between various risk factors and the risk of different pathological types of lung cancer. Additionally, the analyses from many large-scale cancer registries have shown a degree of familial aggregation of lung cancer. To explore lung cancer-related genetic factors, Genome-Wide Association Studies (GWAS) have been used to identify several lung cancer susceptibility sites and have been widely validated. However, the biological mechanism behind the impact of these site mutations on lung cancer remains unclear. Therefore, this study applied the Summary data-based Mendelian Randomization (SMR) model through the integration of two GWAS datasets and four expression Quantitative Trait Loci (eQTL) datasets to identify susceptibility genes. Using this strategy, we found ten of Single Nucleotide Polymorphisms (SNPs) sites that affect the occurrence and development of lung tumors by regulating the expression of seven genes. Further analysis of the signaling pathway about these genes not only provides important clues to explain the pathogenesis of lung cancer but also has critical significance for the diagnosis and treatment of lung cancer.


Author(s):  
Anne Barton

Rheumatoid arthritis (RA) is known to have a genetic component: the evidence comes from twin and family studies as well as genetic studies themselves. Family studies consistently confirm that first degree relatives of patients with RA are at increased risk of developing the condition, supporting a genetic component. The most robust data comes from the Icelandic genealogical database. This chapter covers the basics of genetic studies in RA, designing the genetic study, RA-specific results and insights that can be gained from these. Detailed analyses of selected genetic regions are discussed, alongside genes that may indicate severity. Genetic factors associated with treatment response are also considered. Finally, the role of epigenetics is covered.


2014 ◽  
Vol 54 (6) ◽  
pp. 324 ◽  
Author(s):  
Dora Novriska ◽  
Retno Sutomo ◽  
Amalia Setyati

Background Epilepsy is a neurological disorder that most oftenaffects children. Most cases of epilepsy are found in developingcountries. Children with epilepsy are at risk of behavioral disordersthat can affect their quality of life. Studies on behavioral problemsin children with epilepsy have been limited in Indonesia.Objective To compare behavioral disorders in children withepilepsy to those in normal children, and to assess for possiblefactors associated with the occurrence of behavioral disorders.Methods We conducted a cross-sectional study involving 47children with epilepsy and 46 children without epilepsy, aged 3-16years. Behavioral problems were screened with the Strength andDifficulty Questionnaire (SDQ), Indonesian version. Informationabout EEG description, medication, onset, and duration of epilepsywere obtained from medical records.Results Behavioral problems were found in 19.1% of childrenwith epilepsy and only in 2.2 % of children without epilepsy (PR8.8; 95%CI 1.16 to 66.77; P= 0.015). Significant differences werealso found in the percentage of conduct problems and emotionaldisorders. Multivariate analysis with logistic regression revealedthat the factors associated with behavioral disorders in childrenwith epilepsy were uncontrolled epilepsy (PR 13.9; 95%CI 1.45 to132.4; P=0.023) and focal EEG appearance (PR 19; 95%CI 1.71to 214.43; P=0.017). We also found that uncontrolled epilepsywas a factor related to emotional (PR 6.7; 95%CI 1.66 to 26.76;P=0.007) and conduct problems (PR 6.1; 95%CI 1.35 to 27.29;P=0.019).Conclusion Uncontrolled epilepsy and focal EEG results arefactors associated with increased risk of behavioral problems inchildren with epilepsy. Children with epilepsy should undergobehavioral disorder screening, followed by diagnosis confirmationand treatment.


2021 ◽  
Vol 12 ◽  
Author(s):  
Marius H. Sneller ◽  
Nini de Boer ◽  
Sophie Everaars ◽  
Max Schuurmans ◽  
Sinan Guloksuz ◽  
...  

Background: Individuals with severe mental illness experience increased morbidity and mortality compared to the general population. Adverse effects of antipsychotics, including weight gain, may contribute to the development of metabolic syndrome (MetS), which is associated with increased risks of all-cause and cardiovascular disease mortality. We aim to provide a comprehensive overview of clinical, biochemical and genetic factors associated with MetS among patients with schizophrenia spectrum disorders using second-generation antipsychotics (SGA).Methods: A literature search was performed in Pubmed and Embase to identify all cohort studies, cross-sectional studies and clinical trials investigating associations with MetS in patients with schizophrenia spectrum disorders using SGAs. We extracted and enumerated clinical, biochemical and genetic factors reported to be associated with MetS. We defined factors associated with MetS as factors being reported as associated with MetS in two or more studies.Results: 58 studies were included in this review (n = 12,123). In total, 62 factors were found to be associated with increased risk of MetS. Thirty one out of 58 studies investigated factors that were reported as associated with MetS in two or more studies. With regard to clinical factors, we found gender, higher age, concomitant use of mood stabilizers, higher baseline and current BMI, earlier SGA exposure, higher dose, longer duration of treatment, psychosis and tobacco smoking to be significantly associated with MetS. Furthermore, the biochemical factors hypo-adiponectinemia, elevated levels of C-reactive protein (CRP) and higher white blood cell (WBC) count were identified as factors associated with MetS. Among pharmacogenetic factors, the rs1414334 C-allele of the HTR2C-gene was associated with MetS in patients using SGA.Conclusion: In this systematic review investigating clinical, biochemical and genetic factors associated with MetS in patients using SGAs we found that higher age, higher baseline BMI, higher current BMI and male as well as female gender were positively associated with MetS across all antipsychotics. This study may set the stage for the application of clinical, biochemical and genetic factors to predict the risk of developing MetS in patients using SGAs. Future research is needed to determine which patients using SGAs are at risk to develop MetS in clinical practice.


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