Management of hairy cell leukaemia in pregnancy.

Background: Hairy cell leukaemia (HCL) represents less 1% of all lymphoid neoplasms with cases rarely reported in pregnancy. Management of HCL requires multidisciplinary care to optimise maternal and neonatal outcomes.

Methods: A literature search of Ovid MEDLINE and EMBASE for 'hairy cell leukaemia' and 'Pregnancy' was undertaken.

Addressing the perimenopause: what's blood got to do with it?

A state of the art lecture titled, "Addressing the Perimenopause: What's Blood Got to Do with It?" was presented at the International Society on Haemostasis and Thrombosis (ISTH) Congress in 2024. Perimenopause is when fluctuations of previously cyclically regulated hormones occur prior to menopause, resulting in a number of symptoms that can negatively impact a woman's quality of life. Thrombosis and hemostasis experts are often approached to help investigate and manage clinical issues associated with perimenopause.

SOMANZ position statement for the investigation and management of sepsis in pregnancy 2023.

Background: The Society of Australia and New Zealand (SOMANZ) published its first sepsis in pregnancy and the postpartum period guideline in 2017 (Aust N Z J Obstet Gynaecol, 57, 2017, 540). In the intervening 6 years, maternal mortality from sepsis has remained static.

Aims: To update clinical practice with a review of the subsequent literature.

Update on pulmonary embolism in pregnancy and post-partum: The Society of Obstetric Medicine of Australia and New Zealand Position Statement on Pulmonary Embolism in Pregnancy and Post-partum.

In this clinical review we highlight aspects of the diagnosis and management of pulmonary embolism (PE) in pregnancy and post-partum and how this may impact on antenatal and postnatal management. Investigation for PE in pregnancy is challenging and includes appropriate patient selection and knowledge of the risks and benefits of pulmonary imaging modalities. The complete Society of Obstetric Medicine of Australia and New Zealand Position Statement on Pulmonary Embolism in Pregnancy and Post-Partum comprehensively reviews all aspects of diagnosis, investigation and management and is accessible at https://www.

Maternal thrombin generation and D-dimer levels in obesity and pregnancy: results from the maternal thrombin generation in obesity and pregnancy (MaTOPs) study.

Venous thromboembolic disease (VTE) risk increases five-fold antenatally and 14-fold during the puerperium. Obesity significantly increases this risk. The D-dimer assay and more novel Calibrated Automated Thrombogram (CAT) assay laboratory tests display potential for use in VTE risk stratification in pregnancy, although to date, research in the performance characteristics of these tests in obese and nonobese pregnant populations is limited.

Venous thromboembolism prophylaxis of the obese postpartum patient: A cross-sectional study.

Background: Obesity increases risk of venous thromboembolism (VTE) in obstetric patients regardless of delivery mode and for up to six weeks postpartum.

Aim: This study aimed to examine postpartum pharmacological VTE prophylaxis practices for obese women at an Australian tertiary referral hospital.

Materials And Methods: Medical records were retrieved for obese obstetric patients who delivered during May 2016-May 2017.

Retrospective cohort study comparing the adverse reactions and efficacy of intravenous iron polymaltose with ferric carboxymaltose for iron deficiency anemia.

Objective: To examine the adverse drug reactions (ADRs) and the efficacy of intravenous iron polymaltose and ferric carboxymaltose (FCM) among gynecology/obstetric patients with anemia.

Methods: The present retrospective observational study examined data from anemic obstetrics and gynecology patients who received either iron polymaltose or FCM between January 1, 2011, and April 30, 2015, at The Royal Women's Hospital, Victoria, Australia. Patient demographic data, dosage, ADR documentation, and hemoglobin levels were collected from medical records and compared.

The utility of the Wells clinical prediction model and ventilation-perfusion scanning for pulmonary embolism diagnosis in pregnancy.

Pulmonary embolism is one of the leading causes of mortality in pregnancy in the Western world. No clinical prediction models have been validated in pregnancy. As a result, any pregnant woman presenting with signs possibly consistent with pulmonary embolism is investigated radiologically.

New directions in the diagnosis and treatment of pulmonary embolism in pregnancy.

The diagnosis and management of pulmonary embolism in pregnancy is difficult, because diagnostic procedures and the use of anticoagulants potentially can expose mother and fetus to adverse effects. This article reviews evidence for current best practice and emerging novel techniques for the diagnosis of pulmonary embolism in pregnancy and includes clinical prediction models, biomarkers, and diagnostic imaging that may offer improvement in the diagnosis and investigation of pulmonary embolism in pregnancy in the future. The usefulness of new anticoagulant agents (fondaparinux, rivaroxaban, and dabigatran) in managing pulmonary embolism in future pregnancies is also explored.

Nf1 deficiency cooperates with oncogenic K-RAS to induce acute myeloid leukemia in mice.

Hyperactive RAS signaling is caused by mutations in RAS genes or a deficiency of the neurofibromatosis gene (NF1) and is common in myeloid malignancies. In mice, expression of oncogenic K-RAS or inactivation of Nf1 in hematopoietic cells results in myeloproliferative disorders (MPDs) that do not progress to acute myeloid leukemia (AML). Because NF1 is a RAS-GTPase-activating protein it has been proposed that NF1 deficiency is functionally equivalent to an oncogenic RAS.

Inactivating Icmt ameliorates K-RAS-induced myeloproliferative disease.

Hyperactive signaling through the RAS proteins is involved in the pathogenesis of many forms of cancer. The RAS proteins and many other intracellular signaling proteins are either farnesylated or geranylgeranylated at a carboxyl-terminal cysteine. That isoprenylcysteine is then carboxyl methylated by isoprenylcysteine carboxyl methyltransferase (ICMT).

GGTase-I deficiency reduces tumor formation and improves survival in mice with K-RAS-induced lung cancer.

Protein geranylgeranyltransferase type I (GGTase-I) is responsible for the posttranslational lipidation of CAAX proteins such as RHOA, RAC1, and cell division cycle 42 (CDC42). Inhibition of GGTase-I has been suggested as a strategy to treat cancer and a host of other diseases. Although several GGTase-I inhibitors (GGTIs) have been synthesized, they have very different properties, and the effects of GGTIs and GGTase-I deficiency are unclear.

Rce1 deficiency accelerates the development of K-RAS-induced myeloproliferative disease.

The RAS proteins undergo farnesylation of a carboxyl-terminal cysteine (the "C" of the carboxyl-terminal CaaX motif). After farnesylation, the 3 amino acids downstream from the farnesyl cysteine (the -aaX of the CaaX motif) are released by RAS-converting enzyme 1 (RCE1). We previously showed that inactivation of Rce1 in mouse fibroblasts mislocalizes RAS proteins away from the plasma membrane and inhibits RAS transformation.