To report and review a case of prolactin-producing pituitary tumor presenting with mass effects, hormonal deficiency, and neurogenic diabetes insipidus in a nulliparous woman of Afro-Caribbean descent. The patient presented with dull-aching headaches associated with worsening vision, nausea, and vomiting. The patient also complained of polyuria, nocturia, thirst, polydipsia, and weight gain. Physical examination showed bilateral visual field defects, while investigations revealed hypernatremia and elevated plasma osmolality but decreased urine sodium concentration, osmolality, and specific gravity. Results of the hormonal profile showed high plasma prolactin levels, a low plasma concentration of the antidiuretic hormone, and decreased levels of other anterior pituitary hormones. Imaging revealed a large, uncalcified, cystic pituitary mass extending into adjacent structures and compressing the optic chiasm and internal carotid artery. The outcome of the water deprivation and desmopressin administration tests were consistent with neurogenic diabetes insipidus, and a diagnosis of prolactin-producing pituitary macroadenoma with mass effects, hormonal deficiencies, and neurogenic diabetes insipidus was made. The patient was commenced on medical treatment and referred for histopathological diagnosis and definitive treatment. This report highlights the coexistence of neurogenic diabetes insipidus with a prolactin-producing pituitary macroadenoma presenting with mass effects.

Calciphylaxis, also known as calcific uremic arteriolopathy (CUA), affects small arteries of the skin in patients with end-stage renal failure, dialysis patients, and patients with hypercalcemia. The condition is characterized by the calcification of small blood vessels leading to skin necrosis without inflammation. It is frequently complicated by superimposed infection and bleeding and has a high mortality rate. The rare condition is yet to be documented on the islands of Saint Vincent and the Grenadines. The authors have, therefore, made efforts to document, educate, and discuss this rare presentation in a 65-year-old local Vincentian male with 30 years history of poorly controlled diabetes mellitus and hypertension who commenced hemodialysis two years prior to the presentation for end-stage chronic renal failure. With the increasing incidence and prevalence of diabetes mellitus, hypertension, and complications of chronic kidney disease, and renal failure, this article is written as a case study with a concise literature review on calciphylaxis to provide continuing medical education and increase the level of awareness among medical students and index of suspicion among healthcare providers.

Breast cancer is a leading cause of cancer related death among women worldwide and it is a complex disease characterized by its heterogeneity. The heterogenous characteristic of the breast cancer is responsible for its aggressiveness and treatment resistance. Breast cancer stem cells (BCSCs) are population of heterogenous cells with increased propensity for proliferation, differentiation, migration, invasion and mammosphere formation with increased resistance to treatment. They have ability to initiate and propagate cancer cells population and share similarity with the normal stem cells in relation to their expressions of cell surface markers; Cluster of Differentiation 44 positive (CD44+), Cluster of Differentiation 24 negative/low (CD24-/low) and Alkaline dehydrogenase 1 (ALDH1). MicroRNAs (miRNAs) are responsible for the RNA silencing and post-transcriptional regulation of the gene expression. MicroRNAs (miRNAs) control gene expression by acting as oncogenes or tumor suppressor genes. The epigenetic mechanisms are used for the regulation of miRNAs expression in the breast cancer, and this can be targeted to reverse the cancer progression. This review aims to provide an overview of the pathogenic mechanism of the microRNA’s expressions on the breast cancer stem cells in controlling the prognosis and aggressiveness of breast cancer disease. This is done by highlighting the regulatory mechanism of miRNA expressions on the BCSCs. Dysregulation of the MicroRNAs expression in the breast cancer stem cells and upregulated miRNAs expression were identified in the breast cancer stem cells (BCSCs), including miR-10b, miR-21, miR-155, miR-181, miR-183, miR-210 and miR-221/222, and the downregulated miRNAs expression in BCSCs include Let-7, miR-22, miR-30e, miR-31, miR-103/107, miR-200, miR-205, miR-335, miR-449a, miR-519c, miR-600, miR-708, miR-760. Studies showed association between the miRNA expression and breast cancer metastasis and aggressiveness. MicroRNAs were noticed to have a regulatory effect on neovascularization, drug resistance, and cancer metastasis. They can be used as predictive indicators in determining prognosis of breast cancer following cancer treatment and miRNAs expression can be used to determine the metastatic BCSCs for an efficient targeting mechanism and identification of the metastatic cancer cells. The systematic literature review aims at providing insight into the potential roles of microRNA in oncology especially breast cancers. The data for this study review were obtained from the Medline on OvidSP, includes PubMed of the US National Library of Medicine and the search was done through the University of Bristol Library services. This is to provide an overview of the pathogenic mechanism of microRNAs regulatory effect on the breast cancer stem cells in controlling the prognosis and aggressiveness of breast cancer disease. The review will be providing highlight of the dysregulation of oncogenic and tumor suppressor microRNAs in the breast cancer stem cells and highlighting the roles of miRNAs regulated BCSCs in the pathogenesis, prognosis, and aggressiveness of the breast cancer. We further discuss the biogenesis of miRNAs, regulatory roles of miRNAs on BCSCs, and then summarize the mechanism of miRNAs regulated BCSCs.

The fibroblast growth factor receptor 3 (FGFR3) gene mutations were identified to be involved in the pathogenesis of most chondropathies. The FGFR3 gene encodes the FGFR3 receptor and is involved in the regulation of bone growth by limiting the ossification of long bones. Mutations of the FGFR3 gene result in abnormal cell proliferation and improper cartilage development. We aim to provide an overview of the roles of FGFR3 in skeletal dysplasia by highlighting the pathogenesis, clinical variants of skeletal dysplasia, diagnosis, and their management. Achondroplasia is the most common form of chondropathies, occurring in approximately 1 in 20,000-30,000 live births, and it is the most common form of genetic dwarfism. In over 80% of cases of achondroplasia, the mutation is sporadic, and only 20% are inherited autosomal dominant. Achondroplasia results from a point mutation in the gene encoding the transmembrane portion of FGFR3. Two viable base substitutions are identified in achondroplasia, including a point mutation of guanine substituted for adenine (c.1138G>A); this is identified in approximately 98% of the affected individuals, and transversion of guanine to cytosine (c.1138G>C). Hypochondroplasia is a milder form of chondropathies with an incidence between 1 in 33,000 and 1 in 47,000 live births. Missense mutations of FGFR3 (p.Asn540Lys) are isolated in tyrosine kinase domain I occurring in approximately 60% of cases, and missense mutation of FGFR3 (p.Lys650Asn) identified in the tyrosine kinase domain II of FGFR3. Thanatophoric dysplasia is the most lethal form of chondropathies, with neonatal fetal death secondary to pulmonary hypoplasia. In thanatophoric dysplasia, there is Lys650Met substitution in FGFR3 (Type I) with impairment of endochondral bone growth and a pathogenic variant of p.Lys650Glu substitution in FGFR3 (Type II). In addition, specific amino acid substitution in the FGFR3 gene (G380R) was identified to be associated with severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN). The diagnosis of achondroplasias is routinely made from clinical presentations and radiological findings. FGFR3 molecular genetic testing is performed in children with atypical presentations. In addition, a pre-implantation genetic diagnosis should be available for parents pursuing in-vitro fertilization and embryo implantation procedures. Management of chondropathies includes symptomatic treatment with drugs, surgical intervention, and lifelong follow-up care. Different pharmacological options have been used, including those that directly block FGFR3 activation or regulate signalling pathways controlling chondrocyte proliferation and differentiation.