Review of Literature

Abstract Prolactin (PRL) secreting adenomas are the most common secreting pituitary tumors, accounting for approximately 45% of all pituitary tumours. Giant prolactinomas are a rare subset of macroadenomas, characterized by large size (more than 40 mm in diameter (an arbitrary size), high aggressiveness and massive extrasellar involvement. We describe an unusual giant prolactin producing macroadenoma of pituitary gland in female patients with type 2 diabetes mellitus and its response to cabergoline

Prevalence of diabetes mellitus in a Saudi community

<b>Background and Objectives :</b> Quantifying the prevalence of diabetes mellitus is important to allow for rational planning and allocation of resources. Therefore, we designed this study to determine the prevalence of diabetes among Saudi nationals. <b>Design and Setting :</b> A cross-sectional study among patients attending a primary care clinic in June 2009. <b>Patients and Methods :</b> Patients were interviewed with structured questionnaires to determine the presence of diabetes by questioning for history of the disease, and charts were reviewed to document any diabetic therapies that the patients may have undergone in the past or were undergoing at that time. <b>Results</b> : Of 6024 subjects, diabetes mellitus was present in 1792 (30&#x0025;) patients. The mean (SD) age of the patients was 55.3 (13.2) years. The prevalence of diabetes was 34.1&#x0025; in males and 27.6&#x0025; in females (<i>P</i>&lt;.0001). The mean (SD) age for onset of diabetes in males and females was 57.5 (13.1) and 53.4 (13.1) years, respectively (<i>P</i>&lt;.0001). Females &lt;50 years old had a higher prevalence than males in the corresponding age range-34.1&#x0025; and 25.1&#x0025;, respectively (<i>P</i>&lt;.0001). The prevalence of diabetes decreased in patients older than 70 years. The prevalence of body mass index of &#8805;25 was 72.5&#x0025;. Among patients with diabetes, the prevalence of body mass index of &#8805;25 was 85.7&#x0025; (<i>P</i>&lt;.0001). There was a higher prevalence of obesity (body mass index, &#8805;25) in females (87.7&#x0025;) as compared to males (83.1&#x0025;) (<i>P</i>=.008). <b>Conclusion</b> : The prevalence of diabetes is high among the Saudi population and represents a major clinical and public health problem. A national prevention program to prevent diabetes and address the modifiable risk factors at the community level, targeting high-risk groups, should be implemented soon

Glycogen hepatopathy in a 13-year-old male with type 1 diabetes

Glycogenic hepatopathy (GH ) is a rare cause of serum transaminase elevations in type 1 diabetes mellitus. We describe a 13-year-old male with a history of poorly controlled type 1 diabetes mellitus who presented with hepatomegaly and severe transaminase flares. Liver histology confirmed GH. Treatment consists of improving glycemic control. Hepatomegaly due to excess glycogen storage in poorly controlled type 1 diabetics has been associated with younger patients with poor glycemic control, occurring about 2-4 weeks after starting insulin treatment, and resolving upon glucose stabilization. We conclude that glycogenic hepatopathy can cause hepatomegaly and significant transaminase elevations in individuals with type I diabetes mellitus, The recovery of severe transaminase elevations in this patient illustrates the more benign course of GH, which is a condition with a far better prognosis. Clinician awareness of GH should prevent diagnostic delay and will provide better insight into the prevalence of GH

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease