Hypoglycemia is a common complication in patients with diabetes, mainly in those treated with insulin, sulfonylurea, or glinide. Impairments in counterregulatory responses and hypoglycemia unawareness constitute the main risk factors for severe hypoglycemia. Episodes of hypoglycemia are associated with physical and psychological morbidity. The fear of hypoglycemia constitutes a barrier that impairs the patient’s ability to reach good glycemic control. To prevent hypoglycemia, much effort must be invested in patient education regarding risk factors, warning signs, and treatment of hypoglycemia at an early stage, together with setting personalized goals for glycemic control. In this review, we present a comprehensive update on the treatment and prevention of hypoglycemia in type 1 and type 2 diabetic patients.
Background: Diabetes mellitus is associated with a more severe course of coronavirus disease 2019 . The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes angiotensinconverting enzyme II (ACE2) receptor for host cell entry. We aimed to assess the interactions between antihyperglycemic drugs and the renin-angiotensin system (RAS) and their putative roles in COVID-19. Methods: A literature search was performed using Pubmed to review the interrelationships between hyperglycemia, RAS and COVID-19, and the effects of antihyperglycemic medications. Results: The RAS has an essential role in glucose homeostasis and may have a role in COVID-19-induced lung injury. Some antihyperglycemic medications modulate RAS and might hypothetically alleviate the deleterious effect of angiotensin II on lung injury. Furthermore, most antihyperglycemic medications showed anti-inflammatory effects in animal models of lung injury. Conclusions: Some antihyperglycemic medications might have protective effects against COVID-19induced lung injury. Early insulin therapy seems very promising in alleviating lung injury.
Recent studies suggest that dopamine agonist therapy may be an effective and safe treatment option in a considerable portion of patients with cystic prolactinomas. We suggest that dopamine agonists should be considered as a first-line therapy for cystic prolactinoma in the absence of indications for early surgical intervention.
Background and AimsImmune semaphorins are a large family of proteins involved in the pathogenesis of inflammatory diseases through the regulation of immune homeostasis and tissue inflammation. We aim to assess the possible involvement of semaphorin3A (sema3A) and 4A (sema4A) in peripheral immune responses and bowel tissue inflammation of patients suffering from Crohn’s disease (CD) and ulcerative colitis (UC).Patients and MethodsTwenty-seven CD patients and 10 UC patients were studied and compared to 10 patients followed for acute diverticulitis (disease control) and 12 healthy individuals. All were evaluated for sema3A expression on T regulatory cells (Tregs), serum levels of sema3A and sema4A, and tissue expression of sema3A and sema4A in bowel biopsies.ResultsThe percentage (%) of T regulatory cells (Tregs) expressing sema3A in patients with active CD (64.5% ±14.49%) and active UC (49.8% ±16.45%) was significantly lower when compared to that of healthy controls (88.7% ±3.6%, p< 0.001 and p< 0.0001, respectively). This expression was seen to be in negative correlation with CD activity. Serum levels of Sema4A were significantly lower in patients with CD and UC when compared to that of controls (5.69±1.48ng\ml for CD, 5.26±1.23 ng/ml for UC patients vs 9.74±2.73ng/ml for normal controls, P<0.001). Sema4A was highly expressed in lymphocytes of the lamina propria of CD and UC patients but absent in patients with diverticulitis or in normal individuals.ConclusionsAltered % of Tregs expressing sema3A in patients with inflammatory bowel diseases (IBD) is partially responsible for their failure in preventing CD4+ effector T cell induced inflammation in IBD in peripheral blood. The increased expression of sema4A in bowel biopsies from CD and UC patients is suggestive of its central role in regulating local tissue inflammation in the bowel.
ObJECTIvE: Cushing`s disease during pregnancy is associated with an increased risk for maternal and fetal complications. In recurrent Cushing`s disease following transsphenoidal surgery, and when re-operation is not feasible, medical treatment is usually considered. Cabergoline was found to be effective in reducing hypercortisolism in Cushing's disease. Evolving data concerning the safety of cabergoline use during pregnancy show no significant increase in the rate of complications during pregnancy or the postnatal period. mEThODS: We report a 29-year-old woman, gravida 0, para 0, with recurrent Cushing`s disease, three years after transsphenoidal resection of pituitary aCTh-secreting macroadenoma. Repeated mRI revealed an empty sella with a small gadolinium-enhancing lesion, suspected to be an adenoma remnant on the medial wall of the right cavernous sinus. as the patient was not willing to undergo repeat surgical intervention, treatment with cabergoline was initiated, with a gradual dose titration up to 3.5 mg/week. Clinical improvement ensued, and 4 months later, she conceived spontaneously. after discussing treatment options with the patient, cabergoline treatment at a dose of 2 mg/week was continued throughout pregnancy. RESUlTS: The patient showed complete clinical remission during pregnancy. Consecutive tests of 24-h urinary free cortisol concentration were not found to be elevated. pregnancy and delivery were uneventful except for mild hypothyroidism observed during the second trimester. at full term the patient delivered a healthy female infant, by an elective cesarean section. CONClUSION: This case report demonstrates that cabergoline may be an effective and safe therapeutic option for the treatment of Cushing's disease during pregnancy.Key words: Cabergoline, Cushing's disease, Pregnancy HORMONES 2016, 15(3):453-458 Address for correspondence: Dr. Afif Nakhleh, Endocrinology Department, Bnai Zion Medical Center, 47 Golomb St, Haifa 31048, Israel; Tel.: +972-4-8359931, E-mail: anakhleh@yahoo.com Received: 18-03-2016, Accepted: 26-05-2016 Case report CaSE REpORTA 29 year-old woman, gravida, 0 para 0, was referred to our outpatient clinic with a 3-year history of oligomenorrhea, unexplained weight gain of 20
TO THE EDITOR: The world is watching the progress of coronavirus disease (COVID᎑19) pandemic. Older age and pre-existing medical conditions, specifically diabetes mellitus, hypertension, ischemic heart disease, and chronic lung disease, are associated with a more severe course of . Diabetes mellitus is one of the most prevalent comorbidities among patients hospitalized due to . Data obtained from 21 hospitals in Wuhan, China, showed that 25% of the reported COVID-19 fatalities had a history of diabetes mellitus (33). Diabetes and ambient hyperglycemia were independent predictors for death and morbidity in patients with severe acute respiratory syndrome (14,34). In this letter, we discuss the putative roles of angiotensin-converting enzyme II (ACE2) in glucose homeostasis in patients with type 2 diabetes and COVID-19 and introduce the proposed benefit of early insulin therapy in patients that warrant hospital care.The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme II (ACE2) receptor for host cell entry and the serine protease TMPRSS2 for virus spike protein priming (16). The binding of SARS-CoV-1 Spike protein to ACE2 activates disintegrin and metalloprotease-17 (ADAM17) and induces ACE2 shedding via a process tightly coupled with TNF-␣ production (15). AD-AM17-mediated ACE2 shedding facilitates SARS-CoV-1 entry and induces tissue damage by TNF-␣ production (15). Interestingly, Kuba et al. (22) found that SARS-CoV-1 infection downregulates ACE2 expression in the mice lungs, and this downregulation was associated with the severity of lung injury. Considering that SARS-CoV-1 and SARS-CoV-2 share Ͼ70% sequence in the Spike protein (31), SARS᎑CoV᎑2 infection might also downregulate the ACE2 expression in the same manner and play a role in the pathological process of the lung injury. ADAM17-mediated ACE2 ectodomain shedding might compromise the renin-angiotensin system (RAS) compensatory axis by impairing ACE2 enzymatic activity or its ability to process angiotensin II on the cell surface. Recently, Monteil et al. (23) showed that human recombinant soluble ACE2 significantly blocks SARS-CoV-2 infections, providing a rationale that soluble ACE2 might not only protect from lung injury but also block the SARS-CoV-2 from entering target cells.ACE2 is expressed in several tissues including the kidney and recognized to be renoprotective by degrading angiotensin II to angiotensin(1-7) (9). The ACE2 receptor protects against lung injury by modulating of the RAS and decreasing angio-tensin II levels (19). Accumulating evidence supports the protective roles of ACE2 in diabetes. ACE2 is expressed in the pancreas and several insulin-sensitive tissues and might play important roles in glucose homeostasis. First, ACE2 deficiency leads to altered glucose metabolism; ACE2-knockout mice showed a -cell defect associated with a decrease in insulin secretion in a manner that is not dependent on angiotensin II but may reflect the collectrin-like action of ACE2 (2, 24). In the db/db mouse...
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