Platelet count has been shown to be lower and mean platelet volume (MPV) to be higher in acute myocardial infarction (MI). However, it is not known whether these changes persist post-MI or if these measures are able to distinguish between acute thrombotic and non-thrombotic MI. Platelet count and MPV were measured in 80 subjects with acute MI (thrombotic and non-thrombotic) and stable coronary artery disease (CAD) at cardiac catheterization (acute phase) and at >3-month follow-up (quiescent phase). Subjects were stratified using stringent clinical, biochemical, histological, and angiographic criteria. Outcome measures were compared between groups by analysis of variance. Forty-seven subjects met criteria for acute MI with clearly defined thrombotic (n = 22) and non-thrombotic (n = 12) subsets. Fourteen subjects met criteria for stable CAD. No significant difference was observed in platelet count between subjects with acute MI and stable CAD at the acute or quiescent phase. MPV was higher in acute MI (9.18 ± 1.21) compared to stable CAD (8.13 ± 0.66; P = 0.003) at the acute phase but not at the quiescent phase (8.48 ± 0.58 vs 8.94 ± 1.42; P = 0.19). No difference in platelet count or MPV was detected between thrombotic and non-thrombotic subsets at acute or quiescent phases. The power to detect differences in these measures between thrombotic and non-thrombotic subsets was 58%. Higher MPV at the time of acute MI is not observed by 3 months post-MI (quiescent phase). Platelet count and MPV do not differ in subjects with thrombotic versus non-thrombotic MI. Further investigation is warranted to evaluate the utility of these measures in the diagnosis of acute MI.
Introduction: Dexamethasone (dex) crosses placenta, suppresses fetal ACTH and reduces level of adrenal androgens in fetus with Congenital Adrenal Hyperplasia (CAH). This reduces virilization of female genitalia and its associated risk of emotional distress and need for reconstructive surgery (1). As organogenesis begins at 6 weeks, pre-natal treatment with dex must be started at 6-7 weeks. However, dex is a category C drug and its use is associated with birth defects, reduced birth weight and decreased cognitive function. Clinical Case: A 30-year-old African American (AA) female at 25 weeks gestation was referred to the Endocrine clinic after being lost to follow up for two years for management of 21-hydroxylase deficient CAH-virilizing type in pregnancy. She recalls being diagnosed with CAH around 2 years of age, was followed by Pediatric Endocrinology and has been maintained on oral steroids. Her birth and family history are unknown as she is adopted. She had clitoromegaly and underwent clitoral reduction surgery at 8yrs of age. She has had extensive hirsutism but denied having menstrual irregularities or problems conceiving besides one miscarriage at 10 weeks gestation, 1 year prior to current pregnancy. She had an uncomplicated pregnancy 3 years ago and delivered a boy whose genetic testing was negative for CAH. She was on prednisone then. She had history of non-compliance and was switched to dex 0.75 mg nightly 2 years ago. She did not follow with up Endocrine for the last 2 years as she was asymptomatic and had her dex refilled by primary care physician and had been taking it regularly. Her current pregnancy had been going well. She now has a female fetus with a different AA partner who does not have personal or family history of CAH. Genetic testing of father to see if he is a carrier could not be done, and patient refused chorionic villous sampling to determine fetus’ risk of CAH. Given unknown risk of female fetus having CAH and potential complications of dex, we recommended switching to hydrocortisone (HC) 10mg BID. Clinical Lesson: Endocrine society recommends against treatment of CAH in pregnant women with dexamethasone except in cases of prenatal treatment of CAH of female fetuses which is performed at few selected centers (2). In the case above, patient conceived on dex and continued dex for first 25 weeks of her pregnancy until seen by Endocrinologist. By that time, acute decision-making period was over. Female fetus whose risk of CAH is unknown was exposed to dexamethasone and has possible risk of developing complications. This case emphasizes importance of correct steroid treatment early in pregnancy, multidisciplinary approach in management of such patients and importance of endocrine follow up for all CAH patients especially those of reproductive age. (1) Clin Endocrinol (Oxf). 2010 Oct;73(4):436-44 (2) J Clin Endocrinol Metab. 2018 Nov 1;103(11):4043-4088
Prolonged Hypoglycemia from Insulin Degludec Background: Patients with type 2 diabetes treated with insulin degludec compared with insulin glargine had a reduced risk of overall symptomatic hypoglycemia (1). This is primarily due to former’s long half-life (25 hours) and lack of trough levels. Moreover, insulin degludec’s pharmacokinetics is not affected by renal impairment and no dose adjustment is needed in impaired renal function (2). Case: 75 y/o female with history of type 2 diabetes, chronic kidney disease stage III, pancreatitis and pancreatic cyst status post drainage presented with frequent episodes of symptomatic hypoglycemia.Patient was switched from insulin glargine to degludec 6 units(U) daily and continued on aspart 6 units(U) TID and metformin 500mg BID three months prior to presentation. When seen in clinic two months later, she had frequent episodes of blood glucoses (BG) in 40s-50s mg/dl. Degludec was reduced to 5U and aspart to 1U for 1 carb serving, maximum 3U per meal. Two weeks later she was seen in primary care clinic with BG of 36 mg/dl when all insulin was stopped. One week later she was seen in the emergency room with BG of 37mg/dl. She was treated and discharged home. Three days later she continued to have symptomatic hypoglycemic episodes 1-2 times a day, (BG 40s mg/dl), especially in fasting state and was then hospitalized.On admission, her BG was 66mg/dl. She was started on dextrose drip. Labs showed glomerular filtration rate (GFR) of 30.1 ml/min/1.73m 2 which had reduced from 54.1 ml/min/1.73m 2 three months ago when degludec was started. Her fasting insulin, pro-insulin levels, C-peptide, beta-hydroxy butyrate, IGF1 were in normal range, along with simultaneous plasma glucose of 144 mg/dl. She had normal liver function, TSH and a normal response to ACTH stimulation test. She received IV hydration with improvement in GFR to 40.3 ml/min/1.73m 2 . She was encouraged to eat more as patient had poor appetite since her pancreatic cyst drainage four months ago. She was observed for two days in the hospital and her BG remained in 154 to 213 mg/dl with one value of 306 mg/dl. She was discharged on metformin 500 mg daily and aspart 2U if BG > 250mg/dl. Subsequent follow up one and four weeks later showed no episodes of hypoglycemia. Conclusion: The case above illustrates prolonged action of degludec causing hypoglycemia 10 days after stopping prescription dose (0.1U/kg) of degludec, which has not been previously reported before.Reduced oral intake potentiated hypoglycemic episodes. Practitioners should be aware of potential prolonged hypoglycemia from degludec. (1) The SWITCH 2 Randomized Clinical Trial. JAMA. 2017;318(1):45-56 (2) Clin Pharmacokinet. 2014 Feb;53(2):175-83
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