Development and internal validation of a clinical score to predict neonatal hypoglycaemia in women with gestational diabetes.

INTRODUCTION: Gestational diabetes (GD) is a risk factor for neonatal hypoglycaemia (NH), but other factors can increase this risk. OBJECTIVES: To create a score to predict NH in women with GD. METHODS: Retrospective study of women with GD with a live singleton birth between 2012 and 2017 from the Portuguese GD registry. Pregnancies with and without NH were compared. A logistic regression was used to study NH predictors. Variables independently associated with NH were used to score derivation. The model's internal validation was performed by a bootstrapping. The association between the score and NH was assessed by logistic regression. RESULTS: We studied 10216 pregnancies, 410 (4.0%) with NH. The model's AUC was 0.628 (95%CI: 0.599-0.657). Optimism-corrected c-index: 0.626. Points were assigned to variables associated with NH in proportion to the model's lowest regression coefficient: insulin-treatment 1, preeclampsia 3, preterm delivery 2, male sex 1, and small-for-gestational-age 2, or large-for-gestational-age 3. NH prevalence by score category 0-1, 2, 3, 4, and ≥5 was 2.3%, 3.0%, 4.5%, 6.0%, 7.4%, and 11.5%, respectively. Per point, the OR for NH was 1.35 (95% CI: 1.27-1.42). A score of 2, 3, 4, 5 or ≥6 (versus ≤1) had a OR for NH of 1.67 (1.29-2.15), 2.24 (1.65-3.04), 2.83 (2.02-3.98), 3.08 (1.83-5.16), and 6.84 (4.34-10.77), respectively. CONCLUSION: Per each score point, women with GD had 35% higher risk of NH. Those with ≥6 points had 6.8-fold higher risk of NH compared to a score ≤1. Our score may be useful for identifying women at a higher risk of NH.

Association between foetal sex and adverse neonatal outcomes in women with gestational diabetes.

AIMS: Foetal male sex is associated with adverse perinatal outcomes. However, studies evaluating the impact of foetal sex on perinatal outcomes in women with gestational diabetes (GDM) are scarce. We studied whether male new-born sex is associated with neonatal outcomes, in women with GDM. METHODS: This is a retrospective study based on the national Portuguese register of GDM. All women with live-born singleton pregnancies between 2012 and 2017 were eligible for study inclusion. Primary endpoints under analysis were neonatal hypoglycaemia, neonatal macrosomia, respiratory distress syndrome (RDS) and neonatal intensive care unit (NICU) admission. We excluded women with missing data on the primary endpoint. Pregnancy data and neonatal outcomes between female and male new-borns were compared. Multivariate logistic regression models were built. RESULTS: We studied 10,768 new-borns in mothers with GDM, 5635 (52.3%) male, 438 (4.1%) had neonatal hypoglycaemia, 406 (3.8%) were macrosomic, 671 (6.2%) had RDS, and 671 (6.2%) needed NICU admission. Male new-borns were more frequently small or large for gestational age. No differences were observed on maternal age, body mass index, glycated haemoglobin, anti-hyperglycaemic treatment, pregnancy complications or gestational age at delivery. In the multivariate regression analysis, male sex was independently associated with neonatal hypoglycaemia [OR 1.26 (IC 95%: 1.04-1.54), p = 0.02], neonatal macrosomia [1.94 (1.56-2.41), p < 0.001], NICU admission [1.29 (1.07-1.56), p = 0.009], and RDS [1.35 (1.05-1.73, p = 0.02]. CONCLUSIONS: Male new-borns have an independent 26% higher risk of neonatal hypoglycaemia, 29% higher risk of NICU admission, 35% higher risk of RDS, and almost twofold higher risk of macrosomia, compared to female new-borns.

Thyrotropin Secreting Pituitary Adenoma: A Clinical Case of Postoperative Re-Onset Thyrotoxicosis with Adenoma Recurrence.

We report a case of a 19-year-old young male presenting with thyrotoxicosis with inappropriately elevated TSH. Magnetic resonance imaging revealed a pituitary adenoma (8.2 × 9.7 mm), TRH stimulation test showed abnormal blunted TSH response, and serum glycoprotein hormone alpha-sub-unit was elevated. He had no family history of thyroid disease and TRß genetic testing excluded resistance to thyroid hormone action. The diagnosis of thyrotropin-secreting pituitary adenoma (TSHoma) was presumed and long-acting somatostatin analogue was promptly initiated. After two months of octreotide treatment, serum TSH and FT3 returned to within normal ranges. Tumour resection by transsphenoidal surgery was performed and, ten days after surgery, clinical hypothyroidism was achieved, despite detectable TSH levels (TSH 1.02 µU/ml[RR 0.27-4.2]). Although the patient remained euthyroid for the following three years, there was a gradual biochemical elevation in the levels of TSH, FT4, and FT3 over time, reaching serum values above the normal limit in the third year after surgery. Imaging did not show neoplasm recurrence at this point. After two years, the patient presented with clinical manifestations of re-onset thyrotoxicosis, with MRI revealing a T2 hypersignal oval area compatible with a pituitary adenoma. Adenectomy was performed. Histopathological and immunohistochemical analyses revealed a pituitary adenoma with transcription factor PIT1 expression and positivity for TSH and PRL. TSHoma treatment may not be always effective in the first therapeutic approach and recurrences are a possibility, making follow-up essential. The present case highlights the heterogeneity of post-treatment cure criteria and their limitations. LEARNING POINTS: Thyrotropin-secreting pituitary adenomas are rare benign tumours. Proper diagnosis can be challenging, requiring TSH autonomous production and differentiation from resistance to thyroid hormone action (RTH).Undetectable TSH levels one week after surgery and/or positive T3 suppression test or no response to TRH stimulation test seem to be the criteria with the best prognostic value post-treatment.Close clinical, biochemical and imaging follow-up is crucial to detect TSHoma recurrence.

Maternal height as a predictor of glucose intolerance in the postpartum and its relationship with maternal pre-gestational weight.

PURPOSE: Short stature predicts higher risk of developing type 2 diabetes. We studied the association between height and glucose intolerance in women with gestational diabetes mellitus (GDM) and whether this association differed according to body mass index (BMI). METHODS: Retrospective study of the Portuguese GDM registry. EXCLUSION CRITERIA: missing data on postpartum oral glucose tolerance test (OGTT) or BMI. ENDPOINT: postpartum glucose intolerance (diabetes mellitus or prediabetes on the 6-8 weeks postpartum OGTT). Women were divided by mean height and compared. A multivariate logistic regression was used, and the analysis was stratified by BMI (cut-off: 30 kg/m2) and interaction was tested. RESULTS: We included 7402 women; mean height was 161.9 ± 6.2 cm. Taller women had lower BMI and lower rates of glucose intolerance (6.8 vs. 8.8%, p = 0.002). Women with BMI < 30 kg/m2 were taller than those with obesity. Height associated with glucose intolerance. The multivariate adjusted OR of glucose intolerance was 0.98 (95% CI 0.96-0.99), p = 0.001, per 1 cm increase in height. This association was only observed in women with BMI < 30 kg/m2: OR 0.97 (95% CI 0.95-0.99), < 0.001. There was no such association in women with BMI ≥ 30 kg/m2: OR 0.99 (95% CI 0.97-1.02), p = 0.65. P for interaction between BMI and height was 0.09. CONCLUSIONS: In non-obese pre-gestational women, height is inversely associated with postpartum glucose intolerance. Per 1 cm increase in height, women present a 3% decrease in the risk of developing diabetes mellitus or prediabetes.

The prognostic impact of magnesium in acute heart failure is different according to the presence of diabetes mellitus.

Background: Hypermagnesemia predicts mortality in chronic heart failure (HF); however, in acute HF, magnesium does not seem to be outcome-associated. Diabetes mellitus (DM) frequently associates with altered magnesium status. We hypothesized that DM might influence the prognostic impact of magnesium in acute HF. Methods: This is a retrospective cohort study of hospitalized patients with acute HF. Patients without data on admission serum magnesium were excluded. Follow-up: 1 year from hospital admission. Primary end point: all-cause mortality. Patients were divided according to median serum magnesium (1.64 mEq/L). The Kaplan-Meier survival method was used to determine survival curves according to magnesium levels. The analysis was stratified according to the presence of DM. A multivariable Cox regression analysis was used to study the prognostic impact of magnesium. Results: We studied 606 patients. The mean age was 76 ± 12 years, 44.1% were male, 50.7% had DM, and 232 (38.3%) died during follow-up. Median magnesium was 1.64 (1.48-1.79) mEq/L. Patients with magnesium ≥1.64 mEq/L had higher 1-year mortality [141 (46.4%) vs 91 (30.1%), P < .001]. After adjustments for age, sex, history of atrial fibrillation, systolic blood pressure, heart rate, ischemic etiology, B-type natriuretic peptide, estimated glomerular filtration rate, alcohol consumption, antihyperglycaemic agents or glycated hemoglobin, admission glycemia, New York Heart Association class IV, and severe left ventricle systolic dysfunction, serum magnesium ≥1.64 mEq/L was associated with higher mortality only in patients with DM: HR 1.89 (95% confidence interval: 1.19-3.00), P = .007, and 1.27 (95% confidence interval: 0.83-1.94) and P = .26 for non-DM patients. The results were similar if magnesium was analyzed as a continuous variable. Per 0.1 mEq/L increase in magnesium levels, patients with DM had 13% increased risk of 1-year mortality. Conclusions: Higher magnesium levels were associated with worse prognosis only in HF patients with DM.

The prognostic impact of uric acid in acute heart failure according to coexistence of diabetes mellitus.

BACKGROUND AND AIMS: Increased uric acid levels predict higher mortality in heart failure (HF) patients. Patients with diabetes mellitus (DM) appear to have increased xanthine oxidase activity. We aimed to study if the association between uric acid and mortality in acute HF was different according to the coexistence of DM. METHODS AND RESULTS: We studied a cohort of patients hospitalized due to acute HF in 2009-2010. Patients with no uric acid measurement upon admission were excluded from the analysis. FOLLOW-UP: 2 years; endpoint: all-cause mortality. Patients with elevated uric acid (>80.0 mg/L) were compared with those with lower values. We used a multivariate Cox-regression analysis to assess the prognostic impact of uric acid (both continuous and categorical variable: cut-off 80.0 mg/L). The analysis was stratified according to coexistence of DM. We studied 569 acute HF patients, 44.6%male, mean age 76 years, 290 were diabetic. Median admission uric acid: 81.2 mg/L and 52.2%had uric acid >80.0 mg/L. Elevated uric acid predicted all-cause mortality in acute HF only in patients with DM. The multivariate-adjusted HR of 2-year mortality was 1.68 (95 % CI: 1.15-2.46) for diabetic HF patients with uric acid>80.0 mg/L compared to those with lower levels (p = 0.008) and 1.10 (95 % CI: 1.03-1.18) per each 10 mg/L increase in uric acid (p = 0.007). In non-diabetic HF patients, uric acid was not associated with mortality. CONCLUSIONS: Increased uric acid predicts ominous outcome in acute HF patients with diabetes, however, it is not prognostic associated in non-diabetics. Uric acid may play a different role in acute HF depending on DM status.

Not All Pulmonary Densifications Are COVID-19: A Case Report About Lemierre's Syndrome.

Lemierre's syndrome is a rare and a life-threatening disease characterized by anaerobic bacteraemia associated with thrombosis of the internal jugular vein. Odynophagia, otalgia, odontalgia, dyspnoea, cough and fever are the most frequent manifestations. We describe a case of a 37-year-old woman who was admitted to the emergency room due to fever, odynophagia, dyspnoea, myalgia, and pleuritic chest pain. She had hypoxaemia and increased systemic inflammatory markers. The chest CT showed parenchymal densification compatible with severe acute respiratory syndrome coronavirus infection, although all three polymerase chain reaction testing were negative. The neck CT showed occlusion of the left cervical internal jugular vein. She was treated with antibiotics and was discharged. With the reported clinical case the authors intend to clarify the importance of differential diagnosis and the diagnosis of other infectious respiratory conditions at the time of a global pandemic.

The utility of prolactin serial sampling and the best prolactin cut-offs associated with persistent hyperprolactinemia.

BACKGROUND: A single prolactin sampling is recommended for the diagnosis of hyperprolactinemia. We aimed to study the utility of the prolactin serial sampling and to determine the best cut-offs associated with persistent hyperprolactinemia. METHODS: Retrospective study of hyperprolactinemic patients [referral prolactin (rPRL)] that underwent prolactin serial samplings. Prolactin at 0 minutes (PRL0'), 20 to 30, and 40 to 60 minutes. The lowest of these last 2 was defined as nadir prolactin (nPRL). Persistent hyperprolactinemia was defined as nPRL above normal. We excluded patients under dopamine receptor agonists. Receiver-operating characteristic (ROC) curves were used to determine the best rPRL and PRL0' cut-offs predicting persistent hyperprolactinemia. RESULTS: We studied 53 patients (3 males). Median rPRL 48.0 ng/mL (39.5-72.5), PRL0' 34.3 ng/mL (18.0-50.8) and nPRL 29.5 ng/mL (11.4-44.4). PRL0' was elevated in 35 (66.0%) patients and in 7 of them a normal nPRL was reached; therefore 28 (52.8%) had persistent hyperprolactinemia. The area under curve (AUC) for the association between rPRL and persistent hyperprolactinemia was 0.70 (95%CI: 0.56-0.84); best cut-off: 53.4 ng/mL [sensitivity 53.6%, specificity 80.0%, positive predictive value (PPV) 75.0%, and negative predictive value (NPV) 60.6%]. In the 35 patients with elevated PRL0', the AUC was 0.92 (95%CI: 0.81-1.00); best cut-off: 35.2 ng/mL (sensitivity 85.7%, specificity 85.7%, PPV 60.0%, and NPV 96.0%). CONCLUSIONS: Approximately 1/3 of the patients reached a normal PRL0'. In an additional 20%, prolactin normalized after serial samplings. Patients with rPRL >53.4 ng/mL had 75% probability of having persistent hyperprolactinemia and those with PRL0' <35.2 ng/mL had a 96% probability of not having persistent hyperprolactinemia.

Glucose variability predicts 6-month mortality in patients hospitalized with acute heart failure.

In diabetes mellitus (DM), glycaemic fluctuations associate with higher oxidative stress than sustained chronic hyperglycaemia and glucose variability increases the risk of chronic diabetic complications. Our hypothesis was that higher glucose variability would associate with mortality after an acute heart failure (HF) episode. We retrospectively analysed patients with DM hospitalized with acute HF between 2009 and 2010. Patients with < 2 point-of-care glucose values/day were excluded. Glucose coefficient of variation (GCV) was defined as (glucose standard deviation/mean glucose) × 100. Patients were categorized according GCV ≤ 30.0 and > 30.0%. Follow-up: 6-months. Endpoint: all-cause mortality. A Cox-regression analysis was used to study the association of glucose variability with 6-month mortality. We studied 214 diabetic patients with acute HF, 49.1% male, mean age 76 years. Mean glycaemia during hospitalization was 187 ± 50 mg/dL, hypoglycaemia (< 70 mg/dL) was reported in 21 patients and mean GCV was 28.3 ± 7.6%. Patients with GCV > 30.0% had higher mean glycaemia, more hypoglycaemic episodes and higher HbA1c; they were also more often treated with insulin. Patients were similar concerning age, gender, comorbidities, left ventricular systolic dysfunction and ischemic heart disease. During the 6-month follow-up, 38 (17.8%) patients died. Patients with GCV > 30.0% had a HR of 6-month mortality of 2.21 (95% CI: 1.16-4.21), p = 0.02. This association with more than twofold higher short-term mortality was independent of main confounders. Elevated glycaemic variability in acute HF admissions of patients with DM predicts short-term mortality. Patients with GCV > 30.0% have an independent more than twofold higher risk of 6-month death after an acute HF hospitalization.

SIADH in the context of localised Herpes-Zoster infection.

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