Mild Hypertriglyceridemia Research Articles

Conditions Associated With Hypertriglyceridemia in Adult Patients in a Tertiary Care Center in Basrah, Iraq.

Background Hypertriglyceridemia (HTG) is one of the major modifiable risk factors for the development of several metabolic diseases. Determining the factors associated with HTG is an important step for increasing awareness of the problem and proper planning of health programs for HTG prevention. This study aimed to determine the conditions associated with HTG in adult patients in Basrah, Iraq. Methodology This retrospective study was conducted at Faiha Specialized Diabetes Endocrine and Metabolism Center (FDEMC) in Basra, southern Iraq, in January 2024. The data were retrieved from the center database of 37,133 subjects registered from 2008 to 2023 (16,284, 43.8% males and 20,849, 56.2% females) who attended the FDEMC in Basra due to different reasons. Results The most common causes of HTG were type 2 diabetes mellitus (T2DM) (29,799, 80%), obesity (19,914, 53.63%), and smoking (7,309, 12.68%). The age group of 18-45 years displayed higher triglyceride (TG) levels (281.1 ± 210.1 mg/dL) than other age groups. Furthermore, male patients had higher TG levels than females (288.0 ± 196.3 mg/dL vs. 268.9 ± 165.9 mg/dL). Regarding body mass index, overweight and obese patients had higher mean TG levels (284.4 ± 182.1 mg/dL and 281.7 ± 184.6 mg/dL, respectively). Current and ex-smokers had higher TG levels (305.1 ± 212.2 mg/dL and 283.4 ± 161.3 mg/dL, respectively) than non-smokers (272.5 ± 175.4 mg/dL). Moderate HTG was the most common category encountered in 24,137 patients (65%), followed by mild HTG (12,705, 34.2%). Very few patients had severe (264, 7%) or very severe HTG (27, 0.07%). Male patients had more frequent severe and very severe HTG than females. Conclusions The most common conditions associated with HTG were T2DM, obesity, and smoking. Smoker males were prone to severe and very severe HTG.

Effects of hypertriglyceridemia with or without NEFA elevation on β-cell function and insulin clearance and sensitivity.

Hypertriglyceridemia is a risk factor for developing type 2 diabetes (T2D) and might contribute to its pathogenesis either directly or through elevation of non-esterified fatty acids (NEFAs). This study aimed at comparing the glucometabolic effects of acute hypertriglyceridemia alone or combined with NEFA elevation in non-diabetic subjects. Twenty-two healthy lean volunteers underwent two 5-h intravenous infusions of either saline or Intralipid, without (n=12) or with heparin (I+H; n=10) to activate the release of NEFAs. Oral glucose tolerance tests (OGTTs) were performed during the last 3h of infusion. Insulin sensitivity, insulin secretion rate (ISR), model-derived β-cell function, and insulin clearance were measured after 2h of lipid infusion and during the OGTTs. In fasting conditions, both lipid infusions increased plasma insulin and ISR and reduced insulin clearance, without affecting plasma glucose and insulin sensitivity. These effects on insulin and ISR were more pronounced for I+H than Intralipid alone. During the OGTT, the lipid infusions markedly impaired glucose tolerance, increased plasma insulin and ISR, and decreased insulin sensitivity and clearance, without significant group differences. Intralipid alone inhibited glucose-stimulated insulin secretion (i.e. β-cell glucose sensitivity) and increased β-cell potentiation, whereas I+H had neutral effects on these β-cell functions. In healthy non-obese subjects, mild acute hypertriglyceridemia directly reduces glucose tolerance, insulin sensitivity and clearance, and has selective and opposite effects on β-cell function that are neutralized by NEFAs. These findings provide new insight into plausible biological signals that generate and sustain insulin resistance and chronic hyperinsulinemia in the development of T2D.

New approaches to triglyceride reduction: Is there any hope left?

Triglycerides play a crucial role in the efficient storage of energy in the body. Mild and moderate hypertriglyceridemia (HTG) is a heterogeneous disorder with significant association with atherosclerotic cardiovascular disease (ASCVD), including myocardial infarction, ischemic stroke, and peripheral artery disease and represents an important component of the residual ASCVD risk in statin treated patients despite optimal low-density lipoprotein cholesterol reduction. Individuals with severe HTG (>1,000 mg/dL) rarely develop atherosclerosis but have an incremental incidence of acute pancreatitis with significant morbidity and mortality. HTG can occur from a combination of genetic (both mono and polygenic) and environmental factors including poor diet, low physical activity, obesity, medications, and diseases like insulin resistance and other endocrine pathologies. HTG represents a potential target for ASCVD risk and pancreatitis risk reduction, however data on ASCVD reduction by treating HTG is still lacking and HTG-associated acute pancreatitis occurs too rarely to effectively demonstrate treatment benefit. In this review, we address the key aspects of HTG pathophysiology and examine the mechanisms and background of current and emerging therapies in the management of HTG.

Fospropofol disodium versus propofol for long-term sedation during invasive mechanical ventilation: A pilot randomized clinical trial

Study objectiveFospropofol disodium is a propofol prodrug that is water-soluble and has a reduced risk of bacterial contamination and hypertriglyceridemia compared with propofol. Prior to implementing a large randomized trial, we investigated the feasibility, initial efficacy, and safety of fospropofol disodium compared with propofol in long-term mild-to-moderate sedation in intensive care units (ICUs). DesignSingle-centered, prospective, unblind, randomized, parallel-group clinical trial. SettingThe general ICU of university-affiliated teaching hospital. PatientsAdult patients (n = 60) expected to have mechanical ventilation for >24 h were enrolled and randomly assigned to the fospropofol or propofol group.Interventions: The fospropofol group received continuous fospropofol disodium infusions and the propofol group received continuous propofol infusions. The sedation goal was a score of −3 to 0 on the Richmond Agitation and Sedation Scale (RASS). MeasurementsThe primary outcome was the percentage of time spent in the target sedation range without rescue sedation. Safety outcomes were based on adverse events. Blood samples were collected to measure formate concentration in plasma. Main resultsThe median dose was 4.33 (IQR, 3.08–4.94) mg/kg/h in the fospropofol group and 1.96 (IQR, 1.44–2.94) mg/kg/h in the propofol group. The median percentage of time spent in the target RASS range without rescue sedation was identical in both groups, with 83.33% (IQR, 74.43%–100.00%) in the fospropofol group and 83.33% (IQR, 77.45%–100.00%) in the propofol group (p = 0.887). At least one adverse event was identifed in 23 (76.7%) fospropofol patients and 27 (90.0%) propofol patients. The most common adverse events were tachycardia and hypotension. No paresthesia, catheter-related bloodstream infection or propofol infusion syndrome in both groups was reported. Three patients in the fospropofol group had mild hypertriglyceridemia, and nine patients in propofol group had hypertriglyceridemia (mild in eight patients and moderate in one patient) (10% versus 30%, p = 0.104). The formate concentration in plasma was very low, and no significant difference was identified at any time point between the two groups. ConclusionsFospropofol disodium appears to be a feasible, effective and safe sedative for patients receiving invasive mechanical ventilation with long-term sedation.

Isolated hepatomegaly became Her’s – a case report

Glycogen storage diseases (GSDs) are a group of inherited metabolic disorders caused by mutations in one of the several enzymes involved in glycogen synthesis or breakdown. GSD VI is caused by mutations of PYGL gene encoding hepatic glycogen phosphorylase on chromosome 14q22.1, which has a major role in glycogen metabolism. We report a case of 2year old girl child presented with complaints of slowly progressive abdominal distention of one year duration. Abdominal examination revealed hepatomegaly (liver span 9cm). Lab investigations revealed mild anemia, hypertriglyceridemia and normal liver function. Liver biopsy showed marked elevation of glycogen content in liver with structurally normal glycogen which was consistent with GSD. Sanger sequencing done to identify the subtype of GSD showed PYGL gene mutation, pathogenic variant of type-VIGSD. In the case of isolated hepatomegaly, a glycogen storage disease must be considered in the differential diagnosis and Sanger sequencing must be done for confirmation and prognostication

Evaluation of equations for calculating LDL-cholesterol in patients with concomitant hypertriglyceridemia and low LDL-cholesterol: is there a preferred equation?

It is critical to reliably estimate Low Density Lipoprotein Cholesterol (LDL-C) in patients with concomitant hypertriglyceridemia and low LDL-C. We retrospectively compared the performances of the Friedewald (LDL-F), Martin-Hopkins (LDL-MH) and Sampson (LDL-SA) equations against a direct homogeneous LDL-C assay (dLDL-C) on observations presenting mild hypertriglyceridemia (triglycerides between 1.69 and 3.9 mmol/L) and low LDL-C (< 2.58 mmol/L). Observations were stratified according to their LDL-C. Agreement of the equations with dLDL-C was assessed using Intraclass Correlation Coefficients (ICC) with an agreement cut-off of 0.9, and analysis of Bland-Altman plots. Independently of the LDL-C stratum evaluated, the three equations failed to meet the 0.9 ICC cut-off, although their agreement with dLDL-C improves as LDL-C increases. Analysis of Bland-Altman plots shows a downwards discordance of LDL-F with dLDL-C, and an upwards discordance of LDL-MH and LDL-SA with direct LDL-C. LDL-MH resulted in the least observations outside the Bland-Altman limits of agreement. While no equation can be deemed satisfactory enough to replace direct assays in patients with low LDL-C and concomitant hypertriglyceridemia, LDL-MH seems to perform better than the other equations in estimating LDL-C in these patients.

The nature and characteristics of hypertriglyceridemia in a large cohort with type 2 diabetes

AimsTo determine the prevalence of mild, moderate and severe hypertriglyceridemia (HTG) in a large, diverse healthcare system cohort with type 2 diabetes (T2D) and to study associations between triglyceride levels and demographic factors, glycemic control, body weight and to investigate whether triglyceride levels associate with markers of fatty liver and renal disease. Methods19,086 individuals with T2D were studied between 2015 and 2020. We compared groups with normotriglyceridemia (<150 mg/dl [<1.7 mmol/l]), mild (150-199 mg/dl [1.7–2.25 mmol/l]), moderate (200-499 mg/dl [2.26–5.64 mmol/l]) or severe HTG (>499 mg/dl [>5.64 mmol/l]). We also performed univariate and multivariate correlational analyses with triglyceride level as a continuous variable. Results39 % had triglyceride levels ≥150 mg/dl (<1.7 mmol/l), 19 % had moderate and 2 % had severe HTG. There was a lower proportion of Blacks in all HTG categories compared to Whites. There was no overall gender difference in prevalence except that severe HTG was more common in men and as HTG severity worsened mean age fell. Triglycerides correlated with HbA1c and associated with BMI, LDL-C, diastolic BP, transaminases and urine albumin/creatinine ratio, independent of HbA1c. ConclusionThis study fills gaps in our knowledge of the distribution and clinical associations of HTG in T2D and characterizes the features of the small but important group with severe HTG. We demonstrate the influence of age, sex and race, confirm the moderate effects of glycemic control and obesity on triglyceride level, and provide evidence that triglyceride levels may be a marker for fatty liver and nephropathy independent of glycemic control.

Prospective Validation of a Machine Learning Model for Low-Density Lipoprotein Cholesterol Estimation.

We aim to prospectively validate a previously developed machine learning algorithm for low-density lipoprotein cholesterol (LDL-C) estimation. We retrospectively and prospectively evaluated a machine learning algorithm based on k-nearest neighbors (KNN) according to age, sex, healthcare setting, and triglyceridemia against a direct LDL-C assay. The agreement of low-density lipoprotein-k-nearest neighbors (LDL-KNN) with the direct measurement was assessed using intraclass correlation coefficient (ICC). The analysis comprised 31,853 retrospective and 6599 prospective observations, with a mean age of 54.2 ± 17.2 years. LDL-KNN exhibited an ICC greater than 0.9 independently of age, sex, and disease status. LDL-KNN was in satisfactory agreement with direct LDL-C in observations with normal triglyceridemia and mild hypertriglyceridemia but displayed an ICC slightly below 0.9 in severely hypertriglyceridemic patients and lower in very low LDL-C observations. LDL-KNN performs robustly across ages, genders, healthcare settings, and triglyceridemia. Further algorithm development is needed for very low LDL-C observations.

Abstract #1185237: Tamoxifen Induced pancreatitis in a non-diabetic patient with hypertriglyceridemia

Tamoxifen is a selective estrogen receptor modulator (SERM) used in breast cancer treatment. It interferes with triglyceride metabolism causing hypertriglyceridemia and can precipitate pancreatitis. We report a case of a non- diabetic middle-aged woman with a history of mild hypertriglyceridemia who presented with acute pancreatitis while on chronic tamoxifen treatment for breast cancer.

Severe hypertriglyceridemia in the course of ketoacidosis in a patient with newly diagnosed type 1 diabetes mellitus

BACKGROUND: One of the most serious complications in delayed diagnosis of DKA is hypertriglyceridemia (HTG), Prevalence of mild hypertriglyceridemia is found in about 50% of patients with diabetic ketoacidosis (DKA). Prevalence of severe hypertriglyceridemia [TG &gt; 22.4 mmol/L (&gt; 1959 mg/dL)] was found in about 1–8% of adults with DKA, but few data have been reported in children with severity ranging from asymptomatic to severe acute pancreatitis. CASE PRESENTATION: A 2-year-old-girl with a 2 weeks history of generalized weakness, polydipsia, polyuria, and vulvar candidiasis was admitted to the Intensive Care Unit with clinical signs of DKA. Our patient was met the diagnostic criteria for DKA (pH 7.1, HCO3- 8.8 mmol/L, BE -21.1 mmol/L), glucose level of &gt; 22 mmol/L (556 mg/dl). Initial biochemical analysis showed hyperlipidemia [TG 11470 mg/dL (131.1 mmol/L)], amylase 28 U/L. Her blood demonstrated a grossly lipemic appearance and her lipemic condition disturbed the results of other biochemical blood investigations. The objective of this case report is to present and describe the clinical features, laboratory investigations, case management, and natural course of hypertriglyceridemia in a 2-year-old girl with DKA. CONCLUSIONS: Lipemia secondary to severe HTG may exist in new-onset T1DM with DKA. Diabetic lipemia can be caused not only by profound insulin deficiency. An additional factor which should be taken into consideration in very young children is breastfeeding, which is associated with increased mean total cholesterol (TC) and LDL levels. Moreover, severe hypertriglyceridemia may result in mutations of genes encoding lipoprotein lipase (LPL).

A More Atherogenic Lipoprotein Status Is Present in Adults With Type 2 Diabetes Mellitus Than in Those Without With Equivalent Degrees of Hypertriglyceridemia

ObjectivesThe impact of type 2 diabetes (T2DM) on biomarkers denoting lipoprotein compositional status was studied in mild and moderate hypertriglyceridemia (HTG). Diabetic dyslipidemia pathophysiology could contribute to differences in lipoprotein compositional status, which could be reflected in the preferred cardiovascular disease risk prediction markers in HTG: non–high-density lipoprotein cholesterol (non-HDLC) and apolipoprotein B (apoB). MethodsA total of 2,775 fasting lipid profiles from a tertiary care lipid clinic were analyzed as 2 subgroups (with and without T2DM), stratified by triglyceride (TG) levels: normotriglyceridemia (TG 0.01 to 1.7 mmol/L), mild HTG (TG 1.71 to 5 mmol/L) and moderate HTG (TG 5.01 to 10 mmol/L). The mean non-HDLC:apoB ratio in each TG stratum and subgroup was analyzed. We also used linear regression to assess the correlation between non-HDLC and apoB. ResultsThe mean non-HDLC:apoB ratio was increased in both subgroups in patients with mild and moderate HTG, compared to those with normotriglyceridemia. In moderate HTG, the mean non-HDLC:apoB ratio in the subgroup with T2DM was significantly lower than the subgroup without T2DM. In mild and moderate HTG, the subgroup with T2DM had a stronger correlation between non-HDLC and apoB than did the subgroup without T2DM. Discussion and conclusionsIn mild and moderate HTG, adults with T2DM exhibit lipid profiles that represent a different and more atherogenic lipoprotein compositional status, when compared with adults without T2DM. For the same severity of HTG, the lipoprotein compositional status in diabetic dyslipidemia suggests that there is increased abundance of smaller non-HDL particles and their remnants, which are highly atherogenic.

Tolerance and response to ketogenic therapy in neonates and infants younger than 4 months. Case series in a hospital center in Medellin, Colombia.

Ketogenic therapy (KT) studies have focused in children older than 2 years and adults. Recently its efficacy in infants has been reported, but there are few studies in this age group. We report a case series of nine newborn and children younger than 4 months of age with refractory epilepsy treated with KT. We retrospectively reviewed charts of children treated at our center between 2015-2021. Data was collected on seven patients. Six patients began having seizures on day one of life, one had seizures starting on day 45. Different epilepsy etiologies were found. KT was started as soon as 9 days of life. The average age at which ketogenic therapy was started was 24 days of life. Initially, the diet was started at 1:1 or 2:1 ratio, and was progressed to a 4:1 ratio. After one month of KT 5/7 patients experienced a significant reduction in seizure frequency (>50%) and 2/7 had complete seizure control. At six months, 4/7 patients achieve complete seizure freedom and 1/7 had >50% seizure reduction. Two patients were lost to follow-up. None of our patients reported gastrointestinal side effects that required diet adjustments. One patient had mild and one mild hypertriglyceridemia. Even though evidence about KT in young children are starting to emerge, our experience shows it can be successful in controlling seizure burden without considerable adverse effects. There is great research potential regarding KT in young children.

The role of comorbid hypertriglyceridemia and abdominal obesity in the severity of acute pancreatitis: a retrospective study

BackgroundThe effect of comorbid hypertriglyceridemia (HTG) and abdominal obesity (AO) on acute pancreatitis (AP) remains unclear. The aim of this study was to explore the effect of comorbid HTG and AO and discuss which is the dominant disorder.MethodsIn this study, 1219 AP patients who presented with HTG or AO were stratified into four groups: non-HTG + non-AO, HTG + non-AO, non-HTG + AO, and HTG + AO.ResultsThe 328 patients with comorbid HTG + AO were much younger (42.29 ± 11.77), mainly male (79.57%), and had higher TG levels, larger waist circumferences, and more past medical histories than the patients in the other three non-comorbid groups (P < 0.001). The comorbidity group developed more incidences of persistent organ failure and local complications (P < 0.05). Multivariate logistic regression analysis showed that AO (OR = 3.205, 95% CI = 1.570–6.544), mild HTG (OR = 2.746, 95% CI = 1.125–6.701), and moderate to very severe HTG (OR = 3.649, 95% CI = 1.403–9.493) were independent risk factors for persistent respiratory failure (P < 0.05). Age > 60 years (OR = 1.326, 95% CI = 1.047–1.679), AO (OR = 1.701, 95% CI = 1.308–2.212), diabetes mellitus (OR = 1.551, 95% CI = 1.063–2.261), mild HTG (OR = 1.549, 95% CI = 1.137–2.112), and moderate to very severe HTG (OR = 2.810, 95% CI = 1.926–4.100) were independent risk factors associated with local complications (P < 0.05). Moreover, HTG seemed to be more dangerous than AO. The higher the serum TG level was, the greater the likelihood of persistent respiratory failure and local complications.ConclusionsComorbid HTG and AO will aggravate the severity and increase the incidence of local complications of AP. HTG may play a dominant role of risk in the condition of comorbidity.Chinese clinical trial registryChiCTR2100049566. Registered on 3rd August, 2021. Retrospectively registered, https://www.chictr.org.cn/edit.aspx?pid=127374&htm=4.

Very severe hypertriglyceridemia in a subject with poor glycemic control: a case report with general consideration

Hypertriglyceridemia is defined as a value of fasting serum triglyceride over 150 mg/dl. The classification of hypertriglyceridemia according to the Endocrine Society includes mild and moderate hypertriglyceridemia, severe hypertriglyceridemia and very severe hypertriglyceridemia. Mild and moderate hypertriglyceridemia increases the risk for cardiovascular events while severe and very severe hypertriglyceridemia is a risk factor for acute pancreatitis. Conventional pharmacological therapy of hypertriglyceridemia includes fibrates, niacin, statins, ezetimibe, and omega-3 fatty acid. Other triglyceride-lowering therapies are represented by plasmapheresis and lipoprotein lipase gene therapy. The present work refers to a 55-year-old man without a history of family diabetes mellitus (DM), dyslipidemia, premature coronary artery disease, diagnosed with type 2 DM in 2016, from 2018 on insulin treatment; he was hospitalized for endocrine evaluation. The patient had a history of high blood pressure for approximately 15 years, chronic kidney disease, very severe hypertriglyceridemia, and chronic obstructive pulmonary disease. The patient followed treatment with hypoglycemic, hypolipemic, low-salt diet, fibrates, statins, omega-3 fatty acid.

Prevalence of severe hypertriglyceridemia and pancreatitis in familial partial lipodystrophy type 2

Familial partial lipodystrophy (FPLD) is a rare Mendelian condition listed in the differential diagnosis of severe hypertriglyceridemia (HTG) and pancreatitis. Here we determined the prevalence of severe HTG and pancreatitis among a cohort of 74 FPLD patients assessed in a lipid clinic. We studied lipid profiles from individuals with either of the two most common pathogenic monoallelic variants in LMNA, namely p.R482Q (N= 51) and p.R482W (N= 23). In total, 28 (37.8%) patients with a mean age of 41.8 ± 14.8 years had diabetes, while 46 (62.2%) patients with a mean age of 35.4 ± 19.4 years had no diabetes. Among patients with and without diabetes, median TG levels (interquartile range) were 2.73 (4.78) and 1.86 (1.66) mmol/L (242 [423] and 165 [147] mg/dL), respectively. Overall, 4 subjects (5.4%) had triglyceride levels > 10 mmol/L (> 885 mg/dL), of whom 3 (4.1%) had a history of hospitalization for acute pancreatitis. All 4 patients with severe HTG had diabetes, i.e. 14.3% of those with diabetes. In contrast, FPLD2 patients without diabetes had only mild HTG, with no instances of severe HTG or pancreatitis. Thus, among this selected lipid clinic cohort with lipodystrophy, severe HTG and pancreatitis in FPLD2 are relatively common when diabetes is present.

Is Machine Learning-derived Low-Density Lipoprotein Cholesterol estimation more reliable than standard closed form equations? Insights from a laboratory database by comparison with a direct homogeneous assay

BackgroundThere is no consensus on the best method to estimate Low Density Lipoprotein-Cholesterol (LDL-C) in routine laboratories. MethodsWe conducted a retrospective study to compare the performances of a Machine Learning (ML) algorithm using the K-Nearest Neighbors (LDL-KNN) method with that of the Friedewald formula (LDL-F), the Martin-Hopkins equation (LDL-NF), the de Cordova equation (LDL-CO) and the Sampson equation (LDL-SA) against direct homogeneous LDL-C assay (LDL-D) in patients who presented to the Laboratories of Hôtel Dieu de France university hospital in Beirut, Lebanon, from September 2017 to July 2020. Agreements between methods were analyzed using Intraclass Correlation Coefficients (ICC) and the Bland-Altman method of agreement. Results31,922 observations from 19,279 subjects were included, with a mean age of 52 ± 18 years and 10,075 (52.3%) females. All methods except LDL-F and LDL-CO exhibited an overall ICC beyond the 0.9 cut-off. LDL-SA, LDL-NF and LDL-KNN were less susceptible to triglyceridemia than LDL-F and LDL-CO, with LDL-KNN resulting in the lesser fraction of points beyond the Bland-Altman limits of agreement. ConclusionAn ML algorithm using LDL-KNN is promising for the estimation of LDL-C as it agrees better with LDL-D than closed form equations, especially in mild and severe hypertriglyceridemia.

Fluphenazine-Induced Severe Hypertriglyceridemia

Introduction: Antipsychotics are known to result in lipid dysregulation, possibly through their effects on weight, appetite and increased glucose intolerance. These effects are seen in varying degrees with both typical and atypical antipsychotics. This results in a cohort of patients with drug-induced hyperlipidemia, who benefit from lipid-lowering therapy. We describe an extreme scenario where the use of fluphenazine resulted in very severe hypertriglyceridemia, in addition to new onset diabetes requiring inpatient management.Case: A 42-year-old man with schizophrenia and a history of mild hypertriglyceridemia presented to the emergency department with one month of polyuria and polydipsia, and a home glucose measurement of >500 mg/dL. Six months earlier, he had been started on fluphenazine for schizophrenia. Laboratory testing at that time showed Hemoglobin A1c of 6.0% and a mild elevation in triglycerides to 188 mg/dL. He endorsed a family history of hypertriglyceridemia and type two diabetes. On physical exam, he appeared healthy with no abnormal focal findings. Labs revealed Hemoglobin A1c of 14% and a triglyceride level of 15,213 mg/dL. His blood samples became rapidly lipemic within a few minutes of the blood draw, corrupting the majority of the lab values. He was admitted to the ICU for continuous IV insulin, which improved his severe hypertriglyceridemia over the course of one week. Fluphenazine was switched to ziprasidone for schizophrenia. Pancreatic autoimmune workup was negative. Once the patient’s triglyceride level was <1000 mg/dL, insulin drip was discontinued and gemfibrozil was started. His triglyceride level at discharge was 449 mg/dL, and decreased to within the normal range over the course of a few months at outpatient follow up.Discussion: The highest on the differential for this case is fluphenazine-associated worsening of pre-existing hypertriglyceridemia in a patient with risk factors for metabolic syndrome. Antipsychotics can result in new-onset or worsening of metabolic syndrome. These patients can usually be managed in the outpatient setting with lipid-lowering therapies and glycemic control. This case represents a rare scenario of a dramatic hypertryglyceridemia and worsening of diabetes secondary to the use of the typical antipsychotic fluphenazine.

Concurrent Diabetic Ketoacidosis and Acute Pancreatitis in Mild Hypertriglyceridemia: An Enigmatic Triangle

Hypertriglyceridemia (HTG) is a well-established cause of acute pancreatitis (AP). Diabetic ketoacidosis (DKA) leads to lipolysis and HTG, and can result in AP. Triad of AP, DKA, and HTG is rare and not fully understood. Usually AP is associated with severe HTG with serum triglyceride (TG) level over 1,000 mg/dL. However, we experienced two cases of AP in DKA with mild HTG with TG level less than 200 mg/dL. Herein, we report these unusual cases and provide a review of the literature about the triad of DKA, HTG, and AP.

Plasma glycerol levels in men with hypertriglyceridemia

When plasma triglyceride is assessed in standard laboratories, it is a measurement of plasma glycerol after hydrolysis of triglycerides into fatty acids and glycerol. In most patients, the plasma level of free glycerol will only marginally influence the measurement of plasma triglyceride. However, in rare cases elevated free glycerol concentrations causes pseudohypertriglyceridemia and blanking for free glycerol becomes important. In this study, we investigated the plasma free glycerol level in 100 adult men with mild to moderate hypertriglyceridemia to assess the need for providing a free glycerol measurement in our clinical biochemistry department. The plasma samples were obtained in our blood sampling facility that receives both in- and outpatients. The highest plasma level of free glycerol observed was 300 µmol/L and in 99% of the investigated men the inclusion of plasma free glycerol in the measurement of plasma triglyceride cause a less than 10% false increase in plasma triglyceride. A weak positive correlation between the plasma levels of free glycerol and triglyceride was observed. When subdividing the cohort into mild and moderate hypertriglyceridemia, the positive correlation was only maintained in the moderate hypertriglyceridemia group that also demonstrated a 23% higher plasma glycerol level than men with mild hypertriglyceridemia. We conclude that even though glycerol blanking is relevant in rare occasions, then this study does not support providing such a measurement in our department. The positive correlation between free glycerol and triglyceride in this cohort likely reflects a shared association with metabolic dysregulation.

Pulmonary Wild Type TTR Amyloidosis in a Post Orthotopic Heart Transplant Patient

Introduction In patients with systemic amyloidosis with pulmonary involvement, the most common amyloid subtype is thought to be light chain (AL) amyloidosis. However, retrospective studies have shown wild-type ATTR (wtATTR) deposits to be an incidental finding at autopsy in 14% of patients despite being rarely symptomatic. Case Report A 70-year-old male presents with progressive NYHA II symptoms and worsening bilateral lower extremity neuropathy nearly three years following orthotopic heart transplantation for wtATTR cardiac amyloidosis. As the donor was low risk, his immediate post-operative course was uncomplicated save for mild coronary allograft vasculopathy and hypertriglyceridemia. Initial workup of his dyspnea revealed normal biventricular function. Given his history of amyloidosis, repeat cardiac biopsy was performed and failed to show evidence of amyloid deposition. A PYP scan was similarly performed without suggestion of cardiac involvement. After failing to improve clinically despite two rounds of antibiotics, he underwent a chest CT demonstrating a new left lower lobe ground-glass opacification with tree-in-bud nodules and PFTs showing mild obstructive disease. Follow-up bronchoscopy with endobronchial biopsy was without evidence of infection, sirolimus-related pneumonitis, or malignancy but curiously did reveal evidence of wtATTR, confirmed by mass spectroscopy. Summary At the present time, wtATTR stabilizers such as tafamidis are not approved in the United States for pulmonary wtATTR amyloidosis nor for amyloid-related polyneuropathy. It remains unknown whether his presenting symptoms are attributable to the wtATTR amyloid infiltrate. One must wonder whether treatment of his pulmonary wtATTR using off-label tafamidis would translate into symptomatic improvement and potentially improve his quality (and perhaps even quantity) of life.