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Case 6–2020: A 34-Year-Old Woman with Hyperglycemia

Presentation of case.

Dr. Max C. Petersen (Medicine): A 34-year-old woman was evaluated in the diabetes clinic of this hospital for hyperglycemia.

Eleven years before this presentation, the blood glucose level was 126 mg per deciliter (7.0 mmol per liter) on routine laboratory evaluation, which was performed as part of an annual well visit. The patient could not recall whether she had been fasting at the time the test had been performed. One year later, the fasting blood glucose level was 112 mg per deciliter (6.2 mmol per liter; reference range, <100 mg per deciliter [<5.6 mmol per liter]).

Nine years before this presentation, a randomly obtained blood glucose level was 217 mg per deciliter (12.0 mmol per liter), and the patient reported polyuria. At that time, the glycated hemoglobin level was 5.8% (reference range, 4.3 to 5.6); the hemoglobin level was normal. One year later, the glycated hemoglobin level was 5.9%. The height was 165.1 cm, the weight 72.6 kg, and the body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) 26.6. The patient received a diagnosis of prediabetes and was referred to a nutritionist. She made changes to her diet and lost 4.5 kg of body weight over a 6-month period; the glycated hemoglobin level was 5.5%.

Six years before this presentation, the patient became pregnant with her first child. Her prepregnancy BMI was 24.5. At 26 weeks of gestation, the result of a 1-hour oral glucose challenge test (i.e., the blood glucose level obtained 1 hour after the oral administration of a 50-g glucose load in the nonfasting state) was 186 mg per deciliter (10.3 mmol per liter; reference range, <140 mg per deciliter [<7.8 mmol per liter]). She declined a 3-hour oral glucose tolerance test; a presumptive diagnosis of gestational diabetes was made. She was asked to follow a meal plan for gestational diabetes and was treated with insulin during the pregnancy. Serial ultrasound examinations for fetal growth and monitoring were performed. At 34 weeks of gestation, the fetal abdominal circumference was in the 76th percentile for gestational age. Polyhydramnios developed at 37 weeks of gestation. The child was born at 39 weeks 3 days of gestation, weighed 3.9 kg at birth, and had hypoglycemia after birth, which subsequently resolved. Six weeks post partum, the patient’s fasting blood glucose level was 120 mg per deciliter (6.7 mmol per liter), and the result of a 2-hour oral glucose tolerance test (i.e., the blood glucose level obtained 2 hours after the oral administration of a 75-g glucose load in the fasting state) was 131 mg per deciliter (7.3 mmol per liter; reference range, <140 mg per deciliter). Three months post partum, the glycated hemoglobin level was 6.1%. Lifestyle modification for diabetes prevention was recommended.

Four and a half years before this presentation, the patient became pregnant with her second child. Her prepregnancy BMI was 25.1. At 5 weeks of gestation, she had an elevated blood glucose level. Insulin therapy was started at 6 weeks of gestation, and episodes of hypoglycemia occurred during the pregnancy. Serial ultrasound examinations for fetal growth and monitoring were performed. At 28 weeks of gestation, the fetal abdominal circumference was in the 35th percentile for gestational age, and the amniotic fluid level was normal. Labor was induced at 38 weeks of gestation; the child weighed 2.6 kg at birth. Neonatal blood glucose levels were reported as stable after birth. Six weeks post partum, the patient’s fasting blood glucose level was 133 mg per deciliter (7.4 mmol per liter), and the result of a 2-hour oral glucose tolerance test was 236 mg per deciliter (13.1 mmol per liter). The patient received a diagnosis of type 2 diabetes mellitus; lifestyle modification was recommended. Three months post partum, the glycated hemoglobin level was 5.9% and the BMI was 30.0. Over the next 2 years, she followed a low-carbohydrate diet and regular exercise plan and self-monitored the blood glucose level.

Two years before this presentation, the patient became pregnant with her third child. Blood glucose levels were again elevated, and insulin therapy was started early in gestation. She had episodes of hypoglycemia that led to adjustment of her insulin regimen. The child was born at 38 weeks 5 days of gestation, weighed 3.0 kg at birth, and had hypoglycemia that resolved 48 hours after birth. After the birth of her third child, the patient started to receive metformin, which had no effect on the glycated hemoglobin level, despite adjustment of the therapy to the maximal dose.

One year before this presentation, the patient became pregnant with her fourth child. Insulin therapy was again started early in gestation. The patient reported that episodes of hypoglycemia occurred. Polyhydramnios developed. The child was born at 38 weeks 6 days of gestation and weighed 3.5 kg. The patient sought care at the diabetes clinic of this hospital for clarification of her diagnosis.

The patient reported following a low-carbohydrate diet and exercising 5 days per week. There was no fatigue, change in appetite, change in vision, chest pain, shortness of breath, polydipsia, or polyuria. There was no history of anemia, pancreatitis, hirsutism, proximal muscle weakness, easy bruising, headache, sweating, tachycardia, gallstones, or diarrhea. Her menstrual periods were normal. She had not noticed any changes in her facial features or the size of her hands or feet.

The patient had a history of acne and low-back pain. Her only medication was metformin. She had no known medication allergies. She lived with her husband and four children in a suburban community in New England and worked as an administrator. She did not smoke tobacco or use illicit drugs, and she rarely drank alcohol. She identified as non-Hispanic white. Both of her grandmothers had type 2 diabetes mellitus. Her father had hypertension, was overweight, and had received a diagnosis of type 2 diabetes at 50 years of age. Her mother was not overweight and had received a diagnosis of type 2 diabetes at 48 years of age. The patient had two sisters, neither of whom had a history of diabetes or gestational diabetes. There was no family history of hemochromatosis.

On examination, the patient appeared well. The blood pressure was 126/76 mm Hg, and the heart rate 76 beats per minute. The BMI was 25.4. The physical examination was normal. The glycated hemoglobin level was 6.2%.

A diagnostic test was performed.


Dr. Miriam S. Udler: I am aware of the diagnosis in this case and participated in the care of this patient. This healthy 34-year-old woman, who had a BMI just above the upper limit of the normal range, presented with a history of hyperglycemia of varying degrees since 24 years of age. When she was not pregnant, she was treated with lifestyle measures as well as metformin therapy for a short period, and she maintained a well-controlled blood glucose level. In thinking about this case, it is helpful to characterize the extent of the hyperglycemia and then to consider its possible causes.


This patient’s hyperglycemia reached a threshold that was diagnostic of diabetes 1 on two occasions: when she was 25 years of age, she had a randomly obtained blood glucose level of 217 mg per deciliter with polyuria (with diabetes defined as a level of ≥200 mg per deciliter [≥11.1 mmol per liter] with symptoms), and when she was 30 years of age, she had on the same encounter a fasting blood glucose level of 133 mg per deciliter (with diabetes defined as a level of ≥126 mg per deciliter) and a result on a 2-hour oral glucose tolerance test of 236 mg per deciliter (with diabetes defined as a level of ≥200 mg per deciliter). On both of these occasions, her glycated hemoglobin level was in the prediabetes range (defined as 5.7 to 6.4%). In establishing the diagnosis of diabetes, the various blood glucose studies and glycated hemoglobin testing may provide discordant information because the tests have different sensitivities for this diagnosis, with glycated hemoglobin testing being the least sensitive. 2 Also, there are situations in which the glycated hemoglobin level can be inaccurate; for example, the patient may have recently received a blood transfusion or may have a condition that alters the life span of red cells, such as anemia, hemoglobinopathy, or pregnancy. 3 These conditions were not present in this patient at the time that the glycated hemoglobin measurements were obtained. In addition, since the glycated hemoglobin level reflects the average glucose level typically over a 3-month period, discordance with timed blood glucose measurements can occur if there has been a recent change in glycemic control. This patient had long-standing mild hyperglycemia but met criteria for diabetes on the basis of the blood glucose levels noted.

Type 1 and Type 2 Diabetes

Now that we have characterized the patient’s hyperglycemia as meeting criteria for diabetes, it is important to consider the possible types. More than 90% of adults with diabetes have type 2 diabetes, which is due to progressive loss of insulin secretion by beta cells that frequently occurs in the context of insulin resistance. This patient had received a diagnosis of type 2 diabetes; however, some patients with diabetes may be given a diagnosis of type 2 diabetes on the basis of not having features of type 1 diabetes, which is characterized by autoimmune destruction of the pancreatic beta cells that leads to rapid development of insulin dependence, with ketoacidosis often present at diagnosis.

Type 1 diabetes accounts for approximately 6% of all cases of diabetes in adults (≥18 years of age) in the United States, 4 and 80% of these cases are diagnosed before the patient is 20 years of age. 5 Since this patient’s diabetes was essentially nonprogressive over a period of at least 9 years, she most likely does not have type 1 diabetes. It is therefore not surprising that she had received a diagnosis of type 2 diabetes, but there are several other types of diabetes to consider, particularly since some features of her case do not fit with a typical case of type 2 diabetes, such as her age at diagnosis, the presence of hyperglycemia despite a nearly normal BMI, and the mild and nonprogressive nature of her disease over the course of many years.

Less Common Types of Diabetes

Latent autoimmune diabetes in adults (LADA) is a mild form of autoimmune diabetes that should be considered in this patient. However, there is controversy as to whether LADA truly represents an entity that is distinct from type 1 diabetes. 6 Both patients with type 1 diabetes and patients with LADA commonly have elevated levels of diabetes-associated autoantibodies; however, LADA has been defined by an older age at onset (typically >25 years) and slower progression to insulin dependence (over a period of >6 months). 7 This patient had not been tested for diabetes-associated autoantibodies. I ordered these tests to help evaluate for LADA, but this was not my leading diagnosis because of her young age at diagnosis and nonprogressive clinical course over a period of at least 9 years.

If the patient’s diabetes had been confined to pregnancy, we might consider gestational diabetes, but she had hyperglycemia outside of pregnancy. Several medications can cause hyperglycemia, including glucocorticoids, atypical antipsychotic agents, cancer immunotherapies, and some antiretroviral therapies and immunosuppressive agents used in transplantation. 8 However, this patient was not receiving any of these medications. Another cause of diabetes to consider is destruction of the pancreas due to, for example, cystic fibrosis, a tumor, or pancreatitis, but none of these were present. Secondary endocrine disorders — including excess cortisol production, excess growth hormone production, and pheochromocytoma — were considered to be unlikely in this patient on the basis of the history, review of symptoms, and physical examination.

Monogenic Diabetes

A final category to consider is monogenic diabetes, which is caused by alteration of a single gene. Types of monogenic diabetes include maturity-onset diabetes of the young (MODY), neonatal diabetes, and syndromic forms of diabetes. Monogenic diabetes accounts for 1 to 6% of cases of diabetes in children 9 and approximately 0.4% of cases in adults. 10 Neonatal diabetes is diagnosed typically within the first 6 months of life; syndromic forms of monogenic diabetes have other abnormal features, including particular organ dysfunction. Neither condition is applicable to this patient.

MODY is an autosomal dominant condition characterized by primary pancreatic beta-cell dysfunction that causes mild diabetes that is diagnosed during adolescence or early adulthood. As early as 1964, the nomenclature “maturity-onset diabetes of the young” was used to describe cases that resembled adult-onset type 2 diabetes in terms of the slow progression to insulin use (as compared with the rapid progression in type 1 diabetes) but occurred in relatively young patients. 11 Several genes cause distinct forms of MODY that have specific disease features that inform treatment, and thus MODY is a clinically important diagnosis. Most forms of MODY cause isolated abnormal glucose levels (in contrast to syndromic monogenic diabetes), a manifestation that has contributed to its frequent misdiagnosis as type 1 or type 2 diabetes. 12

Genetic Basis of MODY

Although at least 13 genes have been associated with MODY, 3 genes — GCK , which encodes glucokinase, and HNF1A and HNF4A , which encode hepatocyte nuclear factors 1A and 4A, respectively — account for most cases. MODY associated with GCK (known as GCK-MODY) is characterized by mild, nonprogressive hyperglycemia that is present since birth, whereas the forms of MODY associated with HNF1A and HNF4A (known as HNF1A-MODY and HNF4A-MODY, respectively) are characterized by the development of diabetes, typically in the early teen years or young adulthood, that is initially mild and then progresses such that affected patients may receive insulin before diagnosis.

In patients with GCK-MODY, genetic variants reduce the function of glucokinase, the enzyme in pancreatic beta cells that functions as a glucose sensor and controls the rate of entry of glucose into the glycolytic pathway. As a result, reduced sensitivity to glucose-induced insulin secretion causes asymptomatic mild fasting hyperglycemia, with an upward shift in the normal range of the fasting blood glucose level to 100 to 145 mg per deciliter (5.6 to 8.0 mmol per liter), and also causes an upward shift in postprandial blood glucose levels, but with tight regulation maintained ( Fig. 1 ). 13 This mild hyperglycemia is not thought to confer a predisposition to complications of diabetes, 14 is largely unaltered by treatment, 15 and does not necessitate treatment outside of pregnancy.

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Key features suggesting maturity-onset diabetes of the young (MODY) in this patient were an age of less than 35 years at the diagnosis of diabetes, a strong family history of diabetes with an autosomal dominant pattern of inheritance, and hyperglycemia despite a close-to-normal body-mass index. None of these features is an absolute criterion. MODY is caused by single gene–mediated disruption of pancreatic beta-cell function. In MODY associated with the GCK gene (known as GCK-MODY), disrupted glucokinase function causes a mild upward shift in glucose levels through-out the day and does not necessitate treatment. 13 In the pedigree, circles represent female family members, squares male family members, blue family members affected by diabetes, and green unaffected family members. The arrow indicates the patient.

In contrast to GCK-MODY, the disorders HNF1A-MODY and HNF4A-MODY result in progressive hyperglycemia that eventually leads to treatment. 16 Initially, there may be a normal fasting glucose level and large spikes in postprandial glucose levels (to >80 mg per deciliter [>4.4 mmol per liter]). 17 Patients can often be treated with oral agents and discontinue insulin therapy started before the diagnosis of MODY. 18 Of note, patients with HNF1A-MODY or HNF4A-MODY are typically sensitive to treatment with sulfonylureas 19 but may also respond to glucagon-like peptide-1 receptor agonists. 20

This patient had received a diagnosis of diabetes before 35 years of age, had a family history of diabetes involving multiple generations, and was not obese. These features are suggestive of MODY but do not represent absolute criteria for the condition ( Fig. 1 ). 1 Negative testing for diabetes-associated autoantibodies would further increase the likelihood of MODY. There are methods to calculate a patient’s risk of having MODY associated with GCK , HNF1A , or HNF4A . 21 , 22 Using an online calculator ( www.diabetesgenes.org/mody-probability-calculator ), we estimate that the probability of this patient having MODY is at least 75.5%. Genetic testing would be needed to confirm this diagnosis, and in patients at an increased risk for MODY, multigene panel testing has been shown to be cost-effective. 23 , 24


Maturity-onset diabetes of the young, most likely due to a GCK variant.


Dr. Christina A. Austin-Tse: A diagnostic sequencing test of five genes associated with MODY was performed. One clinically significant variant was identified in the GCK gene (NM_000162.3): a c.787T→C transition resulting in the p.Ser263Pro missense change. Review of the literature and variant databases revealed that this variant had been previously identified in at least three patients with early-onset diabetes and had segregated with disease in at least three affected members of two families (GeneDx: personal communication). 25 , 26 Furthermore, the variant was rare in large population databases (occurring in 1 out of 128,844 European chromosomes in gnomAD 27 ), a feature consistent with a disease-causing role. Although the serine residue at position 263 was not highly conserved, multiple in vitro functional studies have shown that the p.Ser263Pro variant negatively affects the stability of the glucokinase enzyme. 26 , 28 – 30 As a result, this variant met criteria to be classified as “likely pathogenic.” 31 As mentioned previously, a diagnosis of GCK-MODY is consistent with this patient’s clinical features. On subsequent testing of additional family members, the same “likely pathogenic” variant was identified in the patient’s father and second child, both of whom had documented hyperglycemia.


Dr. Udler: In this patient, the diagnosis of GCK-MODY means that it is normal for her blood glucose level to be mildly elevated. She can stop taking metformin because discontinuation is not expected to substantially alter her glycated hemoglobin level 15 , 32 and because she is not at risk for complications of diabetes. 14 However, she should continue to maintain a healthy lifestyle. Although patients with GCK-MODY are not typically treated for hyperglycemia outside of pregnancy, they may need to be treated during pregnancy.

It is possible for a patient to have type 1 or type 2 diabetes in addition to MODY, so this patient should be screened for diabetes according to recommendations for the general population (e.g., in the event that she has a risk factor for diabetes, such as obesity). 1 Since the mild hyperglycemia associated with GCK-MODY is asymptomatic (and probably unrelated to the polyuria that this patient had described in the past), the development of symptoms of hyperglycemia, such as polyuria, polydipsia, or blurry vision, should prompt additional evaluation. In patients with GCK-MODY, the glycated hemoglobin level is typically below 7.5%, 33 so a value rising above that threshold or a sudden large increase in the glycated hemoglobin level could indicate concomitant diabetes from another cause, which would need to be evaluated and treated.

This patient’s family members are at risk for having the same GCK variant, with a 50% chance of offspring inheriting a variant from an affected parent. Since the hyperglycemia associated with GCK-MODY is present from birth, it is necessary to perform genetic testing only in family members with demonstrated hyperglycemia. I offered site-specific genetic testing to the patient’s parents and second child.

Dr. Meridale V. Baggett (Medicine): Dr. Powe, would you tell us how you would treat this patient during pregnancy?

Dr. Camille E. Powe: During the patient’s first pregnancy, routine screening led to a presumptive diagnosis of gestational diabetes, the most common cause of hyperglycemia in pregnancy. Hyperglycemia in pregnancy is associated with adverse pregnancy outcomes, 34 and treatment lowers the risk of such outcomes. 35 , 36 Two of the most common complications — fetal overgrowth (which can lead to birth injuries, shoulder dystocia, and an increased risk of cesarean delivery) and neonatal hypoglycemia — are thought to be the result of fetal hyperinsulinemia. 37 Maternal glucose is freely transported across the placenta, and excess glucose augments insulin secretion from the fetal pancreas. In fetal life, insulin is a potent growth factor, and neonates who have hyperinsulinemia in utero often continue to secrete excess insulin in the first few days of life. In the treatment of pregnant women with diabetes, we strive for strict blood sugar control (fasting blood glucose level, <95 mg per deciliter [<5.3 mmol per liter]; 2-hour postprandial blood glucose level, <120 mg per deciliter) to decrease the risk of these and other hyperglycemia-associated adverse pregnancy outcomes. 38 – 40

In the third trimester of the patient’s first pregnancy, obstetrical ultrasound examination revealed a fetal abdominal circumference in the 76th percentile for gestational age and polyhydramnios, signs of fetal exposure to maternal hyperglycemia. 40 – 42 Case series involving families with GCK-MODY have shown that the effect of maternal hyperglycemia on the fetus depends on whether the fetus inherits the pathogenic GCK variant. 43 – 48 Fetuses that do not inherit the maternal variant have overgrowth, presumably due to fetal hyperinsulinemia ( Fig. 2A ). In contrast, fetuses that inherit the variant do not have overgrowth and are born at a weight that is near the average for gestational age, despite maternal hyperglycemia, presumably because the variant results in decreased insulin secretion ( Fig. 2B ). Fetuses that inherit GCK-MODY from their fathers and have euglycemic mothers appear to be undergrown, most likely because their insulin secretion is lower than normal when they and their mothers are euglycemic ( Fig. 2D ). Because fetal overgrowth and polyhydramnios occurred during this patient’s first pregnancy and neonatal hypoglycemia developed after the birth, the patient’s first child is probably not affected by GCK-MODY.

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Pathogenic variants that lead to GCK-MODY, when carried by a fetus, change the usual relationship of maternal hyperglycemia to fetal hyperinsulinemia and fetal overgrowth. GCK-MODY–affected fetuses have lower insulin secretion than unaffected fetuses in response to the same maternal blood glucose level. In a hyperglycemic mother carrying a fetus who is unaffected by GCK-MODY, excessive fetal growth is usually apparent (Panel A). Studies involving GCK-MODY–affected hyperglycemic mothers have shown that fetal growth is normal despite maternal hyperglycemia when a fetus has the maternal GCK variant (Panel B). The goal of treatment of maternal hyperglycemia when a fetus is unaffected by GCK-MODY is to establish euglycemia to normalize fetal insulin levels and growth (Panel C); whether this can be accomplished in the case of maternal GCK-MODY is controversial, given the genetically determined elevated maternal glycemic set point. In the context of maternal euglycemia, GCK-MODY–affected fetuses may be at risk for fetal growth restriction (Panel D).

In accordance with standard care for pregnant women with diabetes who do not meet glycemic targets after dietary modification, 38 , 39 the patient was treated with insulin during her pregnancies. In her second pregnancy, treatment was begun early, after hyperglycemia was detected in the first trimester. Because she had not yet received the diagnosis of GCK-MODY during any of her pregnancies, no consideration of this condition was given during her obstetrical treatment. Whether treatment affects the risk of hyperglycemia-associated adverse pregnancy outcomes in pregnant women with known GCK-MODY is controversial, with several case series showing that the birth weight percentile in unaffected neonates remains consistent regardless of whether the mother is treated with insulin. 44 , 45 Evidence suggests that it may be difficult to overcome a genetically determined glycemic set point in patients with GCK-MODY with the use of pharmacotherapy, 15 , 32 and affected patients may have symptoms of hypoglycemia when the blood glucose level is normal because of an enhanced counterregulatory response. 49 , 50 Still, to the extent that it is possible, it would be desirable to safely lower the blood glucose level in a woman with GCK-MODY who is pregnant with an unaffected fetus in order to decrease the risk of fetal overgrowth and other consequences of mildly elevated glucose levels ( Fig. 2C ). 46 , 47 , 51 In contrast, there is evidence that lowering the blood glucose level in a pregnant woman with GCK-MODY could lead to fetal growth restriction if the fetus is affected ( Fig. 2D ). 45 , 52 During this patient’s second pregnancy, she was treated with insulin beginning in the first trimester, and her daughter’s birth weight was near the 16th percentile for gestational age; this outcome is consistent with the daughter’s ultimate diagnosis of GCK-MODY.

Expert opinion suggests that, in pregnant women with GCK-MODY, insulin therapy should be deferred until fetal growth is assessed by means of ultrasound examination beginning in the late second trimester. If there is evidence of fetal overgrowth, the fetus is presumed to be unaffected by GCK-MODY and insulin therapy is initiated. 53 After I have counseled women with GCK-MODY on the potential risks and benefits of insulin treatment during pregnancy, I have sometimes used a strategy of treating hyperglycemia from early in pregnancy using modified glycemic targets that are less stringent than the targets typically used during pregnancy. This strategy attempts to balance the risk of growth restriction in an affected fetus (as well as maternal hypoglycemia) with the potential benefit of glucose-lowering therapy for an unaffected fetus.

Dr. Udler: The patient stopped taking metformin, and subsequent glycated hemoglobin levels remained unchanged, at 6.2%. Her father and 5-year-old daughter (second child) both tested positive for the same GCK variant. Her father had a BMI of 36 and a glycated hemoglobin level of 7.8%, so I counseled him that he most likely had type 2 diabetes in addition to GCK-MODY. He is currently being treated with metformin and lifestyle measures. The patient’s daughter now has a clear diagnosis to explain her hyperglycemia, which will help in preventing misdiagnosis of type 1 diabetes, given her young age, and will be important for the management of any future pregnancies. She will not need any medical follow-up for GCK-MODY until she is considering pregnancy.


Maturity-onset diabetes of the young due to a GCK variant.


We thank Dr. Andrew Hattersley and Dr. Sarah Bernstein for helpful comments on an earlier draft of the manuscript.

This case was presented at the Medical Case Conference.

No potential conflict of interest relevant to this article was reported.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org .

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Clinical pearls, case study: a woman with type 2 diabetes and severe hypertriglyceridemia sensitive to fat restriction.

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Deborah Thomas-Dobersen; Case Study: A Woman With Type 2 Diabetes and Severe Hypertriglyceridemia Sensitive to Fat Restriction. Clin Diabetes 1 October 2002; 20 (4): 202–203. https://doi.org/10.2337/diaclin.20.4.202

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L.S. is a 52-year-old Caucasian woman who was diagnosed with type 2 diabetes in 1988. She developed hypertriglyceridemia 3 years later and hypertension 9 years later. Other medical problems include obesity and diverticulosis. She presents now for screening to determine eligibility for a clinical research protocol using once-daily insulin.

Physical exam reveals a height of 64 inches, a weight of 181 lb, a body mass index of 31 kg/m 2 , and a waist circumference of 40 inches. Blood pressure, well controlled on 20 mg lisinopril (Prinivil) daily, is 104/70 mmHg.

Laboratory results reveal a fasting lipid panel as follows: total cholesterol 214 mg/dl, triglycerides 940 mg/dl, direct HDL cholesterol 24 mg/dl, an invalid LDL cholesterol unobtainable because of the hypertriglyceridemia, and a free fatty acid of 1.1 mEq/l (normal range 0.1–0.6 mEq/l). Hemoglobin A 1c (A1C) is 9.5%, and fasting blood glucose (FBG) is 304 mg/dl. When called to discuss the finding of severe hypertriglyceridema, the patient commented that she had previously had fasting triglycerides as high as 3,000 mg/dl.

L.S. is currently taking metformin (Glucophage), 1,000 mg twice daily, and glipizide (Glucatrol XL), 10 mg twice daily, to control her blood glucose. She is also on gemfibrizol (Lopid), 600 mg twice daily, for hypertriglyceridemia and estradiol (Estraderm) for menopause (topical estrogen does not induce hypertriglyceridemia).

What nutritional modification would be effective in rapidly lowering serum triglycerides when the patient is at risk of pancreatitis?

What treatment strategies can be employed to lower triglycerides, and how effective are they?

How can nutritional modifications improve insulin resistance?

Type 2 diabetes carries a two- to fourfold excess risk of coronary heart disease. The most common pattern of dyslipidemia in patients with type 2 diabetes is elevated triglycerides and decreased HDL levels. 1 Although coexistent increases in small, dense LDL cholesterol particles—not the triglycerides themselves—may be responsible for the increase in cardiovascular risk, hypertriglyceridemia poses a significant burden on society. 2  

In type 2 diabetes, characterized by insulin resistance and insulin deficiency, the pathophysiology of hypertriglyceridemia is an increased hepatic production of triglycerides as well as a decreased lipoprotein lipase activity leading to slower breakdown of VLDL cholesterol and chylomicrons. 3 The American Diabetes Association (ADA) Clinical Practice Recommendations list serum triglycerides ≥400 mg/dl and an HDL level <45 mg/dl for women as indicative of high risk of coronary heart disease. 1  

By both ADA and National Cholesterol Education Program (NCEP III) guidelines, the first goal for this patient is to lower triglycerides to prevent pancreatitis, which not only can result in hospitalization, but also is potentially lethal. 4 Although L.S. is already on the maximum dose of gemfibrozil, her triglycerides are still inadequately controlled.

With triglycerides in this range, she should be alerted immediately to the fact that any alcohol, even that found in over-the-counter cold remedies can trigger pancreatitis until her serum triglycerides are brought down to a safer range (<500 mg/dl). In addition, a single high-fat meal can also trigger pancreatitis.

A severely restricted fat intake (<10% of daily kcal) can effectively bring down serum triglycerides by 20% per day until triglycerides are <500 mg/dl. A diet in which fat is so severely restricted usually brings about weight loss as well. A loss of 2.5 kg body weight would bring an expected 15–20% decrease in serum triglycerides. In addition, aerobic exercise can help to lower serum triglycerides by 10–15%. 2  

Interventions to further decrease serum triglycerides to <200 mg/dl, increase HDL to 45 mg/dl, and decrease LDL to <100 mg/dl should be attempted to decrease the risk of coronary heart disease.

At the first clinic visit, L.S. was advised of the risk of pancreatitis and advised to forego any alcohol and to adhere to severe fat restriction until she has a fasting serum triglyceride level <400 mg/dl. She and her husband are both from the South, and their traditional Southern fare used quite a bit of salt pork, which deleteriously augmented the saturated as well as total fat in her diet. She had been advised to “watch her weight” when her triglycerides were in the 3,000 mg/dl range, but she had been unable to follow that recommendation.

Between clinic visits, L.S. was given written information about a low-fat (10% of kcal) diet, including lists of foods to restrict and foods to encourage until a more thorough meal plan could be developed based on an assessment of her previous dietary patterns. She was advised that this was a short-term, severe dietary change. She had already instituted an exercise program, walking for 1 hour, five times a week regularly.

Two weeks later, when L.S. returned to clinic after following the suggested fat restriction, her lab results showed the following lipid profile: serum total cholesterol 193 mg/dl, serum triglycerides 355 mg/dl, direct HDL cholesterol 32 mg/dl, and LDL cholesterol 90 mg/dl. Her A1C had dropped to 8.8% with no change in therapy for her diabetes, and her FBG was 158 mg/dl. Her fasting free fatty acid level was 0.7 mEq/l. Her weight had dropped by 3 lb.

At this visit, medical nutrition therapy (MNT) was initiated, and the patient was put on 10 units of 75/25 insulin before dinner.

Six weeks later, her A1C had dropped further, to 7%, her FBG was 110 mg/dl, and her weight was down another 2 lb. Her lipid profile was as follows: total cholesterol 181 mg/dl, triglycerides 299 mg/dl, direct HDL cholesterol 32 mg/dl, and LDL cholesterol 89 mg/dl. Her fasting free fatty acid level was now 0.6 mEq/l, the upper level of normal. Meal plan records showed that she was consuming ∼1,500 kcal/day and getting ∼25% of daily kcal from fat.

Commonly, controlling hyperglycemia leads to a decrease in triglycerides. 1 However, in this patient, the clearing of serum triglycerides, the restricted saturated fat, and the weight loss had a substantial impact on improving glucose tolerance without adding further diabetes oral agents. Studies have shown that dietary fat, primarily saturated fat, has adverse effects on insulin sensitivity. 5 Restricting fat intake, especially saturated fat, resulted in a better metabolic profile in regard to both glucose tolerance and fasting serum triglycerides.

Lifestyle changes had been recommended previously; why was L.S. successful this time when she hadn’t been before? The patient offered the following comments when asked this question.

“I was handed written information, but concern about the numbers (hypertriglyceridemia) was never conveyed.”

“They tell you what you need to do, but not how or why to do it.”

“No one sat down and talked with me. I never received individualized attention.”

“If my triglycerides were potentially harmful, why did they not see me sooner than 3 months? Three months was the usual time between visits and again they conveyed no concern.”

In previous attempts to encourage this patient make lifestyle changes, the compliance approach was used, but the benefits of self-care, the costs of not complying, the susceptibility to pancreatitis and cardiovascular disease, and the severity of such elevated triglycerides were not conveyed. A referral to an educator, time spent in assessing eating patterns and teaching alternatives, and more frequent visits or follow-up serve to convey the importance of recommended lifestyle changes. MNT coupled with an empowerment approach through which patients are the primary decision makers is important.

Although lifestyle changes are always recommended as first-line therapy, the approach to helping patients achieve these lifestyle changes in busy office practices is too often insufficient. A new Medicare benefit effective January 2002 allows patients with diabetes access to insurance coverage for MNT. Evidence-based research shows that MNT provided by a registered dietitian experienced in the management of diabetes is clinically effective. 6  

Reducing dietary fat improves body weight, which in turn improves glucose tolerance and hypertriglyceridemia. 7 – 9  

There is evidence that saturated fat may elevate plasma glucose by way of increasing insulin resistance.

MNT for hypertriglyceridemia may be divided into three parts:

  1. When fasting triglycerides are ≥1,000 mg/dl, restrict dietary fat to 10% of kcal until fasting triglycerides fall to <500 mg/dl.

  2. For fasting triglycerides between 1,000 and 500 mg/dl, a ) reduce saturated fat to <7% of energy and dietary cholesterol to 200 mg/day; b ) increase viscous (soluble) fiber to 10–25 mg/day; c ) encourage modest weight loss (5–7% of body weight); and d ) increase physical activity. 10 Monounsaturated fats or carbohydrates can be used to substitute for the decrease in saturated fats.

  3. For fasting triglycerides <500 mg/dl, encourage weight loss and a decrease in simple sugars in addition to the above reduction in saturated fat.

Deborah Thomas-Dobersen, RD, MS, CDE, is a professional research assistant and certified diabetes educator in the Endocrinology Department of the University of Colorado Health Sciences Center in Aurora.

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Diabetes Mellitus Case Study (45 min)

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What additional nursing assessments should be performed at this time?

  • POC glucose
  • Heart and lung sounds and respiratory effort – ensure she is protecting her airway
  • Assess skin and mucous membranes
  • Level of consciousness and orientation

What history questions would you like to ask of the patient and/or her parents?

  • Has she been excessively thirsty or hungry lately
  • Has she been urinating a lot
  • Has she lost weight unintentionally?
  • Is there a history of diabetes in the family?
  • Has she been told previously that she has diabetes?
  • Does she take any medications on a daily basis?

Upon further questioning, the parents report that their daughter has been weak a lot lately. Miss Matthews reports but she’s always hot and exhausted. She reports a 10-pound weight loss over the last 2 months despite eating all the time and agrees that she has been thirsty and peeing a lot.

What diagnostic tests should be run for Miss Matthews?

  • Serum glucose level
  • BMP – electrolytes, anion gap, etc.
  • ABG to assess for acidosis
  • Urine ketones

What is an appropriate response by the nurse?

  • Your daughter has Type 1 diabetes, which means that she has an autoimmune disorder that attacks the cells in her pancreas that make insulin. Type 1 diabetes typically has nothing to do with diet and lifestyle and usually has more to do with genetics.
  • Your daughter’s healthy lifestyle will continue to help her control her blood sugar levels, but unfortunately, there is no cure for type 1 diabetes at this time.

What treatments do you expect to be ordered for Miss Matthews at this time?

  • Miss Matthews will need intensive insulin therapy and IV fluids to counteract the ketoacidosis and bring her blood sugars down.
  • She will then need to be started on long-acting insulin like Lantus and short-acting insulin-like NovoLog for correction with meals.

Miss Matthews is treated for diabetic ketoacidosis over the next 2 days and is now feeling much better. The diabetic nurse educator comes by to teach Miss Matthews how to self-administer SubQ insulin using an insulin pen. Miss Matthews says “I  can’t stand needles, isn’t there a pill I can take instead?”

What is the most appropriate response by the nurse?

Unfortunately, at this time insulin is not available in pill form. It has to be taken via injection. Otherwise, it will not work correctly.

What options does Miss Matthews have for insulin administration?

  • Insulin vial with needles
  • Insulin pen
  • Insulin pump

Miss Matthews is able to demonstrate proper technique for glucose monitoring and self-administration of insulin with the insulin pen. Her blood glucose levels are stable between 140 and 180 mg/dL,  and the provider has said that she could go home today.

In addition to the insulin education, she has already received, what other education topics should be included in discharge teaching for Miss Matthews?

  • Miss Matthews should be taught how to count carbohydrates to determine the amount of insulin required.
  • She should be given a prescribed sliding scale or insulin protocol to follow.
  • Miss Matthews should also be instructed on when to take her long-acting insulin and when to take regular insulin in relation to meal times. It is important that she does not take short-acting insulins without being ready to eat.
  • Miss Matthews should be educated on the possibility of morning hyperglycemia due to the Somogyi effect or Dawn phenomenon, and be given suggestions to try an evening dose of insulin or an evening snack.
  • The importance of follow-up appointments with her primary care provider and/or endocrinologist should be stressed. She should have her Hgb A1c checked every 3 months to start with.
  • She should also be educated on foods to avoid, such as desserts and sweets, and foods that are beneficial, such as fruits and vegetables and high-quality proteins.
  • Miss Matthews should carry some candy or glucose tablets with her in case of a hypoglycemic reaction.

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Nursing Case Studies

Jon Haws

This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

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  • Diabetes & Primary Care
  • Vol:23 | No:02

Interactive case study: Making a diagnosis of type 2 diabetes

  • 12 Apr 2021

Share this article + Add to reading list – Remove from reading list ↓ Download pdf

Diabetes & Primary Care ’s series of interactive case studies is aimed at GPs, practice nurses and other professionals in primary and community care who would like to broaden their understanding of type 2 diabetes.

The three mini-case studies presented with this issue of the journal take you through what to consider in making an accurate diagnosis of type 2 diabetes.

The format uses typical clinical scenarios as tools for learning. Information is provided in short sections, with most ending in a question to answer before moving on to the next section.

Working through the case studies will improve your knowledge and problem-solving skills in type 2 diabetes by encouraging you to make evidence-based decisions in the context of individual cases.

Crucially, you are invited to respond to the questions by typing in your answers. In this way, you are actively involved in the learning process, which is a much more effective way to learn.

By actively engaging with these case histories, I hope you will feel more confident and empowered to manage such presentations effectively in the future.

Colin is a 51-year-old construction worker. A recent blood test shows an HbA 1c of 67 mmol/mol. Is this result enough to make a diagnosis of diabetes?

Rao, a 42-year-old accountant of Asian origin, is currently asymptomatic but has a strong family history of type 2 diabetes. Tests have revealed a fasting plasma glucose level of 6.7 mmol/L and an HbA 1c of 52 mmol/mol. How would you interpret these results?

43-year-old Rachael has complained of fatigue. She has a BMI of 28.4 kg/m 2 and her mother has type 2 diabetes. Rachael’s HbA 1c is 46 mmol/mol. How would you interpret her HbA 1c measurement?

By working through these interactive cases, you will consider the following issues and more:

  • The criteria for the correct diagnosis of diabetes and non-diabetic hyperglycaemia.
  • Which tests to use in different circumstances to determine a diagnosis.
  • How to avoid making errors in classification of the type of diabetes being diagnosed.
  • The appropriate steps to take following diagnosis.

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diabetes mellitus case study with answers


According to McCance and Huether (2019), 9.3 % of the adult population in the United States is affected by Type 2 diabetes mellitus.  Risk factors for developing Type 2 diabetes are family history, hypertension, obesity, and increased age.  Lifestyle choices, genetic factors, and environmental factors combined can all contribute to the development of Type 2 diabetes mellitus. One main issue leading to Type 2 diabetes is insulin resistance in peripheral tissues specifically the muscle, liver, and adipose tissue (McCance & Huether, 2019).

Alpha cells and beta cells are islet cells that are found in the pancreas.  The beta cells are responsible for creating insulin and the alpha cells are responsible for creating glucagon.  The increasingly high glucagon levels cause blood glucose levels to increase leading to the stimulation of gluconeogenesis and glycogenolysis (McCance & Huether, 2019).  Due to the decreased reactiveness of the alpha cells to glucose, the glucagon secretion begins increasing as well.  Amylin which is a beta-cell hormone is responsible for repressing the alpha cells release of glucagon (McCance & Huether, 2019).  In Type 2 diabetes the cells begin to become insulin resistant. This means the needed glucose is unable to get inside of the cells which causes it to accumulate in the blood.  In this case, the insulin receptors are abnormal or missing causing glucose to be locked out of the cells.

The beta cells attempt to keep up with the increased demand for insulin but eventually lose the ability to produce enough.  The beta cells begin to decrease in number and size and eventually fail due to exhaustion (McCance & Huether, 2019).  This leads to hyperglycemia which is the buildup of glucose in the bloodstream.  In an attempt to compensate for hyperglycemia, the pancreas will produce more insulin.  The pancreas will eventually reach exhaustion and no longer be able to compete with the body’s increased demand for insulin.

Our GI hormones (gut hormones) contribute to diabetes & insulin resistance as well.  Ghrelin is a hormone made in the stomach and pancreatic islets that control food intake.  Insulin resistance has been associated with reduced levels of ghrelin.  Incretins are released from the GI tract to increase insulin release, regenerate the beta-cell and provide a barrier to beta-cell damage (McCance & Huether, 2019).  Studies show the incretin glucagon-like peptide 1, (GLP-1) depicts a decrease in beta-cell responsiveness in type 2 diabetes (McCance & Huether, 2019).

Due to hyperglycemia and the current lack of insulin polyphagia, polydipsia and polyuria are classic signs that appear while recurrent infections and visual changes occur later on.  If hyperglycemia continues to progress without treatment microvascular complications such as nephropathy, neuropathy, and retinopathy can occur along with macrovascular complications: cerebrovascular disease, coronary artery disease, and peripheral artery disease (McCance & Huether, 2019).

According to the American Diabetes Association (2015), there are four ways to diagnose Type 2 diabetes

  • Glycated hemoglobin (A1C) test: Diabetics diagnosed using this test will have an A1C of 6.5% or higher
  • Random blood sugar test: Diabetics diagnosed using this test will have a blood sugar of > 200 mg/dL
  • Fasting plasma glucose (FPG): Diabetics diagnosed using this test will have a FPG of 126 mg/dL or higher
  • Oral glucose tolerance test (OGTT): Diabetics diagnosed using this test will have an OGTT of 200 mg/dL or higher.

American Diabetes Association. (2015, January 1). 2. Classification and Diagnosis of Diabetes. Retrieved from https://care.diabetesjournals.org/content/38/Supplement_1/S8.

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2019).  Pathophysiology: the biologic basis for disease in adults and children  (8th ed.). St. Louis, MO: Elsevier.

Proximal gastric motor activity in response to a liquid meal in type I diabetes mellitus with autonomic neuropathy


  • 1 Department of Gastroenterology, University Hospital Utrecht, The Netherlands.
  • PMID: 9539642
  • DOI: 10.1023/a:1018894520557

Disordered gastric emptying occurs in 30-50% of patients with diabetes mellitus. Although the rate of gastric emptying is dependent on the integration of motor activity in different regions of the stomach, there is limited information about the function of the proximal stomach in diabetes mellitus. In the present study the response of the proximal stomach to a liquid meal was examined in eight diabetic patients with autonomic neuropathy and gastrointestinal symptoms and in 10 healthy volunteers, using an intragastric bag connected to an electronic barostat. Postprandial relaxation of the proximal stomach was measured as an increase of intragastric bag volume at a constant pressure level of 1 mm Hg above the intraabdominal pressure. During the experiment the blood glucose levels were maintained within the euglycemic range. Before ingestion of the meal the intragastric bag volume was larger in the diabetic patients than in the healthy volunteers, 234.4 +/- 29.1 ml vs 155.3 +/- 15.3 ml (P = 0.06). The maximum volume was not different in diabetics compared to the healthy controls (386.3 +/- 45.2 ml versus 399.0 +/- 35.2 ml). However, the maximum volume increase was significantly less in diabetics (143.7 +/- 38.6 ml) compared to the controls (231.4 +/- 30.5 ml, P < 0.04). Bloating was inversely correlated with the volume changes, which suggests that impaired relaxation of the proximal stomach may play a role in the genesis of this sensation. In conclusion, this study shows a lower fasting fundal tone and a decrease in volume change of the gastric fundus after a nutrient drink in patients with autonomic neuropathy due to type I diabetes mellitus. These abnormalities may play a role in the abnormal distribution of food, disordered liquid gastric emptying, and in the genesis of the sensation of bloating observed in these patients.

Publication types

  • Research Support, Non-U.S. Gov't
  • Autonomic Nervous System Diseases / etiology
  • Autonomic Nervous System Diseases / physiopathology*
  • Blood Glucose / metabolism
  • Case-Control Studies
  • Diabetes Mellitus, Type 1 / complications
  • Diabetes Mellitus, Type 1 / physiopathology*
  • Diabetic Neuropathies / physiopathology*
  • Food, Formulated
  • Gastric Emptying / physiology*
  • Gastrointestinal Motility / physiology
  • Middle Aged
  • Blood Glucose


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