diabetes type 1 case study evolve

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• Published: 11 March 2019

The reconstructed natural history of type 1 diabetes mellitus

• Paolo Pozzilli 1 , 2 &
• Alberto Signore 3  

Nature Reviews Endocrinology volume  15 ,  pages 256–257 ( 2019 ) Cite this article

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The causes of type 1 diabetes mellitus (T1DM) are unclear; however, a general consensus exists that T1DM is a T cell-mediated autoimmune disease characterized by the selective destruction of insulin-secreting β-cells. Now, two imaging mass cytometry studies of human pancreatic tissue illuminate new biology in the pathogenesis of T1DM.

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Damond, N. K. et al. A map of human type 1 diabetes progression by imaging mass cytometry. Cell Metab. https://doi.org/10.1016/j.cmet.2018.11.014 (2019).

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Wang, Y. J. et al. Multiplexed in situ imaging mass cytometry analysis of the human endocrine pancreas and immune system in type 1 diabetes. Cell Metab. https://doi.org/10.1016/j.cmet.2019.01.003 (2019).

Gepts, W. Pathologic anatomy of the pancreas in juvenile diabetes mellitus. Diabetes 14 , 619–633 (1965).

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Foulis, A. K. & Stewart, J. A. The pancreas in recent-onset type 1 (insulin- dependent) diabetes mellitus: insulin content of islets, insulitis and associated changes in the exocrine acinar tissue. Diabetologia 26 , 456–461 (1984).

Rui, J. et al. B cells that resist immunological attack develop during progression of autoimmune diabetes in NOD mice. Cell Metab. 25 , 727–738 (2017).

Signore, A. et al. Detection of insulitis by pancreatic scintigraphy with 99mTc-labeled IL-2 and MRI in patients with LADA (Action LADA 10). Diabetes Care 38 , 652–658 (2015).

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Unit of Endocrinology and Diabetes, University Campus Bio-Medico, Rome, Italy

Paolo Pozzilli

Centre of Immunobiology, Blizard Institute, Queen Mary, University of London, London, UK

Nuclear Medicine Unit, Department of Medical-Surgical Sciences and of Translational Medicine, “Sapienza” University of Rome, Rome, Italy

Alberto Signore

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Correspondence to Paolo Pozzilli .

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Pozzilli, P., Signore, A. The reconstructed natural history of type 1 diabetes mellitus. Nat Rev Endocrinol 15 , 256–257 (2019). https://doi.org/10.1038/s41574-019-0192-8

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Published : 11 March 2019

Issue Date : May 2019

DOI : https://doi.org/10.1038/s41574-019-0192-8

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Home › Case Studies › The 10 Biggest Research Breakthroughs of 2019

The 10 Biggest Research Breakthroughs of 2019

2019 has been a year of milestones in our mission to cure, treat and prevent T1D – with huge advances in beta cell replacement, new targets for complication treatments, and the first ever therapy to delay the onset of T1D. Let’s look back on the year with ten of the biggest advances from the world of T1D research:

1. Teplizumab delays T1D onset by two years

In a study by JDRF-funded TrialNet , the immunotherapy drug teplizumab was found to delay T1D diagnosis by a median of 2 years in children and adults at high risk. The milestone study was the first ever in humans to show a delay in the onset of T1D, and a huge step forward for research into preventing the condition.

2. Continued support for Australian research

Through the efforts of JDRF advocates, T1D research got a $54.5m bipartisan commitment over the next 5 years. This funding will be directed towards T1D research and also ensure that the Australian Type 1 Diabetes Clinical Research Network (CRN) can continue to support world class Australian research to cure, prevent and treat T1D

3. Rotavirus vaccine may help prevent T1D

A Melbourne study found that the rotavirus vaccine – used to protect children from a nasty stomach virus – may also help to prevent type 1 diabetes. The study found that the rate of T1D diagnosis in children aged under 4 has declined since 2007, the same year the rotavirus vaccine was introduced as a routine infant vaccination.

4. First oral treatment for T1D approved in Europe

The type 2 diabetes drug dapagliflozin was approved for use in type 1 diabetes in the UK and Europe – the first oral medication available for T1D. Dapagliflozin is part of a class of drugs known as SGLT2 inhibitors, and is prescribed as an adjunct (add-on) to insulin therapy. In clinical trials, SGLT2 inhibitors have been shown to reduce blood glucose levels, as well as the amount of insulin a person requires.

5. ENDIA comes to life

The ENDIA study reached a huge milestone when it recruited its 1,500 th and final participant. ENDIA aims to discover the environmental factors that trigger the development of T1D, by studying babies from pregnancy through to 6 months of age. The study has been running since 2013 as part of JDRF’s Type 1 Diabetes Clinical Research Network.

6. Making islet transplantation more accessible

JDRF-funded researchers at the Garvan Institute of Medical Research in Sydney discovered a way of reducing the need for immunosuppressants following an islet transplant . The researchers, led by A/Prof Shane Grey, found that increasing the levels of the A20 protein in islet cells, before a transplant, made the cells less likely to be rejected by the body. With further research, this breakthrough could make islet transplantation available to a much broader group of people with T1D.

7. A new T1D screening program is launched

Type1Screen was launched in Australia and New Zealand for people who have relatives with T1D. The program tests for antibodies that act as markers of T1D risk, and can help detect the condition at its first stages. This early detection can lead to a lower rate of serious complications like diabetic ketoacidosis (DKA).

8. A milestone for beta cell replacement

In the US, JDRF-supported company ViaCyte released exciting results for its beta cell replacement therapy. In a clinical trial, researchers showed that the therapy, known as PEC-Direct, can help people with T1D produce insulin again. PEC-Direct consists of pancreatic precursor cells – stem cells that are programmed to grow into islet cells – in a device that can be implanted under the skin.

9. Functional insulin-producing cells grown in lab

In a world first, JDRF-funded researchers were able to transform human stem cells into clusters of insulin-producing cells that mimic the islets of the pancreas. This new advance in making cells in the lab could make islet transplantations much more effective. When transplanted, these cell clusters begin responding to blood sugar levels within days – much more efficient than the 2-6 weeks it usually takes transplanted cells to become active.

10. New hope for treating complications

A US-based team of researchers discovered 17 new markers in the blood that are associated with a person’s risk of developing kidney complications. These markers have the potential to become targets for new treatments to treat or prevent kidney disease in T1D – and several are already being studied in clinical trials for other autoimmune conditions.

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Evolution may have pushed humans toward greater risk for type-1 diabetes, study shows

August 17, 2010 - By Krista Conger

Gene variants associated with an increased risk for type-1 diabetes and rheumatoid arthritis may confer previously unknown benefits to their human carriers, say researchers at the Stanford University School of Medicine . As a result, the human race may have been evolving in the recent past to be more susceptible, rather than less, to some complex diseases, they conclude.

“At first we were completely shocked because, without insulin treatment, type-1 diabetes will kill you as a child,” said Atul Butte , MD, PhD, assistant professor of pediatric cancer biology and a bioinformatics expert. “Everything we’ve been taught about evolution would indicate that we should be evolving away from developing it. But instead, we’ve been evolving toward it. Why would we have a genetic variant that predisposes us to a deadly condition?”

The researchers speculate that at least some of the risky changes may protect carriers against certain viruses and bacteria — a trade-off that may have made evolutionary sense in the not-too-distant past when infectious diseases were devastating and largely untreatable. It’s not clear, however, whether the beneficial effects arise from the disease-associated mutations themselves, or from neighboring genes that tag along when DNA is divvied up into sperm and eggs.

Butte, who directs the Center for Pediatric Bioinformatics at Lucile Packard Children’s Hospital , is the senior author of the research, published Aug. 17 in Public Library of Science ONE . Graduate student Erik Corona is the first author of the study and conducted the analysis.

The idea that disease-causing genes can be beneficial is not new. The most clear-cut case involves a gene variant that, when present in two copies, causes sickle cell anemia, which can result in severe pain, organ damage and death. Although it seems that natural selection would work to eliminate the disorder, the variant remains prevalent in some areas of Africa because people with just a single copy are less susceptible to malaria. Evolutionarily the trade-off is worth it: Far more people are protected from malaria than ever develop sickle cell anemia even in today’s environment.

Unlike sickle cell anemia, which is caused by a mutation in just one gene, many complex diseases are associated with several variants — specific locations in the DNA where the nucleotide “letters” vary between individuals. These locations are known as SNPs, for single nucleotide polymorphisms. Some of these SNPs are associated with an increased disease risk, while others protect against developing the disease. When calculating an individual’s overall genetic risk, it’s necessary to consider the net effect of all of his or her variants.

Corona picked seven well-known conditions to study: type-1 and type-2 diabetes, rheumatoid arthritis, hypertension, Crohn’s disease, coronary artery disease and bipolar disorder. Previous genome wide association studies have identified severalhundred SNPs associated with each disorder. Corona found that of the top SNPs associated with type-1 diabetes, 80 have been recently increasing in prevalence, meaning that they underwent positive selection. Of these, a surprising 58 are associated with an increased risk of the disorder, while 22 appear protective. Similarly, SNPs associated with an increased risk for rheumatoid arthritis were found to be positively selected. In contrast to type-1 diabetes and rheumatoid arthritis, Corona found that we’re evolving away from a tendency to develop Crohn’s disease (that is, more protective SNPs than risky SNPs have been positivelyselected).

Results for the other three disorders — type-2 diabetes, coronary artery disease and bipolar disorder — showed that protective and risky SNPs were positively selected in about equal proportions. “Now we’re starting to see little hints as to why this might be the case,” said Butte. For example, a recent study in another lab showed that genetic variations in an antiviral response gene called IFIH1 that improve its ability to protect against enterovirus infection (and the resulting severe, potentially deadly, abdominal distress) also increase a carrier’s risk for type-1 diabetes. And scientists who study global disease patterns have long noted that the prevalence of tuberculosis varies inversely with that of rheumatoid arthritis.

“It’s possible that, in areas of the world where associated triggers for some of these complex conditions are lacking, carriers would experience only the protective effect against some types of infectious disease,” said Butte, who pointed out that the cumulative effect of many SNPs in a person’s genome may buffer the effect of any one variant, even if it did raise a person’s risk for a particular condition.

Regardless of the reason, some evolutionary tenets still apply. Healthier people are, presumably, more likely to reproduce and pass those same genes — be they protective or risky — to their offspring. When conditions changed because of differences in diet, exposures or location as populations move around the globe, carriers of the risky SNPs began to develop the conditions we struggle with today.

Corona and Butte are now expanding their investigation to include even more SNPs and diseases. They are also looking at the genetic profile of various types of tumors to see if there’s evidence for positive evolutionary pressure there as well.

“Even though we’ve been finding more and more genetic contributions to disease risk,” said Butte, “that’s not really an appealing answer. There have got to be some other reasons why we have these conditions.”

In addition to Corona and Butte, graduate student Joel Dudley participated in the research. The work was supported by the Lucile Packard Foundation for Children’s Health , the Hewlett Packard Foundation, the Armin and Linda Miller Fellowship Fund, the National Library of Medicine , the National Institute of General Medical Sciences , the National Science Foundation and the Howard Hughes Medical Institute .

More information about Stanford’s Department of Pediatrics, which also supported the work, is available at http://pediatrics.stanford.edu .

About Stanford Medicine

Stanford Medicine is an integrated academic health system comprising the Stanford School of Medicine and adult and pediatric health care delivery systems. Together, they harness the full potential of biomedicine through collaborative research, education and clinical care for patients. For more information, please visit med.stanford.edu .

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• v.19(Suppl 1); 2015 Apr

Type 1 diabetes mellitus-common cases

Surender kumar.

Department of Endocrinology, Sir Ganga Ram Hospital, New Delhi, India

Tight glycemic control in type 1 diabetes mellitus patients is associated with the risk of hypoglycemia. Diabetic patients are forced to change their lifestyle to adjust to the disease condition and survive it. The best way to manage diabetes would be to develop a therapy, which could adjust to the patient's conditions. Here, I present few cases wherein switching to a long-acting basal insulin analog helped combat recurrent hypoglycemic episodes experienced by the patients.

I NTRODUCTION

Tight glycemic control in type 1 diabetes mellitus (T1DM) patients is not possible because of hypoglycemia. Diabetic patients are forced to change their lifestyle to adjust to the disease condition and survive it. The best way to manage diabetes would be to develop a therapy, which could adjust to the patient's conditions.[ 1 ]

A 6-year-old boy presented with classic features of diabetic ketoacidosis, that is, weight loss and extreme weakness and osmotic features. The fasting blood sugar level was 300 mg/dL, postprandial glucose level was 467 mg/dL and hemoglobin A1c (HbA1c) was 7.2%. He was administered with standard intravenous insulin and fluid, which finally brought down the fasting blood glucose level to around 120 mg/dL. He was administered basal-bolus therapy and was discharged. Patient had two episodes of severe hypoglycemia. His parents were worried due to frequent checking of blood glucose levels many times in a day. The challenge was also to avoid urination in bed at night by the child. Otherwise he would get a common cold. The patient remained unconscious in the middle of the night and was fed up with the frequent monitoring of blood sugar. The patient and the parents had severe anxiety, depression, frustration, and disgust. The parents considered diabetes as a curse on their family. He was informed about degludec/injection tresiba, which is not yet approved in children because of lack of experience. The physician explained to them that there was nothing wrong in administering it and is not contra-indicated in T1DM.[ 2 ] The parents were also explained that insulin degludec may even help the child to convert from four injections to one injection a day, and from very frequent monitoring to once in a day. After reviewing the literature about insulin degludec, the parents were finally convinced about it. The patient was then put from basal-bolus to 2 bolus plus 1 basal and finally degludec at 16 U. Over the period of time, blood sugar level came to normal at around 110 mg/dL-pre meal. The patient was trained very well that if he wanted to reduce the frequency of monitoring of blood sugar level, then he had to follow small frequent meals. This made him felt happy because once the sugar was controlled then small amount of sweets was also given. The techniques resulted in good compliance from the patient. The patient did not report any hypoglycemic event over a period of 3 months. This was a big relief for the patient and his parents. Later parents were told that the child may require basal-bolus therapy. The outcomes of this case study were that in case of T1DM the physician should not be very aggressive except during the first 2 weeks of admission. The physician should also try to convince the parents about line of treatment, and educate both the patients and the child. The dose may be gradually stabilized without being aggressive, and this also prevents frequent episodes of hypoglycemia. Hence, gradual tightening of glycemic control is very important. The doctor should analyze the psyche of the patient and his parents.

A 57-year-old female presented with a 13 year history of diabetes. Due to the failure of oral hypoglycemic agents (OHAs) in controlling her sugar levels, for the last 3 years, she was treated with biphasic insulin aspart 30/70. She was a very frequent flier, a regular swimmer and socially very active, and this led her to have irregular meals. Hence, she often go into frequent hypoglycemia and during the last 6 months the patient's average blood glucose level during fasting were 170 mg/dL and postprandial glucose levels varied from 230 to 280 mg/dL. Even after high sugar levels, she fortunately had normal kidney functions. Patient was able to afford an insulin pump, so she was put on one. With the pump, her blood glucose was in control and patient was happy. However she soon realized the limitation of carrying it everywhere she went. These were the true feelings of a patient who was very active while she was on an insulin pump. The physician, after discussing with the patient, started her on insulin degludec and lifestyle modification, especially the diet component. Patient understood these problems and followed the diet. She followed the dietary modification and over 2 months of time, fasting blood glucose was 110 mg/dL, post meals values were around 180 mg/dL. She had only one episode of minor hypoglycemia which was due to delayed meal. The doctor later reduced degludec from 44 U to 40 U and blood glucose was still improving without any episode of hypoglycemia in the last 3 months. The outcome of this case is that with this therapy and dietary modification, a desired level of blood glucose can be achieved, without hypoglycemic risk.

An 80-year-old retired army officer, staying alone, has type 2 diabetes for the last 12 years and renal function test was normal and patient was on insulin along with other OHAs. Despite this, the patient was getting attacks of hypoglycemia, which scared the patient of unconsciousness and even death. The limiting factors were that the patient was staying alone and was dependent upon an attendant to get injections. During the weekends or holidays, the attendant was not on a regular time, and this led to irregular insulin injections, causing hypoglycemic episode to patient. This patient as well was put on insulin degludec and over a period the dose of degludec was also increased. His HbA1c and fasting blood glucose level improved without any episode of hypoglycemia. The outcomes of this case are that degludec along with dietary modifications gave desired diabetes control without any hypoglycemia.

The main barrier to tight glycemic control is hypoglycemia. This can be adjusted with slight dietary modification without changing the therapy.[ 3 ]

Source of Support: Nil

Conflict of Interest: None declared.

R EFERENCES

Nursing Case Study for Type 1 Diabetes

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Michael is a 14-year-old male brought into a small ER by his mother. They were driving a long distance after he competed in a wrestling tournament. He had not felt well on the bus ride with the team so his mother decided he should ride with her. His mother denies a history of chronic illness but did say he had “like a cold but with a stomachache” about 3 months ago.

She also says that he has been very thirsty, and they had to stop several times for him to urinate. She is also worried because he almost missed his wrestling “weight class” parameters because he was significantly lighter this past weekend than he has been in the past. And that is even with him eating more than usual.

What symptoms are most worrisome to the triage nurse?

• He has 2 of the 3 “p’s” – polydipsia (thirst), polyuria (frequent urination), polyphagia (hunger) which are trademarks of diabetes mellitus (DM) and/or diabetic ketoacidosis (DKA). They happen in response to the body lacking insulin and its response is to try to achieve homeostasis with these mechanisms. His weight loss could be indicative of DM as well. 
• They describe a recent viral-like illness which may precipitate a diagnosis of DM (it is thought the body has an inappropriate immune response to the illness leading to DM)

In triage, the nurse obtains a point-of-care blood glucose (BG) level and the machine gives no value. Instead, an error message indicating “hi” displays on the machine.

Why did the nurse do this test? What should they do next?

• Clues point to possible DM or DKA. Getting a BG immediately can help guide care. Always follow the facility protocol/procedure on “hi” or “lo” (often spelled this way on glucometers) readings. The protocol might dictate (standing order) stat venous draw and send it to the lab. It may be advised to try again on a different machine with a new sample. Whatever the guidance, a BG level is imperative for this patient.

Michael is AAO x 4. He complains of a “stomachache” and reports he has nausea and experienced vomiting shortly before arrival. His skin is warm and dry, but his face is flushed. When asked about pain, he says he has a headache, and his vision is blurry. The nurse notices a fruity odor on his breath when obtaining vital signs. 

BP 90/54 mmHg SpO 2 98% on Room Air

HR 122 bpm and regular

RR 26 bpm at rest

The patient and his mother are placed into an exam room immediately and the triage nurse verbally reports this to the accepting nurse.

How does the nurse interpret these symptoms?

• Michael’s symptoms are consistent with hyperglycemia (link here to cheatsheet?) DKA

What orders does the accepting nurse anticipate?

• Labs, ABGs, urinalysis, IV access (bilateral upper extremities, largest possible in case patient deteriorates). One lab, in particular, can give the provider an idea of the last 2-3 month BG average, the hemoglobin A1C.

The provider orders stat labs, urinalysis and ABGs then examines the patient. 

Why stat orders?

• This patient’s condition could deteriorate rapidly, and treatment should begin ASAP. Labs are needed to guide the plan of care. The nurse should watch for changes in the level of consciousness, respiratory changes, his response to potential fluid & electrolyte imbalances. Place on continuous cardiac monitoring as well.

Lab results are as follows:

WBC 15000 cells/mcL

Glucose 420 mg/dl

BUN 21 mg/dl

Creatinine 0.77 mg/dl

Anion gap 12

Glucose positive

Ketones positive

What do these results mean?

• CBC WBC 15000 cells/mcL – an immune response, possibly to viral illness or another issue HgbA1C 9% – indicates the average BG over the past 2-3 months has been about 212mg/dLBMP Glucose 420 mg/dl – hyperglycemia K 5.8 – electrolyte imbalance, can cause cardiac changes and need to monitor closely if IV insulin is started (will need frequent checks of this and BG) BUN 21 mg/dL – fluid imbalance Creatinine 0.77 mg/dL – normal but necessary to check for kidney function Anion gap 12 – indicative of DKAABG – metabolic acidosis Ph 7.25 HCO3 15 PaCo2 35 PaO2 88Urine – indicative of DKA Glucose positive Ketones positive

What medication orders should the nurse anticipate?

• IV fluids, insulin (either IV or SQ). NOTE: only REGULAR INSULIN can be given IV, and if it is, then IV dextrose and potassium chloride should be included in the insulin IV titration protocol/order). SQ insulin may be ordered using a sliding scale. O2 via NC possibly due to potential respiratory concerns (Kussmaul respirations)

The provider tells Michael and his mother that he suspects diabetic ketoacidosis which is not uncommon for new type I diabetics. He plans to transfer Michael to a nearby city via helicopter for a higher level of care.  The patient’s mother asks why he has to be transferred.

How does the nurse explain the transfer to the mother and patient?

• DKA requires monitoring in a critical care unit. Because of his age and new-onset DM, a higher level of care is recommended in order to have access to the best resources

The flight team arrives and assesses the patient. The ER completes a report using SBAR format at the bedside. The patient and his mother are given the chance to ask questions.

What are the transport team’s priorities as they move this patient?

• Airway, breathing, and circulation (ABC) status; Mental status; Volume status.

Upon arrival to the higher level of care, Michael is admitted to the ICU overnight. By the morning he is transferred to a pediatric floor for further observation. His mother remains at his bedside. They plan to return to their home after discharge. 

How should the pediatric medical unit prepare this family for discharge? What specific teaching should be provided?

• Condition-specific education is vital including DM management with medications, exercise, nutrition, psychosocial concerns, preventative care (i.e. vaccinations), parental/family involvement. A specialized diabetic educator and/or dietician would be ideal. Assessing their education preferences and literacy level is important as well. How to give insulin injections and check BG (glucometer use) are key takeaways (have patient and parent return-demonstrate). Case management may need to get involved for prescription/supplies. An endocrinologist may be consulted so education about his specialist is also important.

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Nursing case studies.

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.

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Clinical pearls, case study: type 1 and type 2, too.

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Heidi L. Gassner , Stephen E. Gitelman; Case Study: Type 1 and Type 2, Too?. Clin Diabetes 1 July 2003; 21 (3): 140–141. https://doi.org/10.2337/diaclin.21.3.140

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R.M. is a 17-year-old African-American girl with new-onset diabetes, presumed to be type 2 diabetes. She presented to her pediatrician during the winter months with the classic symptoms of polyuria and polydipsia. She reported weight loss over the preceding weeks, but was otherwise well. Her family history was positive for type 2 diabetes in grandparents and some distant relatives and negative for autoimmune diseases.

Physical examination revealed a blood pressure of 103/53 mmHg, pulse of 79, and temperature of 38°C. Her weight was 60 kg (132 lb, 50–75th percentile), height was 155 cm (61 inches, 10th percentile), and body mass index (BMI) was 25 kg/m 2 (85th percentile). She had acanthosis nigricans and was at Tanner V stage of sexual development.

Urinalysis revealed a glucose level of >1,000 mg/dl and ketones of 40 mg/dl. Her initial laboratory studies included a blood glucose measurement of 726 mg/dl, bicarbonate of 21 mmol/l (normal range 23–32 mmol/l), venous pH of 7.37, hemoglobin A 1c (A1C) of 8.6%, and C-peptide of 1.0 ng/ml (normal range 0.6–3.2 ng/ml).

R.M. was admitted to the hospital for subcutaneous insulin therapy, fluids, and diabetes education. She was discharged to her home on metformin, 500 mg twice daily, and a split-mixed insulin regimen of NPH and lispro at ∼1 unit/kg/day, with two-thirds being taken in the morning and one-third in the evening. She was also started on a fixed carbohydrate, reduced-fat meal plan.

At her first follow-up visit 1 month later, R.M. was found to be positive for islet cell autoantibodies (ICAs), glutamic acid decarboxylase (GAD) antibodies, and ICA-512 antibodies. Her A1C was 7.8%. Her insulin doses had been slowly decreased, with glucose levels consistently <150 mg/dl and total daily insulin requirements of ∼0.5 units/kg/day. Her metformin was discontinued given her positive antibody studies and near-euglycemic blood glucose range.

At another follow-up 3 months later, R.M. was still off metformin, and her blood glucose levels were in a euglycemic range on <0.4 units/kg/day (10 units of NPH with 4 units of lispro at breakfast and 6 units of NPH with 3 units of lispro at dinner). Her A1C was 5.9%. She had not required any adjustments for high blood glucose levels.

How does one distinguish between type 1 diabetes and type 2 diabetes?

When should autoantibodies be measured?

In patients who have type 1 diabetes with evidence of insulin resistance, what treatment options are available?

Most practitioners today would have assumed that this adolescent had recent-onset type 2 diabetes. The risk factors include non-Caucasian ancestry, positive family history, presence of acanthosis in someone with an elevated BMI, and hyperglycemia without ketoacidosis. 1  

In the past, type 1 diabetes would account for the majority of diabetes seen in this age-group. Yet, the national obesity epidemic has changed the types of diabetes being seen, especially in pediatrics. The most recent National Health and Nutrition Examination Survey noted that 30% of adolescents are now overweight, 2 and there has been a commensurate rise in the number of cases of type 2 diabetes found in adolescents. 3 Recently, in a cohort of obese adolescents, 20% were noted to have impaired glucose tolerance, and 4% had undiagnosed type 2 diabetes. 4 In some pediatric diabetes practices, type 2 diabetes now accounts for 25–50% of the patient population, and this continues to increase. 1  

The incidence of type 2 diabetes in American adolescents is highest among African-Americans, Latinos, and Asians. 1 For the African American population, this increased risk for type 2 diabetes results at least in part from the fact that African-American prepubertal children and adolescents have greater insulin resistance than their Caucasian counterparts, even when matched for BMI. 5 , 6  

Given the increase of obesity in our society, we expect that many children who present with new-onset diabetes will have evidence of obesity and acanthosis, which are strongly suggestive of type 2 diabetes. Yet, rather than assume that they have type 2 diabetes, clinicians must test for autoantibodies to clarify the underlying etiology.

R.M. was found to have positive antibodies directed against the β-cells and thus, clearly, has autoimmune-mediated type 1 diabetes. However, she also has evidence of insulin resistance, which is found in type 2 diabetes. Some have referred to this condition as “double diabetes,” or “type 1.5 diabetes.”

Multiple studies have shown that up to 90% of new-onset type 1 diabetic patients will have evidence of at least one antibody at diagnosis, and ∼40–50% will have two or more. 7 Tests for four autoantibodies are now available through commercial laboratories. The traditional assay to measure ICAs involves incubating a patient’s serum with a section of normal pancreas and assessing reactivity via indirect immunoflurosence. The other three antibody tests now available are for GAD, ICA-512 (also known as IA-2 or tyrosine phosphatase), and insulin autoantibodies (IAAs). The IAA measurement must be obtained within 10 days to 2 weeks from the initiation of exogenous insulin therapy, because exogenous insulin may induce antibody positivity.

Although most patients with type 1 diabetes are autoantibody-positive, ethnicity confers notable differences and may make confirmation of type 1 diabetes more difficult. African-American adolescents with new-onset type 1 diabetes have up to a fourfold greater chance of exhibiting no autoantibodies compared to their Caucasian counterparts (17.4 vs. 4.6%, respectively). 8 Thus, African-American adolescents with type 1 diabetes may initially present as antibody-negative, which may prove misleading in making therapy decisions.

The presence of autoantibodies has important implications for patient care. In the U.K. Prospective Diabetes Study, subjects presumed to have type 2 diabetes, yet who were noted to have one or more autoantibodies, progressed more rapidly to β-cell failure and required insulin therapy. 9 Up to 90% of patients who were positive for ICA and GAD antibodies required insulin within 6 years. 9  

In this case, had one assumed that this was a case of type 2 diabetes and treated R.M. solely with metformin, the patient may have done well initially, during her honeymoon phase. However, she would have been at high risk for progression to diabetic ketoacidosis as her honeymoon period waned or when faced with an intercurrent illness or stress. Furthermore, intensive insulin therapy is one potential means to prolong the honeymoon phase and protect endogenous insulin secretion, 10 and she would have been denied this potential benefit.

Despite the evidence that R.M. has type 1 diabetes, we must return to considerations about type 2 diabetes. Although she tested positive for autoantibodies, she did present with acanthosis nigricans, an elevated BMI, a positive family history, and was from a higher-risk ethnic group. If we had studied her formally, she would almost certainly have exhibited increased insulin resistance, and she may have ultimately developed type 2 diabetes later in life if she had not had earlier autoimmune destruction of her β-cells.

One question to consider is whether there is a role for insulin sensitizers in such a situation. Metformin may be a useful addition to insulin for adolescents with type 1 diabetes and insulin resistance. 11 Preliminary studies have found that metformin lowered A1C, decreased insulin dosage, and caused no weight gain in adolescents with type 1 diabetes and poor metabolic control. 11 Clinicians initiating such therapy must carefully inform the patient and family about the risks of lactic acidosis and the increased risk for hypoglycemia with combined therapy. Further studies with metformin and other insulin sensitizers (such as thiazolidinediones) are needed before this will become established therapy.

For R.M., we elected to continue her subcutaneous low-dose insulin regimen at 0.4 units/kg/day during the honeymoon phase, but we may consider adding metformin therapy in the future.

With the surge in obesity, we are witnessing a rise in type 2 diabetes, especially among children and adolescents. These patients often present in puberty, at a time of increased insulin resistance.

All pediatric patients who are diagnosed with new-onset diabetes need antibody studies obtained to distinguish type 1 from type 2 diabetes in order to provide appropriate therapies. Autoantibodies may not always be positive in African Americans with new-onset type 1 diabetes.

Patients who have type 1 diabetes and evidence of insulin resistance may benefit from the addition of metformin as an insulin-sensitizing agent. However, the use of metformin in these patients is still under investigation and has not yet gained approval from the Food and Drug Administration.

Heidi L. Gassner, MD, is a pediatric endocrine fellow, and Stephen E. Gitelman, MD, is an associate professor of clinical pediatrics in the Department of Pediatric Endocrinology at the University of California, San Francisco.

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