Type 2 Diabetes Case Study Newly Diagnosed With Rheumatoid

A Case of Newly Diagnosed Chronic Myelomonocytic Leukemia with Rheumatoid Arthritis Presentation

Gabriel McCoy* and William Edenfield
University of South Carolina, School of Medicine Greenville, Greenville Health System, USA
Corresponding Author :Gabriel McCoy
University of South Carolina
School of Medicine Greenville
Greenville Health System, USA
Tel: (864) 455-7992
E-mail:[email protected]
Received May 13, 2014; Accepted September 08, 2014; Published September 12, 2014
Citation: McCoy G, Edenfield W (2014) A Case of Newly Diagnosed Chronic Myelomonocytic Leukemia with Rheumatoid Arthritis Presentation. J Clin Case Rep 4:414. doi:10.4172/2165-7920.1000414
Copyright: © 2014 McCoy G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Clinical Case Reports

View PDF Download PDF Tables & Figures


We describe a case of newly diagnosed chronic myelomonocytic leukemia that presented with predominantly rheumatologic symptoms. In addition to the deletion of chromosome 12p, marrow cytogenetics also revealed a unique translocation, t(x:4). This finding was not a constitutive abnormality. We report this unusual chromosomal abnormality and hypothesize about the potential immunogenicity of the gene product and its relation to the patient’s rheumatologic complaints.

Chronic myelomonocytic leukemia (CMML); Rheumatoid arthritis; Immunogenic protein
MDS: Myelo Dysplastic Syndrome; FISH: Fluorescence In situ Hybridization; RA: Rheumatoid Arthritis; ALL: Acute Lymphocytic Leukemia; AML: Acute Myelogenous Leukemia
There are greater than 10,000 newly diagnosed cases of myelodysplastic syndromes in the United States each year [1]. Chronic myelomonocytic leukemia (CMML) is a myelodysplastic disease with myeloproliferative features. Not uncommonly, CMML presents with varying autoimmune phenomena. Vasculitis, polychondritis, and polyarthritis have been associated with myelodysplastic diseases such as CMML [2-5]. As many as 10% of patients diagnosed with myelodysplastic syndromes (MDS) have autoimmune manifestations which range from vasculitis to glomerulonephritis [2]. CMML diagnosis requires a peripheral monocytosis of greater than 1×109/L for at least 3 months without presence of a Philadelphia chromosome or BCR-ABL mutation or PDGFRA/B rearrangement and less than 20% blasts in the peripheral blood and bone marrow. Additionally, there must be presence of dysplasia in at least one myeloid lineage. If dysplasia is not present, then diagnosis may be made using all of the previous requirements with either an acquired clonal cytogenetic, molecular genetic abnormality, or a monocytosis that has persisted for at least 2 months with exclusion of alternative causes [6].
CMML is typically diagnosed in patients aged 65-75 and with a 2:1 male predominance. Symptoms typically range from skin rash, to splenomegaly, to weight loss, but can be variable. CMML may be subcategorized into CMML-1 and CMML-2. CMML-1 has presence of less than 5% blasts in blood or less than 10% in bone marrow. CMML- 2 is diagnosed with 5-19% blasts in the blood or 10-19% blasts in the bone marrow or Auer rod presence [6].
The molecular underpinning of the autoimmunity seen in CMML is not well understood. Chromosomal translocations play an important role in the varied manifestations of CMML. For example, a noted case of chronic inflammatory demyelinating polyneuropathy has been reported which was caused by a translocation t(3:8)(q26:q24). These autoimmune manifestations have been largely treated with immunosuppression by steroidal intervention for symptomatic relief [4].
CMML is associated with multiple translocations in 10% of cases. Of this group of translocations, 86% are balanced, and 14% are unbalanced. The chromosomes which are most commonly involved in descending order are 3, 1, 7, 2, 11, 5 and 12 [3] A unique feature of this case is the finding of a deletion of chromosome 12p resulting in the loss of the ETV6 gene and t(x:4)(q26:21) translocation. This translocation involves the region of DNA that has been associated with rheumatoid arthritis.
Case Report
A 61 year old Caucasian male initially presented with the complaint of malaise, arthragias, and lower extremity edema. He noted anorexia and energy loss accompanied by increasing dyspnea on exertion for the past few months. His review of systems was otherwise negative aside from a twenty pound weight loss over the last month.
On physical exam, the patient has significant lower extremity swelling and edema extending to the waist. Neck exam revealed tenderness over the right neck without lymphadenopathy or jugular venous distention or thyroid tenderness. Cardiac exam revealed only tachycardia. No ecchymosis was noted over the skin or mucous membranes. Joint exam revealed reduced range of motion of all joints without effusions. Initial labs showed the following abnormal results: WBC was 28.3×109/L with hemoglobin of 10.4 mmol/L and platelet level of 33×109/L. Total protein was decreased along with albumin (2.0 g/dL). Alkaline phosphatase was elevated (149 U/L). Haptoglobin was normal. The differential on the complete blood count revealed a monocytic hyperproliferation at 27% with (1%) band cell, (6%) lymphocytes, (13%) myelocytes, (1%) promyelocyte, (1%) blast cells, and (51%) segmented neutrophils. Erythrocyte sedimentation rate (ESR) was (90 mm/hr), prothrombin time (PT) was (15.1 s), international normalized ratio (INR) was (1.2), fibrinogen was (659 g/L) and d-dimer was (3.71 ng/ml). The patient underwent a battery of serological tests for rheumatologic and hematological abnormalities (Table 1).
Bone marrow biopsy pathology
The bone marrow biopsy showed hypercellular marrow (Figure 1) with fibrosis. Dysplastic features were seen in megakaryocytes and myeloid cells. Marrow cellularity was estimated at approximately 70% with many increased myeloid cells of all stages. Dysplastic erythroid precursors were also demonstrated (Figure 2).
Bone Marrow flow cytometry: 78% mature granulocytes, 2% lymphocytes, 10% monocytes, 7% erythroid precursors and 3% blasts. 1% CD19-positive B cells present, 1% CD3-positive t cells.
FISH: There was rearrangement of ETV6 (TEL) (12p 13.2), No PDGFRA: 4q12 rearrangements noted. A deletion of (12p) containing the region encoding for ETV6 gene was noted. The bone marrow was also negative for BCR-ABL mutation.
Demonstrated the t(x:4) which was not constitutive based on subsequent buccal swab karyotyping.
The patient was evaluated by a rheumatologist and appeared to have a constellation of autoimmune manifestations. The elevation in rheumatoid factor, ANA, anti-CCP, and decreased complement was felt to be consistent with rheumatoid arthritis. The patient was diagnosed with rheumatoid arthritis (RA) was placed on high dose methylprednisolone (125 mg/week). Upon further outpatient follow up, the patient maintained a monocytosis greater than 1×109/L for three months. He was diagnosed with CMML and offered the option between decitabine and azacitidine. After discussion of the options; the patient chose treatment with decitabine over azacitidine. He experienced a significant improvement of his symptoms, and has been transfusion independent with improving blood counts since discharge from the hospital.
The autoimmune manifestations which this patient experienced initially may be explained by means of a positive rheumatoid factor and anti-cyclic citrullinated peptides (CCP). There have been reports that CD 14+ abnormal monocytes signal B cells to produce IgM-RF and thus play a role in pathogenesis of RA in addition to clinical and serological manifestations of RA. Increased bone marrow production of these monocytes may cause serological findings of RA [7]. However, this patient had normal CD14 on flow cytometry which makes this pathophysiology unlikely.
The translocation of (x:4) seems like a more plausible cause for the elevation in rheumatoid factor. Serological markers such as rheumatoid factor (RF) and anti-CCP in rheumatoid arthritis have been shown to have some association with the X chromosome genes (namely TIMP1, and IL9R genes) [8]. If these gene loci were part of the translocation, this may offer a credible reason that both anti-CCP and RF were elevated. These markers for rheumatoid arthritis have been reported with mutations in both TIMP1 and IL9R [8].
The combination of leukocytosis without infectious source, thrombocytopenia, and monocyte hyperproliferation, was suspicious for underlying bone marrow dysfunction. The decision to do a bone marrow biopsy should be done in this situation to elucidate the causative factor for the confounding serological findings. CMML was diagnosed based on the absence of Philadelphia chromosome, and absence of a PDGFRA rearrangement on FISH from bone marrow samples. There was a peripheral monocyte proliferation greater than 1×109/L documented for 3 months, less than 20% blasts, and bone marrow pathological findings consistent with both myeloproliferative and dysplastic features. Furthermore, the cytogenetic abnormalities appear clonal and confined to the bone marrow, thus confirming this is CMML. The presence of less than 5% blasts peripherally and less than 10% in marrow suggests this case was CMML-1.
The arthralgia’s and hypocomplementemia may be partially explained by the unique translocation of t(x:4). This translocation may be responsible for elevated transcription of an immunogenic protein which facilitates the fixation of complement and auto immune reaction. This subsequently led to lowered complement level, positive ANA, and increased immunoglobulin. CMML has been noted to cause autoimmune manifestations in a variety of different presentations [1]. Additionally, it has been associated with various translocations in presentation. It may be possible that these varieties of translocations create a wide spectrum of autoimmune symptoms based on the translocation and resultant protein. The translocation found in this case is not typically seen with CMML cases.
Myeloid neoplasms and meylodysplastic syndromes have been associated with deletions of short arm of chromosome 12 [9]. Among the most commonly seen gene rearrangement on this chromosome associated with hematological malignancies is the ETV6 gene [10]. The ETV6 gene has the function of transcription repression and is expressed biologically in myeloid cells significantly more than other cells. It is required for hematopoiesis and development of vascular structures [9,11]. This gene sequence has been shown to be associated with CMML, fibrosarcoma, childhood ALL, and AML through translocations and rearrangements [5]. In this case, by virtue of deletion of 12p and thus ETV6 gene, there is potential loss of transcription regulation of monocytes and proliferation occurs.
The t(x:4) mutation was found to be isolated to the bone marrow and not consistent with a germ-line mutation. This segregation to the bone marrow strongly suggests that this translocation plays an important part in the expression of the disease in this case. We hypothesize that this protein is responsible for fixing complement in this patients’ blood and creating the rheumatologic manifestations seen clinically. The variability of translocations associated with CMML may be responsible for the varying clinical presentations of CMML.
In conclusion, more research is needed into the variety of translocations associated with myelodysplastic syndromes and the causative factors that are associated with the various autoimmune presentations of this disease. This case report shows that there are many unique presentations of serious hematological diseases which may manifest as other diseases. Most profoundly, this case outlines a unique and novel translocation and deletion of a chromosome which has not been described in CMML concurrently. Efforts are underway to identify the genes involved and the putative protein product of the t(x:4) demonstrated in this case.
  1. Ma X, Does M, Raza A, Mayne ST (2007) Myelodysplastic syndromes: incidence and survival in the United States. Cancer 109: 1536-1542.
  2. Saif MW, Hopkins JL, Gore SD (2002) Autoimmune phenomena in patients with myelodysplastic syndromes and chronic myelomonocytic leukemia. Leuk Lymphoma 43: 2083-2092.
  3. Fain O, Braun T, Stirnemann J, Fenaux P (2011) [Systemic and autoimmune manifestations in myelodysplastic syndromes]. Rev Med Interne 32: 552-559.
  4. Isoda A, Sakurai A, Ogawa Y, Miyazawa Y, Saito A, et al. (2009) Chronic inflammatory demyelinating polyneuropathy accompanied by chronic myelomonocytic leukemia: possible pathogenesis of autoimmunity in myelodysplastic syndrome. Int J Hematol 90: 239-242.
  5. Hamidou MA,Derenne S, Audrain MA, Berthelot JM, Boumalassa A, et al. (2000) Prevalence of rheumatic manifestations and antineutrophil cytoplasmic antibodies in haematological malignancies. A prospective study. Rheumatology (Oxford) 39: 417-420.
  6. Parikh SA,Tefferi A (2012) Chronicmyelomonocytic leukemia: 2012 update on diagnosis, risk stratification, and management. Am J Hematol 87: 610-619.
  7. Hirohata S,Yanagida T, Koda M, Koiwa M, Yoshino S, et al. (1995) Selective induction of IgM rheumatoid factors by CD14+ monocyte-lineage cells generated from bone marrow of patients with rheumatoid arthritis. Arthritis Rheum 38: 384-388.
  8. Burkhardt J, Petit-Teixeira E, Teixeira VH, Kirsten H, Garnier S, et al. (2009) Association of the X-chromosomal genes TIMP1 and IL9R with rheumatoid arthritis. J Rheumatol 36: 2149-2157.
  9. Hess JL (2001) Chronic Myelomonocytic Leukemia (CMML). Atlas Genetic Cytogenetics Oncology Haematology July.
  10. Wlodarska I,Mecucci C, Baens M, Marynen P, van den Berghe H (1996) ETV6 gene rearrangements in hematopoietic malignant disorders. Leuk Lymphoma 23: 287-295.
  11. Weizmann Institute of Science. Human Gene Database.

Tables and Figures at a glance

Table 1


Figures at a glance

Figure 1Figure 2
Post your comment

Recommended Journals

Recommended Conferences

  • World Cardiology Conference
    17-18 September,2018 Tin Shui Wai, Hong Kong
  • Clinical and Experimental Dermatology
    November 02 - 04, 2018 San Francisco, USA

View More

Article Usage

  • Total views: 12391
  • [From(publication date):
    September-2014 - Mar 11, 2018]
  • Breakdown by view type
  • HTML page views : 8610
  • PDF downloads : 3781
Select your language of interest to view the total content in your interested language

1. UK Prospective Diabetes Study (UKPDS) Group Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837–853 [PubMed]

2. UK Prospective Diabetes Study (UKPDS) Group Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998;352:854–865 [PubMed]

3. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med 2008;359:1577–1589 [PubMed]

4. Ray KK, Seshasai SR, Wijesuriya S, et al. Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials. Lancet 2009;373:1765–1772 [PubMed]

5. Nathan DM, Buse JB, Davidson MB, et al. American Diabetes Association. European Association for the Study of Diabetes Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy: a consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetologia 2009;52:17–30 [PubMed]

6. Duckworth W, Abraira C, Moritz T, et al. VADT Investigators Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med 2009;360:129–139 [PubMed]

7. Patel A, MacMahon S, Chalmers J, et al. ADVANCE Collaborative Group Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560–2572 [PubMed]

8. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee.Canadian Diabetes Association 2008 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2008;32(Suppl.1):S1–S201

9. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetologia 2012;55:1577–1596 [PubMed]

10. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract 2009;15:540–559 [PubMed]

11. DeFronzo RA, Eldor R, Abdul-Ghani M. Pathophysiologic approach to therapy in patients with newly diagnosed type 2 diabetes. Diabetes Care 2013;36(Suppl. 2):S127–S138 [PMC free article][PubMed]

12. Bennett WL, Odelola OA, Wilson LM, et al. Evaluation of guideline recommendations on oral medications for type 2 diabetes mellitus: a systematic review. Ann Intern Med 2012;156:27–36 [PubMed]

13. Shah BR, Hux JE, Laupacis A, Zinman B, van Walraven C. Clinical inertia in response to inadequate glycemic control: do specialists differ from primary care physicians?Diabetes Care 2005;28:600–606 [PubMed]

14. Abbas A, Blandon J, Rude J, Elfar A, Mukherjee D. PPAR-γ agonist in treatment of diabetes: cardiovascular safety considerations. Cardiovasc Hematol Agents Med Chem 2012;10:124–134 [PubMed]

15. Riche DM, King ST. Bone loss and fracture risk associated with thiazolidinedione therapy. Pharmacotherapy 2010;30:716–727 [PubMed]

16. Idris I, Warren G, Donnelly R. Association between thiazolidinedione treatment and risk of macular edema among patients with type 2 diabetes. Arch Intern Med 2012;172:1005–1011 [PubMed]

17. Lewis JD, Ferrara A, Peng T, et al. Risk of bladder cancer among diabetic patients treated with pioglitazone: interim report of a longitudinal cohort study. Diabetes Care 2011;34:916–922 [PMC free article][PubMed]

18. Azoulay L, Yin H, Kristian BF, Assayag J, Majdan A, Pollak MN, Suissa S. The use of pioglitazone and the risk of bladder cancer in people with type 2 diabetes: nested case-control study. BMJ 2012;344:e3645 [PMC free article][PubMed]

19. Neumann A, Weill A, Ricordeau P, Fagot JP, Alla F, Allemand H. Pioglitazone and risk of bladder cancer among diabetic patients in France: a population-based cohort study. Diabetologia 2012;55:1953–1962 [PMC free article][PubMed]

20. McCulloch DK, Nathan DM, Mulder JE. Sulfonylureas and meglitinides in the treatment of diabetes mellitus [article online], 2013. Available from www.uptodate.com Available from http://www.uptodate.com/contents/diabetes-melitus-type-2-treatment-beyond-the-basics Accessed 28 March 2013

21. Kahn SE, Haffner SM, Heise MA, et al. ADOPT Study Group Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy. N Engl J Med 2006;355:2427–2443 [PubMed]

22. Caputo S, Andersen H, Kaiser M, Karnieli E, Meneghini LF, Svendsen AL. Effect of baseline HbA1c on glycemic control and diabetes management following initiation of once-daily insulin detemir in real-life clinical practice. Endocr Pract. 21 January 2013 [Epub ahead of print] [PubMed]

23. Gerstein HC, Miller ME, Byington RP, et al. Action to Control Cardiovascular Risk in Diabetes Study Group Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008;358:2545–2559 [PMC free article][PubMed]

24. Currie CJ, Peters JR, Tynan A, et al. Survival as a function of HbA(1c) in people with type 2 diabetes: a retrospective cohort study. Lancet 2010;375:481–489 [PubMed]

25. Riddle MC, Karl DM. Individualizing targets and tactics for high-risk patients with type 2 diabetes: practical lessons from ACCORD and other cardiovascular trials. Diabetes Care 2012;35:2100–2107 [PMC free article][PubMed]

26. Stoffers DA, Kieffer TJ, Hussain MA, et al. Insulinotropic glucagon-like peptide 1 agonists stimulate expression of homeodomain protein IDX-1 and increase islet size in mouse pancreas. Diabetes 2000;49:741–748 [PubMed]

27. Denker PS, Dimarco PE. Exenatide (exendin-4)-induced pancreatitis: a case report. Diabetes Care 2006;29:471. [PubMed]

28. Buse JB, Rosenstock J, Sesti G, et al. LEAD-6 Study Group Liraglutide once a day versus exenatide twice a day for type 2 diabetes: a 26-week randomised, parallel-group, multinational, open-label trial (LEAD-6). Lancet 2009;374:39–47 [PubMed]

29. Rebours V, Boutron-Ruault MC, Schnee M, et al. The natural history of hereditary pancreatitis: a national series. Gut 2009;58:97–103 [PubMed]

30. Elashoff M, Matveyenko AV, Gier B, Elashoff R, Butler PC. Pancreatitis, pancreatic, and thyroid cancer with glucagon-like peptide-1-based therapies. Gastroenterology 2011;141:150–156 [PMC free article][PubMed]

31. Bjerre Knudsen L, Madsen LW, Andersen S, et al. Glucagon-like Peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology 2010;151:1473–1486 [PubMed]

32. Singh S, Chang H-Y, Richards TM, Weiner JP, Clark JM, Segal JB. Glucagonlike Peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study. JAMA Intern Med2013;173:534–539 [PubMed]

33. Prasad-Reddy L, Williams KL. Incretin-based therapies: A focus on safety concerns and emerging uses. Formulary 2012;47:369–377

34. Ussher JR, Drucker DJ. Cardiovascular biology of the incretin system. Endocr Rev 2012;33:187–215 [PMC free article][PubMed]

35. Delahanty LM, Peyrot M, Shrader PJ, Williamson DA, Meigs JB, Nathan DM, DPP Research Group Pretreatment, psychological, and behavioral predictors of weight outcomes among lifestyle intervention participants in the Diabetes Prevention Program (DPP). Diabetes Care 2013;36:34–40 [PMC free article][PubMed]

36. Johnson M, Jones R, Freeman C, et al. Can diabetes prevention programmes be translated effectively into real-world settings and still deliver improved outcomes? A synthesis of evidence. Diabet Med 2013;30:3–15 [PMC free article][PubMed]

37. Kappe C, Patrone C, Holst JJ, Zhang Z, Sjoholm A. Metformin protects against lipoapoptosis and enhances GLP-1 secretion from GLP-1-producing cells. J Gastroenterolol 2013;48:322–332 [PubMed]

38. Calvert JW, Gundewar S, Jha S, et al. Acute metformin therapy confers cardioprotection against myocardial infarction via AMPK-eNOS-mediated signaling. Diabetes 2008;57:696–705 [PubMed]

39. Chaiteerakij R, Yang JD, Harmsen WS, et al. Risk factors for intrahepatic cholangiocarcinoma: association between metformin use and reduced cancer risk. Hepatology 2013;57:648–655 [PMC free article][PubMed]

40. Mazzone PJ, Rai H, Beukemann M, Xu M, Jain AK, Sasidhar M. The effect of metformin and thiazolidinedione use on lung cancer in diabetics. BMC Cancer 2012;12:410. [PMC free article][PubMed]

41. Schramm TK, Gislason GH, Vaag A, et al. Mortality and cardiovascular risk associated with different insulin secretagogues compared with metformin in type 2 diabetes, with or without a previous myocardial infarction: a nationwide study. Eur Heart J 2011;32:1900–1908 [PubMed]

42. Fuhlendorff J, Rorsman P, Kofod H, et al. Stimulation of insulin release by repaglinide and glibenclamide involves both common and distinct processes. Diabetes 1998;47:345–351 [PubMed]

43. Raz I, Eldor R, Cernea S, Shafrir E. Diabetes: insulin resistance and derangements in lipid metabolism. Cure through intervention in fat transport and storage. Diabetes Metab Res Rev 2005;21:3–14 [PubMed]

44. Schernthaner G, Currie CJ, Schernthaner G-H. Do we still need pioglitazone for the treatment of type 2 diabetes? A risk-benefit critique in 2013. Diabetes Care 2013;36(Suppl. 2):S155–S161 [PMC free article][PubMed]

45. Macconell L, Pencek R, Li Y, Maggs D, Porter L. Exenatide once weekly: sustained improvement in glycemic control and cardiometabolic measures through 3 years. Diabetes Metab Syndr Obes 2013;6:31–41 [PMC free article][PubMed]

46. Ban K, Hui S, Drucker DJ, Husain M. Cardiovascular consequences of drugs used for the treatment of diabetes: potential promise of incretin-based therapies. J Am Soc Hypertens 2009;3:245–259 [PubMed]

47. Kieffer TJ, McIntosh CH, Pederson RA. Degradation of glucose-dependent insulinotropic polypeptide and truncated glucagon-like peptide 1 in vitro and in vivo by dipeptidyl peptidase IV. Endocrinology 1995;136:3585–3596 [PubMed]

48. Agersø H, Jensen LB, Elbrønd B, Rolan P, Zdravkovic M. The pharmacokinetics, pharmacodynamics, safety and tolerability of NN2211, a new long-acting GLP-1 derivative, in healthy men. Diabetologia 2002;45:195–202 [PubMed]

49. Ross SA, Ekoé JM. Incretin agents in type 2 diabetes. Can Fam Physician 2010;56:639–648 [PMC free article][PubMed]

50. Raz I, Eldor R. Rational therapy for diabetes: early recognition of adverse effects and avoidance of disruptive false alarms. Diabetes Metab Res Rev 2012;28:321–324 [PubMed]

51. Garg R, Chen W, Pendergrass M. Acute pancreatitis in type 2 diabetes treated with exenatide or sitagliptin: a retrospective observational pharmacy claims analysis. Diabetes Care 2010;33:2349–2354 [PMC free article][PubMed]

52. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 2008;371:569–578 [PubMed]

53. Iyer SN, Tanenberg RJ, Mendez CE, West RL, Drake AJ., 3rd Pancreatitis associated with incretin-based therapies. Diabetes Care 2013;36:e49. [PMC free article][PubMed]

54. Butler AE, Campbell-Thompson M, Gurlo T, Dawson DW, Atkinson M, Butler PC. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:2595–2604 [PMC free article][PubMed]

55. Shin JA, Lee JH, Kim HS, Choi YH, Cho JH, Yoon KH. Prevention of diabetes: a strategic approach for individual patients. Diabetes Metab Res Rev 2012;28(Suppl. 2):79–84 [PubMed]

0 Thoughts to “Type 2 Diabetes Case Study Newly Diagnosed With Rheumatoid

Leave a comment

L'indirizzo email non verrà pubblicato. I campi obbligatori sono contrassegnati *