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Autoantibodies to Insulin and Dysglycemia In CASE STUDIES Autoantibodies to Insulin and Dysglycemia in People With and Without Diabetes: An Underdiagnosed Association Praveen Valiyaparambil Pavithran, Nisha Bhavani, Rohinivilasam Vasukutty Jayakumar, Arun Somasekharan Menon, Harish Kumar, Vadayath Usha Menon, Vasantha Nair, and Nithya Abraham he potential effects of inhibito- In this article, we describe our ry immunoglobulins to insulin experience with patients who pre- Twere first described in insulin- sented with glycemic excursions treated patients many decades ago resulting from insulin autoantibodies (1). This antibody response is thought from a single university referral teach- to occur in at least 40% of patients ing center in South India. on insulin therapy (2). Subsequent Spontaneous Hyperinsulinemic case reports documented glycemic Hypoglycemia excursions in the form of markedly increased insulin requirements and Case Presentation unpredictable hypoglycemic episodes, At the Department of Endocrinology both of which were attributable to in- of Amrita Institute of Medical sulin autoantibodies (3). Sciences in Kochi, Kerala, India, a Autoantibodies to insulin also can large tertiary care center, between occur occasionally in patients who 2008 and 2014, we diagnosed eight have not been previously exposed to cases in which insulin autoantibodies insulin. Autoimmune hypoglycemia could be implicated as the etiological resulting from high titers of insulin factor responsible for spontaneous autoantibodies have been reported, hyperinsulinemic hypoglycemia. One patient presented exclusively with mostly from Japan, as a rare cause of postprandial hypoglycemia–related hyperinsulinemic hypoglycemia (4). symptoms, whereas the others pre- There has only been one confirmed sented with a combination of fasting case of autoimmune hypoglycemia and postprandial symptoms. During reported from India (5). The esti- the same time period, there were mation of insulin autoantibodies is only seven cases of histopathological- an integral part of the diagnosis in ly proven insulinomas diagnosed in such cases. our center. Apart from insulin, other inciting All the patients underwent a agents implicated include sulfahydryl mixed-meal challenge test, fol- group–containing drugs and alpha- lowed by a supervised fast. Samples Department of Endocrinology, Amrita lipoic acid (ALA). Autoimmune Institute of Medical Sciences, Kochi, India were collected to measure insulin hypoglycemia also has been reported Corresponding author: Praveen and C-peptide when the patients Valiyaparambil Pavithran, pravvp@gmail. to be associated with autoimmune were symptomatic, with blood glu- com disorders and plasma cell dyscrasias cose levels of <55 mg/dL. Insulin DOI: 10.2337/diaclin.34.3.164 (6). Spontaneous resolution has been autoantibodies were estimated by reported in a few cases of autoim- radiobinding assay. A postprandial ©2016 by the American Diabetes Association. Readers may use this article as long as the work mune hypoglycemia, and a dramatic rise of glucose after the mixed meal is properly cited, the use is educational and not response to steroids was seen in some was demonstrable in all patients. for profit, and the work is not altered. See http:// creativecommons.org/licenses/by-nc-nd/3.0 other cases that manifested both Imaging of the pancreas by a for details. hypoglycemia and hyperglycemia. multi-detector computed tomography 164 CLINICAL.DIABETESJOURNALS.ORG PAVITHRAN ET AL . TABLE 1. Clinical and Biochemical Details of Eight Patients With Autoimmune Hypoglycemia Case Case Case Case Case Case Case Case 1 2 3 4 5 6 7 8 Age (years)/sex (F/M) 69/F 28/F 60/M 62/F 65/M 42/F 66/M 41/M Symptoms: postprandial (P), P F C P C P F C fasting (F), or combined (C) Duration of symptoms 2 2 2 3 3 1 3 3 (months) Inciting agent ALA Carbimazole None None None None None None Insulin (µIU/mL) 68.5 1,410 163 113 >300 73 >300 10,080 C-peptide (ng/mL) 5.6 2.9 2.3 5.2 9.3 7. 2 6.2 20 Insulin autoantibodies >50 >300 >50 >50 >50 >50 >50 >50 (normal <0.4 U/mL) (ELISA) Other relevant results Serum electrophoresis No M No M No M No M No M band band band band band Antinuclear antibody Negative testing Remission characteristics: S S S P P S P P spontaneous (S) or after (20 mg) (20 mg) (40 mg) (40 mg) oral prednisolone for 3 months (P [dosage]) M band, monoclonal protein band, a serum electrophoresis finding suggestive of multiple myeloma. pancreatic protocol was also per- Table 1 provides patients’ clinical and agents, presented with diabetic ke- formed. Other relevant investigations biochemical details. toacidosis (DKA) precipitated by a such as serum protein electrophoresis Onset was abrupt in all eight urinary tract infection, for which she were done to exclude myeloma and patients. In one patient, the inciting was started on insulin. One month af- benign gammaglobinopathy in older agent was carbimazole prescribed for ter starting insulin, she had recurrent patients. Endoscopic ultrasound Graves’ disease. In another patient, nocturnal hypoglycemic episodes with was performed in three patients. ALA, which was used as a health postprandial hyperglycemia. The basal Interestingly, urine ketones were supplement, could be implicated. component of her basal-bolus insulin positive in two patients during the Patients with less severe presenta- regimen was then stopped, but even 72-hour fasting. tions had spontaneous remission while only using an ultra-short-acting Insulin was estimated by che- within 3 months. All of the severe analog insulin at dinner, she had miluminescent microparticle cases responded to steroid therapy at documented early-morning hypogly- immunoassay with an analytic sen- doses of 0.5–0.75 mg/kg/day, which cemia. Despite discontinuing insulin sitivity of <1 µIU/mL. C-peptide were tapered and stopped within 3 for 72 hours, she continued to expe- was estimated by electrochemilu- months. None of the patients had a rience nocturnal hypoglycemia with minescence immunoassay on the recurrence. Three patients had other random venous plasma glucose of 54 Elecsys system (Roche Diagnostics, autoimmune comorbid diseases mg/dL. A critical sample showed an Mannheim, Germany) with an ana- (patient 2: Graves’ disease, patient 3: insulin level of 1,901 µIU/mL and lytical sensitivity of 0.01 ng/mL. pernicious anemia and autoimmune C-peptide level of 11 ng/mL, which Insulin autoantibodies were esti- hypothyroidism, and patient 7: auto- ruled out exogenous insulin–related mated by radiobinding assay in Quest immune hypothyroidism). hypoglycemia. Several postprandial > Diagnostics (Nichols Institute, San Glycemic Fluctuations in People glucose levels were 400 mg/dL. She Juan Capistrano, CA). Less than 0.4 With Diabetes Taking Insulin was then suspected to have autoim- U/mL was considered an undetectable mune hypoglycemia. Insulin antibod- titer. In one patient, insulin autoan- Case 1 Presentation ies were elevated >50 U/mL. She was tibody estimation was carried out A 67-year-old woman with type 2 di- started on prednisolone 0.5 mg/kg by enzyme-linked immunosorbent abetes for the past 10 years, previously and two doses of short-acting insu- assay (ELISA; positive: >15 U/mL). well controlled on oral hypoglycemic lin before breakfast and lunch. She VOLUME 34, NUMBER 3, SUMMER 2016 165 CASE STUDIES had a partial remission at the end of Questions Insulin autoantibodies are mostly 2 weeks; 6 weeks after initiation of 1. In what clinical circumstances polyclonal in origin and are mostly treatment, she had a full remission, should insulin autoantibody syn- of the immunoglobulin G class. They and the steroids were tapered. drome be suspected? can be of high affinity/low binding 2. What are the biochemical and capacity or low affinity/high binding Case 2 Presentation hormonal indicators of autoim- capacity (8). The latter is often asso- A 75-year-old man with type 2 dia- mune hypoglycemia? ciated with clinical manifestations. betes for 6 years who was on insu- 3. What are the available These antibodies are virtually indis- lin therapy for the past 4 years was management strategies for dys- tinguishable from the antibodies seen detected to have carcinoma of the glycemia resulting from insulin in up to 70% of children with type 1 colon 1 year before presentation. He autoantibodies? diabetes. When the antibody titers are underwent a hemicolectomy and was very high, there may be clinical mani- Commentary later diagnosed with liver metastasis festations resulting from the ability of and cirrhosis of the liver. He was on We described above two scenarios in these antibodies to act as temporary bavacizumab and chemotherapy for which we believe insulin autoantibod- storehouses of insulin, which prevents the disease, which was staged as T4 ies played a pathogenic role—patients its action, and then the subsequent M1. His glycemic control was erratic without diabetes who have hyperin- release of the stored insulin, which 1 month before presentation, and he sulinemic hypoglycemia and those causes hypoglycemia. This explains was admitted with DKA five times with diabetes who have wide glyce- the characteristic increase in blood during this period and once had lactic mic excursions on insulin. These cases glucose in the immediate postpran- acidosis requiring dialysis. His blood offer insights that may be useful in dial period and the hypoglycemia glucose was controlled only with in- the management of similar cases in observed later. Possible alternative travenous insulin infusion; when he resource-limited settings. explanations include direct stimu- was shifted back to subcutaneous in- Autoimmune responses and their latory effects of the antibodies on sulin, he slipped back into DKA. propensity for leading to disease the pancreas and the crosslinking of At presentation, he was on deglu- states are well known. It is, however, insulin-insulin receptor complexes dec and three-times-daily short-acting very rare for a protein hormone to by the insulin antibodies, resulting insulin. His random blood glucose elicit an antibody response and still in potentiation or prolongation of was 520 mg/dL, and his DKA was rarer for that response to manifest insulin action (6).
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