Introduction: Insulin resistance occurs most commonly in association with obesity but may result from multiple causes, e.g. medications, lipodystrophy, or antibodies to insulin or insulin receptors. We review a case of an unusual presentation of insulin resistance. We highlight challenges of diagnostic testing and treatment when there are cost limitations. Clinical Case:A 41 year old Hispanic male with T2DM and a history of well-controlled BPD on quetiapine only presents for management of diabetes. His current treatment is metformin and a TDD of 170 U human insulin; A1C is 12.2%. He was diagnosed at age 32 via routine lab tests. At diagnosis BW was 96.4 kg, BMI 29, BP 100/70, CHOL 152, TG 247, HDL 35, LDL 68. Physical exam was unremarkable without acanthosis or lipodystrophy. Anti-GAD, anti-islet cell antibodies, insulin and C-peptide levels were ordered, but not obtained due to cost. He was managed with lifestyle modification for 2 years with maintenance of A1C <7%. At age 35 he developed symptomatic hyperglycemia with A1C 9.4% and was started on metformin and glyburide. At age 36 A1C was >11%, with no change in BW. Glargine 5 U was added, and glyburide was changed to glipizide. Glargine was increased to 40 U without changes in glycemia. At age 37 glipizide was stopped, and he could not afford glargine. He was switched to 70/30 human insulin. Insulin dosages were progressively increased to 220 U a day with no change in glycemia. Liraglutide was tried but not continued due to cost, and quetiapine was switched to trazodone without improvement in A1C. LFTs, CBC, HIV, Hepatitis C and B have been negative. The patient has had multiple visits for education with documented adequate disease understanding and performance of injections. Nonadherence was suspected; for its evaluation, the patient was observed in clinic self-injecting 30 U of regular insulin (brought from home); fasting was confirmed for 3hrs post-injection. BG was 327mg/dL pre-injection and 326mg/dL 3hrs post-injection. Insulin antibodies were requested but not obtained due to cost. Insulin receptor antibodies are not commercially available in the US. Potential empiric strategies, e.g. the NIH protocol for insulin type B resistance (rituximab + dexamethasone + cyclophosphamide) was considered but cost is a limitation. We discussed steroids or methotrexate for possible antibody mediated insulin resistance versus a trial of thiazolidinedione, which has been reported to decrease severe insulin resistance in patients with lipodystrophy. The patient opted to initially try a thiazolidinedione. Conclusion:Although poor adherence has not been excluded, the patient appears to have no response to high doses of injected human insulin, suggesting extreme insulin resistance. Cost limitations preclude optimal diagnostic evaluation. Empiric treatment with low cost options potentially may provide diagnostic information as well as efficacious treatment.
Case PresentationA 29-year-old man with unspecified mood disorder, childhood attention deficit hyperactivity disorder, and 2 prior suicide attempts with zolpidem and methadone presented with altered mental status as a transfer from an outside hospital. The patient was found in his truck outside of a grocery store by a bystander who contacted emergency medical services. At the time, he was noted to have seizure-like activity. He had an empty shopping bag in his possession with 14 empty loperamide (Imodium®) bottles, each were supposed to contain 24 tablets. The patient was taken to the nearest medical facility where he was found to be in status epilepticus. After no response to 4 mg intravenous (IV) lorazepam, he was then intubated for airway protection. Propofol infusion was started and a loading dose of levetiracetam 1600 mg IV was administered. Despite medical management, he continued to show evidence of seizure-like activity. Due to the lack of a neurology service at the hospital, the patient was transferred to our academic medical center.On arrival, patient was intubated, sedated and hemodynamically stable. Sedation was paused to allow a thorough neurologic examination, at which time, he became agitated and was not redirectable. However, he did not exhibit seizure activity. Toxicology service was consulted for suspected loperamide overdose.
Background: Subacute thyroiditis (SAT) is a transient inflammatory disorder of the thyroid gland, whereas Hashimoto thyroiditis (HT) is an autoimmune disorder. These two disease entities have quite different pathogenic mechanisms and typically do not co-occur. The objective of this report is to describe a patient with HT with eventual evolution into SAT to euthyroid. We review the diagnostic challenges of an uncommon presentation of Hashimoto thyroiditis with SAT. Clinical Case:52-year old female diagnosed with Hashimoto thyroiditis with subsequent development of hypothyroidism 10 years ago presented to our endocrinology clinic for the management of hyperthyroidism. She was diagnosed previously 10 years ago with reported elevated TSH, low FT4 and positive antibody testing assumed to include elevated anti-thyroid peroxidase. Therefore, at the time of her diagnosis she was started on levothyroxine 25 mcg daily and increased over time to 75 mcg daily. Approximately several months prior to her clinic visit with us, she began having a sore throat with subsequent development of voice hoarseness and tachycardia associated with palpitations lasting persistently for 1 month. She endorsed symptoms 2 months prior with having pain in her lower anterior neck described as non-radiating, intermittent and sharp associated with voice hoarseness, palpitations, racing heart and jitteriness that was exacerbated while palpating area. Her symptoms have since improved to having mild voice hoarseness. Her past medical history aside from hypothyroidism is Celiac disease and migraines. Her medications included Erenumab 70 mg once monthly and sumatriptan 100 mg as needed. During her evaluation, her blood pressure was 120/75, heart rate 72 bmp, temperature 36.0 C. Her physical exam was remarkable for mild tenderness of the anterior inferior midline neck without obvious masses or lesions. Ultrasound of her neck revealed heterogenous echotexture of the entire thyroid gland is noted with diffuse increased vascularity. The right thyroid lobe measured 4.2 x 1.0 x 1.5 cm and left thyroid lobe measures 4.0 x 1.0 x 1.3 cm without focal lesion is noted within either lobe. The soft tissues of the neck are unremarkable. There are no abnormal masses or fluid collections. Visualized lymph nodes are unremarkable in size and did not demonstrate increased vascularity. These findings were consistent with thyroiditis. Laboratory values obtained during her initial symptoms revealed slight hyperthyroidism with a TSH 0.05 mU/L (normal range, 0.8 to 1.7 mU/L) and FT4 2.0 ng/dL (normal range, 0.45 - 4.50 ng/dL), therefore her treatment with levothyroxine was discontinued. She was not started on any additional treatment as her symptoms were self-resolving. Repeat laboratory values in 4 weeks showed completely normal thyroid laboratory value with TSH 4.36 mU/L (normal range, 0.8 to 1.7 mU/L) and FT4 1.1 ng/dL (normal range, 0.45 - 4.50 ng/dL). Conclusion: HT is thought to be autoimmune in origin with lymphocytic infiltration and fibrosis. Early in the disease course, hyperthyroidism may result from destruction of the thyroid gland cells. HT is known to be a life-long disorder with essentially a non-functional thyroid. It is well established that SAT may evolve to HT and that HT may transform in Grave’s disease. Additionally, painful HT mimicking SAT has also been reported. There have been few reported cases of HT progressing into hyperthyroidism secondary to SAT and further resolution to euthyroid function.
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