We have previously reported that there is a strong association between unnecessarily ordered thyroid USGs and unnecessarily requested Endocrinology (Endo) consultations. Unnecessary consults consume time and resources, delay appropriate consults, and have even been proposed as a factor in the over-diagnosis of clinically innocuous thyroid cancers. We have examined the impact on the consumption of clinical resources. The database consisted of 201 new Endo consults, each accompanied by a pre-consult thyroid USG. The consult requests were graded as appropriately requested (APPROP), optionally requested (OPT), or unnecessarily requested (UNNEC). The USG requests were likewise graded as APPROP, OPT, or UNNEC. The USGs were also graded on their degree of contribution to the request for a consultation, specifically, as having a significant role (SIGNIF), a minor role (MIN), or little or no role (NONE). The impact of the UNNEC consults was categorized as (a) the initial Endo consult, a resource that would not have been utilized were an UNNEC consult not submitted, and (b) resources that probably would have been utilized were the UNNEC consults not submitted but would have been managed by and costed to the referring provider instead of to the Endo provider. Such resources included follow-up Endo visits and relevant USGs and blood tests, Of the 201 consults with associated USGs, 156 (77.6%) consults were APPROP, 23 (11.4%) were OPT, and 22 (10.9%) were UNNEC. Conversely, 157 (78.1%) of the USGs were APPROP, 11 (5.5%) were OPT, and 33 (16.4%) were UNNEC. With respect to the association of consults with their accompanying USGs, Among APPROP requested consults, 87.8% of the associated USGs were also APPROP while only 7.7% were associated with UNNEC USGs. Among UNNEC requested consults, 31.8% of the associated USGs were APPROP while 68.2% were associated with UNNEC USGs. Regarding the resource utilization borne by an Endo clinic as a consequence of the submission of 21 UNNEC consults for the two years after the initial consultation, each UNNEC consult had consumed, on average, 5.9 (1 + 2.6 + 2.3) [initial + Yr 1 + Yr 2 follow-ups] Endo clinic visits, 0.9 (0.5 + 0.4) USGs [excludes the USG associated with initial consultation] and 4.1 (2.2 + 1.9) blood work orders and reviews. No follow-up FNAs or thyroid surgeries were performed. Endocrine care from any source would be best served by reducing both the unnecessary utilization and the unnecessary assignment of relevant resources.
There is considerable evidence that some Borrelial (Lyme spirochetal) proteins share significant antigenic properties with several thyroid-related proteins (e.g. TSH receptor, thyroglobulin, thyroid peroxidase) and can induce thyroid autoimmunity, sometimes associated with Hashimoto’s thyroiditis and perhaps also a “destructive thyroiditis” such as “silent” thyroiditis or “Hashitoxicosis.” As an acute illness, Lyme disease may also constitute a “non-thyroidal illness” capable of perturbing thyroid function tests without causing thyroid dysfunction. We report a 22-year old woman admitted with an acute paranoid schizophrenia, thyroid function tests consistent with autoimmunity, transient thyrotoxicosis (tachycardia, lid-lag, brisk DTR’s) and a greatly reduced radioiodine uptake. The thyroid was not palpably enlarged, nodular or tender. On screening assay, reactivity was demonstrated to 4 of 13 Borrelial proteins. Anti-Lyme IgM but not IgG, antibodies, were positive. This was consistent with recent Lyme disease infection. Serum TSH (NL: 0.358-3.74 mcU/ml), Free T4 (NL: 0.76-1.46 ng/dl), and Free T3 (NL: 2.18-3.98 pg/ml) were, respectively: Day1: 0.087 mcU/ml (suppressed), 1.52 ng/dl (slightly elevated), 2.07 pg/ml (slightly reduced); Day2: 0.148 (suppressed), 1.18 (normal), no FT3; Day4: 0.827 (normal), no FT4 or FT3; Day5: 1.66 (normal), 0.89 (normal), 1.77 (low). Anti-Tg and Anti-Peroxidase antibodies were both moderately elevated. Thyroid Stimulating Immunoglobulins were not elevated. The radioactive iodine uptake on Day4 was 2.8% (NL: 15-30% at 24 hr). Thyroid ultrasonogram was normal. An attractive explanation is that Lyme disease triggered a “destructive thyroiditis,” perhaps but not necessarily mediated by thyroid autoimmunity. This would account for the brief interval of thyrotoxicosis accompanied by a very low radioiodine uptake. Alternatively, Lyme disease, as an acute process, would expectedly be capable of eliciting the thyroid function abnormalities of “non-thyroidal illnesses” in general, as would acute psychosis, well-known to often resemble Graves’ disease at admission.
Background Lithium is a drug used in the management of psychiatric condition such as acute mania and bipolar disorder. Lithium is generally known to decrease thyroid hormone synthesis and release, causing hypothyroidism and thyromegaly. Much less commonly, lithium can cause elevated thyroid function tests; we describe such a case. Clinical Case A 21-year-old man with bipolar disorder and polysubstance abuse, presented with acute mania and was started on Lithium. Baseline TSH was 1.42 [0.358-3.74 µIU/mL], but one week after starting Lithium, TSH was 0.1 uIU/mL [0.358 - 3.74 µIU/mL] with free T4 of 0.95 [0.76-1.46 ng/dL]. Three weeks later, TSH was 0. 01 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.52 ng/dL [0.76 - 1.46 ng/dL], FT3 6.16 pg/mL [ 2.18 - 3.98 pg/mL], total T3 221 ng/dL [76–181 ng/dL]. Six weeks after starting Lithium, TSH remained suppressed at <0. 005 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.66 ng/dL [0.76 - 1.46 ng/dL], FT3 6.21 pg/mL [ 2.18 - 3.98 pg/mL]. During this time the patient's only complaint was tremor, with no other symptoms of hyperthyroidism. Physical exam showed mild tachycardia, with no evidence of thyroid eye disease, and the thyroid gland was normal size and nontender. TSI was negative with normal thyroglobulin and iodine levels, negative thyroglobulin and peroxidase antibodies. Lithium was in the therapeutic range. Thyroid US was normal without thyromegaly, normal echogenicity and color flow and without nodules or masses. I-123 thyroid uptake and scan showed low uptake and no nodules. The patient was diagnosed with Lithium-induced silent thyroiditis. He was treated with propranolol 10 mg PO BID for tremors, which was stopped later, due to bradycardia and dizziness. Due to persistent suppression of TSH and elevated FT4 and FT3 eight weeks after initiation of Lithium, this was discontinued, and Depakote was started. Conclusion Prior studies have shown that Lithium-induced thyrotoxicosis occurs in 2.7 cases/per 1000 person-years, with Lithium-associated Graves’ disease in 1.4 cases/1000 person-years, and silent thyroiditis only in 1.3 cases/per 1000 person-years. Although rare, our case highlights the importance of considering silent thyroiditis in patients treated with lithium and hyperthyroidism. References: K. K. Miller and G. H. Daniels, Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clinical Endocrinology 2001; 55, 501-508Kibirige et al. Spectrum of lithium induced thyroid abnormalities: a current perspective. Thyroid Research 2013; 6: 3 Presentation: No date and time listed
Case 1 74-year-old Caucasian male with dysphagia, s/p laryngeal carcinoma, partial laryngectomy and past radiotherapy, was referred for breast enlargement with some increase over the last few years. He denied tenderness or breast discharge, but reported bilateral testicular atrophy, which he attributed to agent orange red exposure. Although married for 53 years, he did not have biological children. He had decreased libido, and denied testicular trauma, urinary symptoms, or history of infections, opiate, steroids abuse, or OTC herbal supplements. Pituitary MRI for head injury was normal. Physical exam-HT= 180.3 cm; 172 cm arm span, bilateral testicular atrophy. Laboratory findings: [PO4= 3.2mg/dL (2.5-4.9); Calcium=9.2 mg/dl(8.5-10.1);Magnesium =2.1 mg/dl(1.7-2.4); Vit D,25 OH=52.9 ng/mL (30–100); PTH =54.9 pg/ml (18.4-80.1),;FSH =41.7 mIU/mL(0 .7-10.8); LH=27.5 mIU/mL (1.2-10.6);Prolactin=4.5 ng/mL(2.5 -7.4); total Testosterone 81 ng/dL (250–1100); free testosterone 4.5pg/mL (30. 0-135. 0); Sex HBG 63 nmol/L (10–57); Estradiol <11.80 pg/mL(<11-39.8); Tumor marker BHCG <2mIU/mL (<5 mIU/ml; Cortisol, am=15.5 ug/dl (5.3-22.5);PSA=.260 ng/mL (0. 0- 4. 0)]. Karyotype analysis=47, XXY [15]/46, XX[5]. With supernumerary X chromosome, consistent with KS. DXA= osteopenia in AP spine and severe osteoporosis in other areas: femur neck left T-Score of -3.1. Right femur neck T-Score=-3. 0, total left femur T-Score= -2.9, right total femur T-Score of -2.9, left forearm radius 33% T-Score=-2.8. Mammogram: mild bilateral gynecomastia, L>R, Testosterone supplementation and intravenous zoledronic acid therapy were started. Case 2 74-year-old Caucasian male referred for low energy, generalized weakness, decreased libido and gynecomastia, long thin arms/legs and "difficulty building muscle". He was taking OTC "testosterone enhancers" herbals only. He reported no biological children. Physical exam: height 187.3 cm, with sparse body hair, absent facial hair, gynecomastia, small testes. Laboratory: [total testosterone=40 ng/dl; free testosterone=5.2 pg/ml; SHBG=40 nmol/L;LH=16.1 mIU/ml; FSH=31.8 mIU/ml; Prolactin=4.3 ng/ml; BHCG <3 mIU/ml; Estradiol=33.60 pg/m] Karyotype: mosaic KS 47, XXY[16]/46,XY[4] with additional X chromosome in 16/20 metaphase cells. DXA =normal bone density. Clinical symptoms and testosterone levels improved after starting testosterone supplementation. Discussion Hypogonadism is an important cause of male osteoporosis. Testosterone is known to regulate male bone metabolism both indirectly by aromatization to estrogens and directly through the androgen receptor on osteoblasts, promoting periosteal bone formation during puberty and reducing bone resorption during adult life. Early onset testosterone deficiency, as in KS, is an important risk factor for osteoporosis, although it is seen in only 40% of patients. Aromatization of testosterone into estradiol from adiposity, may also contribute to normal BMD in some patients. Therefore, it is important to recognize that osteoporosis is not always present in all Klinefelter's patients, even without testosterone therapy and that various phenotypes may account for discrepant conditions, as in these cases. Presentation: No date and time listed
Introduction: Hypoglycemia (HYPO) in non-diabetic patients is an unusual scenario and presents a diagnostic challenge, resulting in serious consequences for patients. We describe the case of an elderly non-diabetic male who developed severe persistent HYPO. Case: A 78-year-old male with history of macroprolactinoma taking bromocriptine, Hashimoto's hypothyroidism, initially treated with low dose L-thyroxine, followed by Graves' hyperthyroidism, Parkinson’s disease (PD), osteopenia was noted to have hypoglycemia (54 mg/dL) on routine lab work. When questioned, he admitted to having had years of lightheaded episodes, "feeling jittery", which improved within minutes after eating sugary foods. His wife mentioned that he “loved to eat sweets” and high simple carbohydrate meals(CARBS). Physical exam - orthostatic hypotension and mild resting tremors, both attributed to PD. Continuous glucose monitoring (CGMS) was performed for 2 weeks which documented HYPO overnight while sleeping, fasting and between meals. The HYPO was associated more frequently with sweet bedtime snacks. Laboratory- Glucose tolerance test was stopped due to HYPO with symptoms. ACTH=19 pg/mL (nl 0-47), AM Cortisol 19.4 microg/dL (nl 5.3-22.5), fasting blood glucose 83 mg/dL(nl 70-99), fasting insulin 6.9 mIU/L( nl 0-24.9), proinsulin 16.9 pmol/L ( nl <=18.8 pmol/L), c-peptide 1.39 ng/mL( nl 0.81-3.85), beta-OH butyrate 0.072 mmol/L( nl 0.020-0.270). Islet cell Ab was normal. Gastric emptying study was negative. Although the dose of bromocriptine was reduced due to HYPO, it continued. He was advised to decrease intake of CARBS, eat small, high protein and fat meals with frequent snacks. On subsequent visits, he reported less hypoglycemic episodes with improved energy level and general well-being, which was confirmed by CGMS. Discussion: Although a wide range of diseases can cause HYPO in nondiabetic patients, differences in characteristics between non-diabetic HYPO and diabetic HYPO have not been well studied. Common underlying diseases associated with HYPO include malignancies, cerebrovascular diseases, infection, major organ failure, and alcohol-related disorders. In addition, comorbidities linked with HYPO include sepsis, kidney diseases, and alcohol dependence, pneumonia, liver diseases and insulin abuse. Malnutrition, alcohol, infection, and post gastrectomy are the leading causes of nondiabetic hypoglycemia. In addition, methimazole use has been associated with insulin autoimmune syndrome resulting in HYPO due to interaction of sulfhydryl group with disulfide bond in the insulin molecule Conclusion: Clinicians should be aware of the potential for hypoglycemia in non-diabetic patients, due to other etiologies, which can also result in severe and possibly life-threatening sequelae. An in-depth evaluation, including the use of CGMS can assist in determining underlying causes.
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