If I Throw Up My Thyroid Meds When I Wake Should I Take It Again
J Neurogastroenterol Motil. 2010 Oct; xvi(4): 428–432.
Thyrotoxic Vomiting: A Example Report and Possible Mechanisms
Soyeon Shim
1Department of Internal Medicine, Wonkwang University Sanbon Infirmary, Gunpo, Gyeonggi-exercise, Korea.
Han Seung Ryu
2Digestive Disease Inquiry Institute, Wonkwang University Schoolhouse of Medicine, Iksan, Jeollabuk-exercise, Korea.
Hyo Jung Oh
1Section of Internal Medicine, Wonkwang University Sanbon Hospital, Gunpo, Gyeonggi-exercise, Korea.
Yong Sung Kim
2Digestive Illness Research Institute, Wonkwang University School of Medicine, Iksan, Jeollabuk-practise, Korea.
Received 2010 Aug 21; Revised 2010 Sep 29; Accepted 2010 Oct ii.
Abstract
The symptoms related to gastrointestinal (GI) tract are sometimes master complaints in patients with endocrine disease. Thyrotoxicosis is a rare, only notable cause for unexplained and repeated airsickness. Here, we report an adolescent patient with thyrotoxicosis who was initially presented with repeated vomiting and epigastric pain. A thirteen-year-old female was referred to a GI outpatient section for evaluation of vomiting and intestinal pain from a pediatric clinic. Esophagogastroduodenoscopy revealed acute gastritis with duodenogastric reflux and suspicious reflux esophagitis of minimal modify, but at that place was no significant improvement later treatment and equally a effect she was admitted to the emergency room. She was afterwards diagnosed equally Graves' affliction because an initial laboratory exam at the GI outpatient department revealed thyroid stimulating hormone < 0.01 µIU/mL and additional blood tests showed elevated thyroid hormones and positive thyroid stimulating hormone receptor antibiotic. The airsickness and epigastric pain improved remarkably subsequently treatment with antithyroid drugs. Clinicians should consider the possibility of thyrotoxicosis in patient with unexplained and repeated airsickness.
Keywords: Adolescent, Thyrotoxicosis, Vomiting
Introduction
Airsickness is one of the most common symptoms in gastroenterology clinics and commonly originates from gastrointestinal (GI) disorders. Nonetheless, various extraintestinal disorders tin besides cause vomiting.i , ii
Patients with thyroid disorders may present with a broad range of GI symptoms (eg, diarrhea, frequent defecation, constipation, dyspepsia, nausea, vomiting and abdominal pain).three Some patients with masked thyrotoxicosis who lack the unique clinical feature usually presented every bit cardiovascular abnormalities such as heart failure, but too occasionally as GI abnormalities including dysphagia,4 vomiting5 and abdominal hurting.6 We written report a case of an boyish female with undiagnosed thyrotoxicosis who was initially treated for vomiting nether a diagnosis of duodenogastric reflux and reflux esophagitis.
Case Report
A xiii-year-erstwhile female person patient was referred to the GI outpatient department of our hospital from a pediatric clinic to undergo the esophagogastroduodenoscopy for the evaluation of recurrent airsickness that lasted for 8 days. The vomiting usually occurred in the afternoon and was ailing in nature. Although vomiting was not related to food intake, she had avoided eating because of recurrent airsickness. She also complained of nausea, boring epigastric pain and palpitation, but denied diarrhea or melena. She had lost 8 kg of weight over 4 months, and her weight was 39.4 kg (10-25 percentile) and height was 156 cm (50-75 percentile) at presentation. By history and family history were not remarkable. She was in Tanner phase 4. Menarche occurred half dozen months ago, and menstrual cycles were irregular. Physical test revealed a dehydrated tongue, cachexic and anxious appearance. Her blood pressure level was 100/80 mmHg, pulse rate was 110/min, respiratory rate was 20/min and trunk temperature was 36.6℃. There was no definite enlargement or palpable mass on the anterior neck, eye abnormality or lymphadenopathy. The belly was soft with normal bowel audio and there was no straight or rebound tenderness on the belly. Electrocardiography showed sinus tachycardia. Obviously abdominal X-ray showed nonspecific findings. Because she had weight loss and palpitation with anxiety, thyroid stimulating hormone (TSH) was included in the initial laboratory test. Esophagogastroduodenoscopy at the offset visit of GI outpatient department revealed balmy mucosal erythema on Z-line and acute erythematous gastritis with large corporeality of duodenogastric reflux (Fig. 1). Helicobacter pylori rapid urease exam was negative. She was prescribed a proton pump inhibitor, prokinetic and mucosal blanket agent (sucralfate) on the basis of her endoscopic diagnosis with GI section follow upward afterwards two weeks. Her airsickness improved during the showtime 2 days subsequently medication, however, she visited the emergency department (ED) v days later considering of recurred vomiting and dull epigastric pain. Her blood pressure level was 140/lxxx mmHg, pulse rate was 88/min, respiratory charge per unit was 20/min and trunk temperature was 36.8℃. Physical examination revealed balmy epigastric direct tenderness. The doctor of the ED found that she already had blood tests including TSH at GI outpatient department and information technology revealed TSH < 0.01 µIU/mL (normal range 0.35-5.55 µIU/mL). Complete blood count with differential, electrolyte and glucose were within normal limit. A liver part tests showed albumin 4.34 g/dL (normal range three.eight-v.3 yard/dL), total bilirubin 2.47 mg/dL (normal range 0.3-ane.two mg/dL), alkaline metal phosphatase 139 IU/L (normal range 25-100 IU/L), AST thirty IU/Fifty (normal range 0-35 IU/L) and ALT 38 IU/L (normal range 0-35 IU/Fifty). A repeated liver function test at ED showed total bilirubin one.7 mg/dL, alkaline metal phosphatase 133 IU/Fifty, AST xxx IU/50, ALT 42 IU/50 and magnesium and calcium were inside normal limit. Subsequent claret tests for the thyroid showed gratis triiodothyroxine (T3) > 8.0 ng/mL (normal range 0.60-1.81 ng/mL), complimentary thyroxine (T4) > 12.0 ng/dL (normal range 0.89-one.76 ng/dL), TSH receptor antibiotic 37.iv% (normal range ≤ 15.0%), anti-thyroid microsomal antibody 6.22 U/mL (normal range ≤ 3.0 U/mL) and thyroglobulin antibody half-dozen.91 U/mL (normal range ≤ 3.0 U/mL). Thyroid ultrasonography revealed diffusely enlarged glands, decreased parenchymal echogenecity and increased vascularity of both glands (Fig. two). Handling was initiated with propylthiouracil (PTU) 3.75mg/kg/24-hour interval and propranolol i mg/kg/day, after 4 days of handling, vomiting, epigastric pain and palpitation were improved remarkably. She was discharged with a maintenance dose of PTU (iii.75 mg/kg/solar day) without prokinetic or proton pump inhibitor.
Endoscopic findings show mild erythema with whitish turbidity around Z-line (A) and large corporeality of bile-mixed fluid in the gastric lumen with bile stainings on the gastric mucosa (B). Later on suctioning of all fluid and washing the gastric mucosa with water, multiple linear mild erythematous changes on gastric mucosa are observed (C, D).
Ultrasonography of the thyroid glands. Both lobes in the transverse plane reveal diffusely enlarged round lobes and decreased parenchymal echogenecity (A). Doppler exam for correct lobe (B) and left lobe (C) demonstrates increased vascularity.
She was hospitalized once more five days later on because vomiting had recurred. Liver function tests returned to normal limits, only thyroid function tests were still elevated (TSH < 0.01 µIU/mL, costless T3 vi.31 ng/mL and costless T4 v.09 ng/dL). We switched handling from PTU to methimazole 0.four mg/kg/twenty-four hour period and added inorganic iodine (Lugol's solution) for v days to prevent thyroid hormone release. After 3 days, there was no further vomiting, and free T3 and free T4 were decreased to 4.46 ng/mL and 2.24 ng/dL, respectively. She was discharged with a maintenance dose of methimazole (0.4 mg/kg/day) and propranolol (1 mg/kg/day).
After 2 months with methimazole and propranolol maintenance therapy, her symptoms were stable and free T4 returned to normal limits (1.27 ng/dL) despite still having low level of TSH (< 0.01 µIU/mL). Over side by side 16 months with methimazole monotherapy, airsickness has not recurred and she became euthyroid with normalized TSH receptor antibody.
Discussion
GI symptoms such as hyperphagia, diarrhea, and frequent defecation are usually associated with thyrotoxicosis, whereas vomiting, intestinal pain, and dysphagia are uncommon. Although vomiting, nausea and intestinal pain have not been generally included as common presenting symptoms for thyrotoxicosis, a review of 25 newly diagnosed thyrotoxicosis cases reported that the significant number of thyrotoxic patients complained of airsickness (44%), nausea (28%) and abdominal hurting (20%).seven Ane or more of these intestinal symptoms were included as a main complaint in 36% of cases reviewed.7
Interestingly, thyrotoxic vomiting tin occur intermittently, and unique clinical features of thyrotoxicosis including goiter, ophthalmopathy such every bit exophthalmos or hat retraction are rarely associated with cases of thyrotoxic airsickness.5 , 6 , 8 Our patient was diagnosed as hyperthyroidism acquired by Graves' disease based on autoantibodies and sonographic finding. She was xiii-year-old child and the characteristics of pediatric Graves' disease as well brand clinician difficult to diagnose thyrotoxicosis. In pediatric Graves' disease, the size of the thyroid gland is highly variable and the goiter may go unnoticed in patients with a slightly enlarged thyroid gland, and ophthalmic abnormalities are less severe in children than in adults.nine Therefore, children with undiagnosed thyrotoxicosis may initially be referred to cardiologists with a heart murmur, gastroenterologists with GI symptoms and failure to thrive, or psychiatrist because of challenging behavior and school refusal earlier existence referred to an endocrinologist.10
When rare GI symptoms like vomiting present as initial symptoms in patients with thyrotoxicosis and there are no typical features of thyrotoxicosis, it tin can be misdiagnosed as GI disorders. If the doctor is misled to another GI disorder and vomiting is prolonged for several weeks under wrong treatment, this patient non simply can progress to a life-threatening state of affairs, simply too may have many unnecessary tests under suspicion of functional airsickness or even exploratory laparotomy.1 , 6 , xi
In cases of thyrotoxicosis that showed only GI symptoms, diagnostic clues might exist chronicity of symptoms, prominent weight loss and tachycardia.6 , 8 , 12 In our patient, the prominent weight loss over several months, palpitation and anxiety were clues to the suspicion of thyrotoxicosis. Withal, since these symptoms are not pathognomic signs of thyrotoxicosis and often accompanied by other GI symptoms, proper diagnosis is hard and delayed considerably.
There are several possible mechanisms past which thyrotoxic airsickness develops. The first proposed mechanism is an increment in β-adrenergic activity due to an increased number of β-adrenergic receptors.13 There have been several reports of rapid symptomatic comeback after administration of β-blockers before the normalization of thyroid hormones.6 , eight , 12 Based on these reports, it is conceivable that the vomiting in thyrotoxicosis may be attributed to sympathomimetic furnishings of thyroid hormones as dysrhythmias, fever, tremors, palpitations and feet. The rapid symptomatic improvement may reflect the power of β-blockers to reduce the peripheral conversion of thyroxine to triiodothyronine.12
Second, increased thyroid hormones tin can cause emesis. There is a reported case that symptoms were non improved by the administration of β-blockers only improved after thyroid hormone levels normalized.14 In our example, clinical symptoms were temporarily improved past the administration of β-blocker with subsequent recurrence within v days and were completely improved afterward thyroid hormone levels decreased to virtually normal range by Lugol'south solution. The mechanism for vomiting in thyrotoxicosis may be similar to that for vomiting in hyperemesis gravidarum. Increased α-subunit of man chorionic gonadotropin induces secretion of thyroxine through a TSH-like activity.15 However, it is nevertheless controversial whether thyroid hormones themselves act equally an emetic factor in thyrotoxic vomiting, although information technology has been speculated that thyroid hormones stimulate the chemical trigger zone.5
Third, thyroid hormones tin change gastric motility and decrease gastric emptying secondary to the malfunction of the pyloric sphincter. A plausible explanation for this phenomenon is that thyroid hormones alter magnesium homeostasis, and hypomagnesemia affect smoothen muscle straight or autonomic innervations of the upper GI smooth muscle.16 , 17 The rate of gastric emptying is slightly increased after the restoration of euthyroidism18 and postprandial tachygastrias are significantly reduced after antithyroid therapy.19 , 20
4th, the estrogen was suggested an emetic cause in thyrotoxicosis considering there are female predominance in thyrotoxic vomiting and estrogen level could be increased in patients of both sexes with thyrotoxicosis.5 , 21 And then the raised estrogen level may induce nausea and vomiting but in susceptible patients.22
Lastly, it was suggested that functional duodenal obstacle in thyrotoxicosis may nowadays much similar the obstruction in superior mesenteric artery syndrome.14 Possible causes of this obstruction are prominent weight loss, supine position in a patient with prolonged and astringent illness and hypermotility induced volvulus of duodenal tertiary portion.
Thyrotoxic vomiting has a excellent prognosis and unremarkably improved within several days after initiation of antithyroid treatment in the majority of reported cases.5 - eight , 12 However, since our patient was pediatric Graves' disease, nosotros should consider genetic background of Graves' affliction and higher frequency of relapse than adult.nine
In determination, the possibility of atypical thyrotoxicosis should be considered in patients with persistent unexplained vomiting. Since symptomatic improvement is related to the thyroid hormone level, advisable treatment strategies and meticulous surveillance for the thyroid hormone level are mandatory.
Footnotes
Financial support: This work was supported past Wonkwang University 2009.
Conflicts of involvement: None.
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