Case report: Acute Gastroparesis secondary to thyrotoxicosis.
Correspondence:
Marie-Louise von Linstow, MD
Grundtvigs Sidevej 7, 2.-3
1865 Frederiksberg C
Denmark
tel: + 45 33 22 34 20
(e-mail: [email protected])
Key words: gastroparesis; hyperthyroidism; thyrotoxicosis
Many diseases are known to interfere with the normal motility of the stomach, and several causes of gastroparesis have been described. The 2 most well known risk factors are abdominal surgery and diabetes mellitus, followed by viral infections (1,2). Case reports concerning other causes such as hypopituitarism (3), demyelinating disease of the medulla (4), cutaneous herpes zoster (5), multiple sclerosis (6) and Duchennes muscular dystrophy (7) are also available. Still many cases of gastroparesis remain idiopathic. Both diabetic gastroparesis, postsurgical gastroparesis and idiopathic gastroparesis have a bad prognosis, while postviral gastroparesis seems to be transient in its course (2).
Diarrhea, nausea and vomiting and general abdominal pain are well-known complications of hyperthyroidism (8,9,10), but to our knowledge, only a single case report has previously described the association between thyrotoxicosis and gastroparesis (11).
We now present another patient with thyrotoxic gastroparesis, which resolved after treatment of the thyrotoxicosis. The diagnosis of gastroparesis was based on a significant delay in gastric emptying demonstrated by X-ray after the oral administration of a barium meal.
Case report
A 54-year-old woman with a 3-year history of hyperthyroidism (Basedow’s disease) and rheumatic arthritis was hospitalized due to serious epigastric pain of 3-4 days duration. The pain was constantly present, radiating to the back and the right curvature and accompanied by nausea, vomiting and a weight loss of 2-3 kg. Ten years earlier, the patient also had an episode of severe abdominal pain, which resolved spontaneously. Ultrasound at that time showed sedimentation in a very large gall bladder, no cholecystitis. Until the current episode, the patient had been well, except for a salmonella infection one year ago. There was no history of fever, chills, arthralgies, myalgies, neurological symptoms, polyuria or polydipsia, and no history of any recent infection. The actual medication was tbl. Propylthiouracil 100 mg x 3 daily, tbl. penicillamine 150 mg x 1 daily, tbl. Lansoprazol 30 mg x 1 daily and tbl. Codeine 50 mg x 3 daily. The hyperthyroidism was controlled by the general practitioner, and the arthritis by the rheumatologists at the local hospital.
Physical examination revealed a cachectic woman with a pulse of 100, a blood pressure of 200/80 mmHg and a temperature of 37.4 °C. There were no ophthalmic signs of thyroid disease, and no goiter was found. Cardiac and respiratory examinations were normal. Direct and indirect tenderness was found in the epigastrium, without any rebound tenderness or guarding. The electrolytes, glucose, creatinine and liver enzymes were all normal. There was a mild leucocytosis of 14.8x109/l (normal 4.5-11.0x109/l) and a C-Reactive Proteine of 22 mg/l (0-5 mg/l). Thyroid parameters 3 months earlier showed TSH<0.01 mU/l (normal 0.30-4.20 mU/l) and free Thyroxin 31 pmol/l (normal 13-23 pmol/l). An ultrasound examination of the upper abdomen showed a slightly dilated ductus choledochus, no visible gall stones. There was no free air on abdominal X-ray. An upper endoscopy revealed a large peptic ulcer localized between the corpus and the antrum. A biopsy showed no presence of Helicobacter Pylori. The patient was discharged with tbl. Lansoprazol 60 mg daily.
The next day the patient returned with abdominal pain, nausea and alimentary vomiting. The temperature was 37.1 °C. Abdomen was soft and tender. There was no free air or evidence of mechanical obstruction on X-ray, but it showed coprostasis and the patient was treated with laxantia, and penicillamine and codeine treatment was stopped. The next day the patient was febrile (38.0°C) and antibiotics were given for 5 days. There was no evidence of pathological bacteria in 3 successive faeces samples. ERCP was performed and exploded the possibility of gall system pathology. The ulcer was healing up. The patient was discharged after 13 days of hospitalization.
Two days later she returned with severe abdominal pain and fever (temp. 38.7°C). Diarrhea and vomiting were also present. Body weight was now only 38 kg (normal body weight was 48 kg), pulse 90 and blood pressure 145/75 mmHg. The patient was capable of drinking, but had no appetite. The abdomen was tender in the epigastrium and right fossa iliaca. X-ray showed a small amount of fluid in both the large and the small intestine. Blood samples showed leucocytosis (18.7 x 109 /l), CRP 230 mg/l. Plasma glucose, - electrolytes and liver enzymes were all normal. After 10 days of hospitalization, a gastric emptying study was performed. The patient was given a water-barium meal. The roentgenograms demonstrated an exceptionally large hypotonic ventricle with a severe delay in gastric emptying. Six hours after oral administration of barium, it still remained in the stomach (normally the ventricle is emptied within a maximum of 4 hours). An upper endoscopy showed pyloric dysfunction with a total lack of peristaltic muscle contractions.
Thyroid function tests revealed now a relatively severe thyrotoxicosis with a TSH < 0.01 mU/l, free thyroxin 79 pmol/l and a total T3 of 5.3 nmol/l (normal 1.3-2.5 nmol/l). The patient had tremor and tackycardia of 110-120, but no other symptoms of thyrotoxicosis. The dose of Propylthiouracil was increased to 200 mg x 3 daily, and tbl. Propranolol 20 mg x 2 daily was added to the treatment. Four days later the patient’s gastrointestinal symptoms began to improve and she was discharged from the hospital.
Three months later she had gained 8 kg´s of weight, had no nausea and a good appetite. She still experienced 3-4 episodes of loose stool every evening, but no abdominal pain or any severe gastric symptoms were present. Thyroid function tests were normalized.
Many gastrointestinal symptoms are associated with thyrotoxicosis, such as diarrhea and constipation, abdominal pain, nausea and vomiting (8,9,10). The patient reported herein had an abrupt onset of gastroparesis while she was in a thyrotoxic state. From the case report it remains unclear whether the patient had taken her propylthiouracil tablets regularly or not. Moreover it became clear that the patient for some years had taken a nature medicine “the green pill” which contains small amounts of iodine. Both could explain the worsening of the thyrotoxic state. Some reports blame D-penicillamine for cases of autoimmune thyroiditis, although the possible association between D-penicillamine and thyroid function is not fully clear (12). Whether our patient’s treatment with penicillamine could have worsened her thyroid function or not, we can’t say.
In our patient was no history of any viral illness, and other possible causes of the symptoms such as electrolyte disturbances and Addison’s disease were excluded. Codeine is known to interfere with gastric and intestinal motility. Our patient had the treatment stopped 4 weeks before the gastric emptying measurement was performed, and this is therefore unlikely to explain the delay. As the patient suffered from rheumatic arthritis, the possibility of secondary amyloidosis as a potential cause of the gastrointestinal symptoms and delayed gastric emptying has been considered. The patient had no other signs of amyloidosis though, especially no nephropathy. We believe that the relief of gastrointestinal symptoms after treatment of the thyrotoxicosis and the exclusion of other potential causes strongly suggests the hyperthyroidism as the underlying cause of the gastroparesis.
Studies of the effect of thyroid dysfunction on gastric emptying have yielded conflicting results. Some studies have shown accelerated gastric emptying in hyperthyroidism based on a barium suspension (13) or hydrogen breath test (14), and Ikeda et al. reports a higher gastric emptying rate in thyrotoxic rats than in controls (15). On the other hand Brown concluded in an older study that a delay in gastric emptying of barium was characteristic of hyperthyroidism (16). More recent studies seem to agree, that gastric emptying doesn’t differ between hyperthyroid patients and healthy control subjects (17,18).
Isolated cases of hyperthyroidism presenting with severe acute abdominal symptoms have been reported (19-22). All these patients underwent a broad range of invasive investigations including sigmoidoscopy, retrograde pyelography, cystoscopy, renal angiography, cholecystography, gastroscopy, barium meal follow-through and even exploratory laparotomi (20,23). None of these investigations gave an explanation of the symptoms. Only when the thyrotoxicosis was treated, the patients became symptom-free. Common for many of these patients were the delay in diagnosing the thyrotoxicosis; Palmer and Beardwell (19) described a patient with a 3-year history of intermittent abdominal pain. She underwent exhaustive investigations as above mentioned. At last hyperthyroidism was discovered, and she was treated with Carbimazole. Within a month, she had gained 3,2 kg in weight and was symptom-free.
Verbrycke has reported 34 cases of hyperthyroidism with chiefly gastrointestinal symptoms and used the term ‘masked gastro-intestinal hyperthyroidism’ (8). Only in one case, described by Groskreutz, thyrotoxic gastroparesis has been found to be the explanation for acute onset of nausea, vomiting and epigastric pain (11).
The patient we describe, was every time admitted to the department of surgical gastroenterology, and appeared acutely ill. The focus was made on the gastric symptoms and clinical signs, and the possibilities of free air or ileus were excluded and a peptic ulcer accepted as the explanation of the symptoms. Even though it was known that the patient was treated for hyperthyroidism, no connection between the gastric symptoms and thyrotoxicosis was suspected. It is therefore important that clinicians pay attention to gastrointestinal symptoms in thyrotoxic patients and are especially aware of the possible gastroparesis – a condition where abdominal pain and nausea are dominant features (24).
This case illustrates that thyrotoxic gastroparesis can be effectively treated, once it is recognized, in contrast to many other gastroparesis syndromes. Many invasive investigations including exploratory laparotomi can be avoided in these patients if the underlying cause is identified sooner.
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