Graves’ Disease and the Manifestations of Thyrotoxicosis
DeGroot LJ.
ncbi.nlm.nih.gov/books/NBK2...
GASTROINTESTINAL FINDINGS
The appetite is characteristically increased. The effect of this increase is to offset, in part (sometimes completely), the loss of weight that might be expected from the increased catabolism. Indeed, the pattern of weight loss with increased appetite is nearly pathognomonic of thyrotoxicosis, although it may occur in diabetes mellitus and malabsorption or intestinal parasitism. A minority of patients complain of anorexia. Needless to say, they are likely to show the greatest weight loss. Nausea and vomiting are rare, but when they occur, they are serious. They are usually features of severe thyrotoxicosis but may also reflect hypercalcemia. In the presence of hypermetabolism, vomiting leads quickly to dehydration, ketosis, and perhaps avitaminosis.
The incidence of achlorhydria in exophthalmic goiter was found some years ago to be approximately 40% and slightly higher in myxedema [372]. The figures would be lower today. Berryhill and Williams [373]found that 73% showed a return of free hydrochloric acid after surgical thyroidectomy. Gastric enzyme production is decreased, and a mild chronic gastritis may be present [374]. Fasting serum gastrin levels, and responses to arginine, are increased [375].
Abdominal pain is an occasional symptom of thyrotoxicosis. Its nature and origin are obscure. Epigastric pain may suggest ulcer, gallbladder disease, or pancreatitis. Vomiting is sometimes associated with the pain.
The rate of absorption from the gastrointestinal tract is accelerated. The glucose tolerance curve may show an abnormally rapid rise and fall. Absorption of vitamin A is enhanced, and vitamin A formation from carotene is also increased.
Increased frequency of normal bowel movements is common, and occasionally diarrhea occurs. Transit time is decreased, and fat absorption may be impaired to the point of steatorrhea if fat intake is excessive [376].
The liver is frequently palpable in the absence of congestive heart failure, and is typically palpable with heart failure. Evidence of mild to severe liver disease may be found [377]. The plasma albumin level may be below 4 g/dl, and the globulin level above 3 g/dl. Galactose tolerance is impaired. There may be mild elevation of PT. The LFTs can give the impression of viral hepatitis. For example in one survey of 81 thyrotoxic patients, three-fourths had some LFT abnormality, including 31% with elevated bilirubin, 24% with elevated SGOT, 13% with elevated LDH, 26% with elevated SGPT, and 67% with elevated alkaline phosphatase (which of course may reflect bone metabolism). Cholesterol is often depressed. The abnormalities clear with treatment [378]. Bilirubin retention and jaundice are occasionally seen without evidence of congestive heart failure, but they are much more commonly found when this complication is also present. On hepatic biopsy the liver may be entirely normal histologically, even when there are abnormalities in chemical findings; alternatively, there may be evidence of focal collections of lymphocytes, decrease in glycogen, and occasionally death of cells. On electron microscopy, the mitochondria are increased in size and the smooth endoplasmic reticulum is hypertrophic. The glycogen level is decreased [379].The fine stellate scarrings seen in the livers of patients with severe thyrotoxicosis and reported in the earlier literature are rarely observed today. The cause of hepatic disease has been thought to be congestive heart failure, malnutrition, intercurrent infections, and a direct toxic effect of thyroid hormone. Malnutrition must play a role. Congestive heart failure by itself certainly can induce gross abnormalities in liver function, and presumably this insult is worsened by coincident thyrotoxicosis. The splanchnic blood flow is increased in thyrotoxicosis and the arteriovenous oxygen difference is greater than normal, but hepatic anoxia, at least in the portal areas, might occur even without circulatory failure if the metabolic demand for oxygen exceeds the supply.
Several patients who have been jaundiced without signs of congestive heart failure or other cause of hepatic dysfunction have been reported [380]. In two of these patients there was considerable elevation of the indirect-reacting bilirubin level. Studies in one patient showed that conjugation products of glucuronic acid were secreted into the urine in greatly increased quantities. This finding ruled out any absolute deficiency in the glucuronyl transferase enzyme in the liver. It was hypothesized that in certain thyrotoxic patients there is a great increase in metabolites that must be excreted via the glucuronyl transferase enzyme system. Since bilirubin competes relatively inefficiently in this enzyme system, it may be "crowded out" in the presence of an increased quantity of substrates. As a result, it may not be conjugated as rapidly as normally, and its concentration in the serum would therefore rise. All of these patients had residual abnormalities in bilirubin metabolism when euthyroid. This finding suggests that an underlying abnormality was present and was exacerbated by thyrotoxicosis. It is probable that the occasional thyrotoxic and jaundiced patient may actually suffer from an unrecognized separate abnormality, such as Gilbert's disease or posthepatitic liver dysfunction, brought to light by thyrotoxicosis.
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