Ectopic endocrine syndrome

It is recommended that everyone should have some understanding of the cause of the disease called ectopic endocrine syndrome. This is mainly because this disease is caused by excessive secretion of adrenal hormones, which can lead to the occurrence of endocrine tumors in patients. Therefore, the cause of ectopic endocrine syndrome should be treated in time. The following is an introduction to the causes and symptoms of ectopic endocrine syndrome, which you can check out.

The main ones are as follows.

Ectopic adrenocorticotropic hormone (ACTH) syndrome

The most common type of ectopic endocrine syndrome. Among the non-endocrine tumors that cause ectopic ACTH syndrome, bronchogenic carcinoma is mainly pulmonary oat cell carcinoma accounting for 60%, followed by thymic tumors accounting for 15%, and pancreatic endocrine tumors accounting for 10%. Other malignant tumors such as esophagus, stomach, colon, gallbladder, kidney, prostate, breast, ovary, liver and thyroid, pheochromocytoma, neuroblastoma, etc. can also cause it. This non-endocrine tumor mainly secretes large-molecule ACTH (about 35-70%), which has lower biological activity than normal small-molecule ACTH, but their biological effects are the same, both of which can stimulate adrenal cortex hyperplasia and secrete cortisol. Therefore, in addition to the symptoms of the primary tumor, there are also clinical manifestations of Cushing's syndrome, which may even appear earlier than the primary tumor. The prominent manifestations are obvious skin pigmentation, high blood pressure, edema, hirsutism and acne, but the typical sanguinea, centripetal obesity and purple skin striae of Cushing's syndrome are rare. Laboratory examinations showed obvious hypokalemic alkali poisoning, increased blood ACTH and cortisol, increased urinary 17-hydroxysteroid and 17-ketosteroid excretion, and high-dose dexamethasone tests could not inhibit the secretion of cortisol. The intrinsic prognosis was poor, and the main treatment was surgical removal of the primary tumor.

Ectopic hypoglycemia syndrome

Hypoglycemia syndrome is not caused by abnormal insulin secretion, but is also one of the common ectopic endocrine syndromes in clinical practice. Many tumors can cause hypoglycemia, especially giant thoracic and abdominal tumors originating from the mesoderm, such as mesothelioma, neurofibroma, and leiomyoma. There are also malignant tumors, such as fibrosarcoma, neurofibrosarcoma, leiomyosarcoma, as well as liver cancer, kidney cancer, adrenal cortical carcinoma and ovarian cancer. These tumor cells synthesize growth factors, which have a blood sugar-lowering effect similar to insulin. In addition, huge tumor tissues also consume a large amount of blood sugar, resulting in symptoms of hypoglycemia. Its clinical manifestations are similar to those of hypoglycemia caused by insulinoma, but the blood insulin and C-peptide levels of these patients are not high during fasting or hypoglycemia. The hypoglycemic episodes disappeared after tumor resection.

Ectopic antidiuretic hormone (ADH) syndrome

It is also called the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The most common tumor that can cause ectopic ADH secretion is lung cancer (accounting for about 40%), and others include malignant tumors of the thymus, pancreas, duodenum, esophagus and breast. Ectopic ADH has the same biological effect as arginine vasopressin, stimulating the renal tubules to reabsorb water. Therefore, patients mainly show symptoms of water intoxication, dilutional hyponatremia, and hypoosmotic pressure, including fatigue, headache, anorexia, nausea and vomiting. In severe cases, when the blood sodium level is lower than 120mmol/L (120mEq/L), mental symptoms may occur, such as drowsiness, mental confusion, and even convulsions and coma. Laboratory examinations showed low blood sodium level, low plasma osmotic pressure, increased urinary sodium excretion, high urine specific gravity, and elevated plasma ADH level. However, when diagnosing, it is important to differentiate SIADH syndrome from certain intracranial diseases such as brain tumors, brain trauma, cerebrovascular disease, and certain drugs such as morphine, pethidine (Demerol), and barbiturate sleeping pills that stimulate ADH secretion. In addition to treating the primary tumor, people with symptoms of water intoxication should strictly control their water intake, appropriately supplement with hypertonic saline and strengthen diuresis to quickly increase the osmotic pressure and prevent cerebral edema.

Ectopic parathyroid hormone (PTH) syndrome

The main manifestations are symptoms caused by hypercalcemia, such as loss of appetite, nausea, thirst, polydipsia, and polyuria. In severe cases, there may be persistent vomiting, dehydration, drowsiness, and mental disorders. It has been found that malignant tumors of the lung, kidney, bladder, liver, colon, testicle and ovary can cause hypercalcemia, which mainly secrete PTH-like polypeptide and cause ectopic hypercalcemia. The conditions for diagnosing hypercalcemia caused by ectopic PTH are: ① Patients with malignant tumors have high blood calcium and low blood phosphorus at the same time; ② Normal parathyroid function; ③ No bone metastases and other causes that can cause high blood calcium; ④ Blood calcium can decrease after tumor removal. Ectopic PTH syndrome is different from primary hyperparathyroidism in that it progresses rapidly and has a short course. Therefore, patients with ectopic PTH syndrome often do not have urinary stones and obvious bone changes. Therefore, patients with hyperparathyroidism who have any of the following manifestations are suspected of having ectopic PTH syndrome: increased blood alkaline phosphatase without X-ray changes in subperiosteal absorption of the cortex; low blood chloride levels and high blood bicarbonate; hypercalcemia with a positive response to adrenal cortex hormones; weight loss and anemia.

Others In addition, it has been reported that other ectopic hormones that can affect calcium and phosphorus metabolism include prostaglandin E2 (PGE2). PGE2 can be secreted in patients with fibrosarcoma, lung cancer, and medullary thyroid cancer, causing high blood calcium but normal blood phosphorus. In addition, patients with bronchial carcinoid, lung cancer and breast cancer may secrete abnormal calcitonin, and patients with benign bone tumors and hemangiomas have vitamin D resistance (tumoral rickets), all of which affect calcium and phosphorus metabolism.