Painless thyroiditis combined with cystic adenoma of the thyroid

  The patient, female, 46 years old, was admitted to the hospital with the main cause of dizziness, nausea and vomiting for 6 days. The patient presented with dizziness, nausea and vomiting when eating and drinking with no obvious cause 6 days ago, vomit was stomach contents, no obvious symptoms of hypermetabolism such as panic, hand trembling, fear of heat and excessive sweating, etc. She was seen at a local hospital, where thyroid function FT3 and FT4 were higher than normal and TSH was reduced (specific value not known). adenoma? A hypoechoic nodule in the right lobe of the thyroid gland. On the day of admission, thyroid function was checked, showing FT3 16.28 pmol/l, FT4 39.41 pmol/l, TT3 4.41 nmol/l, TT4 346.63 nmol/l, TSH 0.04 mIU/l.
  On the same day, thyroid ECT was performed at the Heping Hospital of Chang Medical University, which showed a “cold” nodule in the left lobe of the thyroid gland and hypo-uptake in the right lobe. The patient denied any history of “cold” before the onset of the disease, no history of fever or sore throat, no neck pain or pressure, no hypermetabolic symptoms such as panic, hand trembling, fear of heat and excessive sweating, etc. The patient was admitted to our department for systematic diagnosis and treatment. Physical examination: body temperature 36.5℃, pulse rate 100 times/min, respiration 20 times/min, blood pressure 118/72mmHg.
  The thyroid gland was large and medium in quality. A nodule of about 2cm*1cm in size was palpable in the left lobe, with positive pressure pain. There were no obvious positive signs in the abdomen, negative tremor sign in both hands, and no edema in both lower limbs.
  Laboratory tests: thyroid function: FT3 16.28 pmol/l, FT4 39.41 pmol/l, TT3 4.41 nmol/l, TT4 346.63 nmol/l, TSH 0.04 mIU/l, erythrocyte sedimentation rate (sedimentation) 5.0 mm/h, thyroid peroxidase antibody (TpoAb) 39.22 IU/l Blood electrolytes: potassium 2.9 mmol/l, sodium 135.4 mmol/l, chloride 102.4 mmol/l, calcium 2.40 mmol/l, lipids: total cholesterol (TC) 2.70 mmol/l, triglyceride (TG) 0.47 mmol/l, thyroid ECT: left lobe of thyroid “cold ECT of the thyroid gland showed that the left lobe of the thyroid gland was “cold” nodule and the right lobe had low uptake function. Ultrasound of thyroid gland showed: multiple mixed masses in bilateral thyroid lobes and bilateral enlarged lymph nodes in the neck. Pathological diagnosis by fine needle aspiration of the thyroid gland: possible lymphocytic thyroiditis combined with hyperthyroidism in the right lobe of the thyroid gland and goiter in the left lobe.
  The patient was admitted to the hospital mainly because of dizziness, nausea and vomiting, without typical hypermetabolic symptoms and signs such as panic, hand tremors, fear of heat and excessive sweating. “Combining with the above case characteristics, the diagnosis of subacute thyroiditis is unlikely, and combined with the results of thyroid needle aspiration, the diagnosis of painless thyroiditis is likely; for the “cold” nodule in the left lobe of the thyroid, ultrasound shows mixed echogenicity, and combined with the results of thyroid needle aspiration, the diagnosis of painless thyroiditis is likely. The ultrasound showed mixed echogenicity, combined with the results of fine needle aspiration of the thyroid gland.
  A cystic thyroid adenoma with intracapsular hemorrhage was considered. The patient was admitted with dizziness, nausea, vomiting, fast heart rate and poor sleep, so she was given symptomatic treatment to slow down heart rate, reduce myocardial oxygen consumption, regulate nerves, improve sleep, correct water-electrolyte disorders and supplement energy support. After the above symptomatic treatment, the patient’s symptoms were relieved, but the thyroid function still showed hyperthyroidism at the time of discharge. Therefore, the patient was advised to pay attention to the review, and surgical treatment of the thyroid cystic adenoma could be performed after the thyroid function returned to normal.
  Discussion: Silent thyroiditis, also known as subacute lymphoblastic thyroiditis and silent thyroiditis, occurs in 10% of cases in the postpartum period. Some scholars include postpartum thyroiditis (PPT), amiodarone (canadalone) thyroiditis, and alpha-interferon-induced thyroiditis in this category. The disease presents with transient, reversible destruction of thyroid follicular cells, focal lymphocytic infiltration, and elevated thyroid peroxidase (TpoAb).
  It is considered a type of autoimmune thyroiditis, with a prevalence of 5%-15% in hyperthyroidism, associated with HLA-DR3, HLA-DR4, and HLA-DR5, and autoimmune disorders in first-degree relatives of 20%-25% of patients. The concept of PPT was first introduced by Amino in 1977. In recent years, there have been many reports of sporadic and painless thyroiditis unrelated to recent pregnancy. Its etiology is currently thought to be related to autoimmune and viral infections. The pathogenesis is now thought to be related to the following factors.
  (1) maternal cellular and humoral immunity is suppressed during pregnancy in order to allow the survival of a fetus with antigens different from those of the mother. Patients with autoimmune thyroid disease may experience a temporary immune rebound after a full-term pregnancy or abortion, with increased antibody titers, destruction of thyroid follicular cells, and a one-time increase in blood thyroid hormone levels leading to hyperthyroidism, followed by hypothyroidism.
  ②Viral infection: causes normal follicular cells to be damaged by a large number of lymphocytes infiltration, thyroid antibody titers are not high, and the tissue is completely repaired after healing.
  ③High iodine load: recent animal experiments have confirmed that iodine has a direct cytotoxic effect on the thyroid gland and can indirectly lead to lymphocyte infiltration, especially in individuals with excessive iodine salt supplementation and TpoAb positivity in iodine-deficient areas.
  The clinical features of the disease are as follows.
  ①Short duration of disease.
  (ii) Transient thyrotoxicosis, which may manifest as mild, moderate or severe hypermetabolic symptoms.
  ③No enlargement or mild enlargement of the thyroid gland and no pain in the thyroid gland.
  ④Decreased radioactive iodine uptake rate.
  (⑤Thyroid ultrasound is not rich in blood flow.
  (6) Lymphocytic infiltration of the thyroid gland.
  Very few patients develop chronic lymphocytic thyroiditis and permanent hypothyroidism. In this case, the clinical manifestations and the results of the relevant ancillary tests were consistent with the above characteristics, so the diagnosis of painless thyroiditis was established.
  The clinical manifestations of painless thyroiditis are complex and varied, and often overlap with other thyroid disorders, leading to a high number of clinical misdiagnoses and missed diagnoses. The disease is easily confused with diffuse toxic goiter (Graves’ disease), subacute thyroiditis, and chronic lymphocytic thyroiditis, and should be distinguished from.
  (1) Elevated serum levels of thyroid hormones and reduced iodine uptake by the thyroid gland, which is a “separation phenomenon”, can be distinguished from Graves’ disease.
  (2) Chronic lymphocytic thyroiditis has a significantly elevated TpoAb, an enlarged and tough thyroid gland, and a clinical history that is inconsistent with this disease.
  There are many similarities between this disease and subacute thyroiditis, but the main difference is the absence of thyroid pain or tenderness and increased blood sedimentation. The histological signs are also different.
  The treatment of painless thyroiditis is divided into two main phases: firstly, the thyrotoxic phase, during which antithyroid drugs and radioiodine therapy should be avoided. β-adrenergic receptor blockers or sedatives can relieve the clinical symptoms in most patients, but in patients with PPT, the above drugs can be secreted through breast milk, so lactating women need to be warned. Glucocorticoids can shorten the course of thyrotoxicosis, but they do not prevent the occurrence of hypothyroidism, so their use is not advocated.
  Secondly, during the hypothyroidism period, treatment is generally not required. If the symptoms are obvious and the goods last for a long time, thyroid hormone can be applied in small doses and discontinued after several months. Permanent hypothyroidism requires lifelong replacement therapy. This patient was in the thyrotoxic stage at the time of admission, but her symptoms were mild, so she was given β-blockers to slow her heart rate, reduce myocardial oxygen consumption, regulate nerves, improve sleep, correct water-electrolyte disorders and supplement energy to support symptomatic treatment, and her symptoms were relieved after the above treatment.
  Painless thyroiditis is a self-limiting disease that usually resolves within 2-6 months and rarely lasts more than a year. About 50% of patients develop hypothyroidism, but most patients return to normal after 2-9 months of hypothyroidism, and only 10%-29% develop permanent hypothyroidism. The high rate of clinical misdiagnosis and mistreatment of this disease often leads to unnecessary antithyroid medication and irreversible surgery and isotope therapy. Therefore, patients with clinically painless mild to moderate thyrotoxicosis need to be alerted to the possibility of this disease.
  Cystic thyroid adenoma is a thyroid disease with a high incidence in China, mostly benign, and its diagnosis is mostly dependent on imaging and pathological examination. In order to prevent or exclude its malignant factors, most of them adopt surgical treatment. In recent years, there are also studies reporting the use of minimally invasive treatment methods such as 32P colloid intervention or ultrasound-guided sclerotherapy of thyroid cystadenoma. This patient has a combination of both of these diseases, and few such cases have been reported.
  The purpose of this paper is to deepen the understanding of the treatment process and clinical thinking of two thyroid diseases, namely painless thyroiditis and cystic thyroid adenoma, through this clinical case, to reduce the rate of clinical underdiagnosis and misdiagnosis of these diseases, and to avoid unnecessary treatment, especially surgery and irreversible treatment such as isotope.