Diagnosis and Treatment > Medication
Search for other papers by Tomomi Nakao in
Google Scholar
PubMed
Search for other papers by Ken Takeshima in
Google Scholar
PubMed
Search for other papers by Hiroyuki Ariyasu in
Google Scholar
PubMed
Search for other papers by Chiaki Kurimoto in
Google Scholar
PubMed
Search for other papers by Shinsuke Uraki in
Google Scholar
PubMed
Search for other papers by Shuhei Morita in
Google Scholar
PubMed
Search for other papers by Yasushi Furukawa in
Google Scholar
PubMed
Search for other papers by Hiroshi Iwakura in
Google Scholar
PubMed
Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Summary
Thyroid storm (TS) is a life-threatening condition that may suffer thyrotoxic patients. Therapeutic plasma exchange (TPE) is a rescue approach for TS with acute hepatic failure, but it should be initiated with careful considerations. We present a 55-year-old male patient with untreated Graves’ disease who developed TS. Severe hyperthyroidism and refractory atrial fibrillation with congestive heart failure aggregated to multiple organ failure. The patient was recovered by intensive multimodal therapy, but we had difficulty in introducing TPE treatment considering the risk of exacerbation of congestive heart failure due to plasma volume overload. In addition, serum total bilirubin level was not elevated in the early phase to the level of indication for TPE. The clinical course of this patient instructed delayed elevation of bilirubin until the level of indication for TPE in some patients and also demonstrated the risk of exacerbation of congestive heart failure by TPE.
Learning points:
-
Our patient with thyroid storm could be diagnosed and treated promptly using Japan Thyroid Association guidelines for thyroid storm.
-
Delayed elevation of serum bilirubin levels could make the decision of introducing therapeutic plasma exchange difficult in cases of thyroid storm with acute hepatic failure.
-
The risk of worsening congestive heart failure should be considered carefully when performing therapeutic plasma exchange.
Search for other papers by Yuri Tanaka in
Google Scholar
PubMed
Search for other papers by Taisuke Uchida in
Google Scholar
PubMed
Search for other papers by Hideki Yamaguchi in
Google Scholar
PubMed
Search for other papers by Yohei Kudo in
Google Scholar
PubMed
Search for other papers by Tadato Yonekawa in
Google Scholar
PubMed
Search for other papers by Masamitsu Nakazato in
Google Scholar
PubMed
Summary
We report the case of a 48-year-old man with thyroid storm associated with fulminant hepatitis and elevated levels of soluble interleukin-2 receptor (sIL-2R). Fatigue, low-grade fever, shortness of breath, and weight loss developed over several months. The patient was admitted to the hospital because of tachycardia-induced heart failure and liver dysfunction. Graves’ disease with heart failure was diagnosed. He was treated with methimazole, inorganic iodide, and a β-blocker. On the day after admission, he became unconscious with a high fever and was transferred to the intensive care unit. Cardiogenic shock with atrial flutter was treated with intra-aortic balloon pumping and cardioversion. Hyperthyroidism decreased over 10 days, but hepatic failure developed. He was diagnosed with thyroid storm accompanied by fulminant hepatitis. Laboratory investigations revealed elevated levels of sIL-2R (9770 U/mL). The fulminant hepatitis was refractory to plasma exchange and plasma filtration with dialysis, and no donors for liver transplantation were available. He died of hemoperitoneum and gastrointestinal hemorrhage due to fulminant hepatitis 62 days after admission. Elevated circulating levels of sIL-2R might be a marker of poor prognosis in thyroid storm with fulminant hepatitis.
Learning points:
-
The prognosis of thyroid storm when fulminant hepatitis occurs is poor.
-
Liver transplantation is the preferred treatment for fulminant hepatitis induced by thyroid storm refractory to plasma exchange.
-
Elevated levels of soluble interleukin-2 receptor might be a marker of poor prognosis in patients with thyroid storm.
Search for other papers by Catarina Roque in
Google Scholar
PubMed
Search for other papers by Ricardo Fonseca in
Google Scholar
PubMed
Search for other papers by Carlos Tavares Bello in
Google Scholar
PubMed
Search for other papers by Carlos Vasconcelos in
Google Scholar
PubMed
Search for other papers by António Galzerano in
Google Scholar
PubMed
Search for other papers by Sância Ramos in
Google Scholar
PubMed
Summary
Primary adrenal lymphoma is a rare malignancy. It frequently presents bilaterally and with symptoms of adrenal insufficiency. Amiodarone may induce secondary organ dysfunction, and thyrotoxicosis develops in 15% of cases. The symptomatology of both conditions is nonspecific, especially in the elderly, and a high suspicion index is necessary for appropriate diagnosis. A 78-year-old female presented to the emergency department with confusion, nausea and vomiting. She had recently been to the emergency department with urinary tract infection, vomiting and acute hypochloremic hyponatremia. Upon re-evaluation, the leukocyturia persisted and because of TSH 0.01 µU/mL and free-T4 68 (10–18) pmol/L, she was admitted to the Endocrinology ward. Further evaluation supported amiodarone-induced thyroiditis type 2. Sepsis ensued, in the setting of nosocomial pneumonia. Hemodynamic instability, hyponatremia, hypoglycemia and vomiting raised the suspicion of adrenocortical insufficiency. Fluid resuscitation and hydrocortisone led to clinical improvement, and adrenal insufficiency was admitted. The thoracoabdominal tomography suggested an endobronchic primary lesion with hepatic and adrenal secondary deposits (6.6 and 7 cm), but this was confirmed neither on pleural effusion nor on bronchofibroscopic fluid analyses. The adrenals were not accessible for biopsy. Despite high-dose hydrocortisone maintenance, the patient died before definite diagnosis. The autopsy confirmed primary non-Hodgkin lymphoma.
Learning points:
-
Primary adrenal lymphoma is a rare cause of adrenal insufficiency, but progression can be fast and fatal.
-
Hyperpigmentation is frequently absent.
-
The presenting symptoms are nonspecific and might mimic infection. Disproportion of the general state with signs of specific organ symptomatology is a diagnostic clue.
-
Infection may precipitate adrenal crisis and worsen thyroid function with further adrenal insufficiency exacerbation.
-
In the context of thyrotoxicosis, there may be little clinical response to a therapeutic trial with standard dose glucocorticoids.
-
High-dose glucocorticoid substitution may be required to achieve clinical stability in thyrotoxic patients.
