Pheochromocytoma Diagnosed During First Trimester of Pregnancy.

Pheochromocytomas are rare catecholamine-secreting tumors that occur in 0.002% of pregnancies. These tumors result in high maternal and fetal morbidity and mortality unless diagnosed in early stages of development, because excess levels of catecholamines cause vasoconstriction of both maternal and uteroplacental vasculature. Paroxysmal hypertension is the most common manifestation, but its variability in presentation and similarity to other pregnancy-related conditions often make diagnosis of pheochromocytoma difficult. Thus, it is essential to consider underlying pathological causes of hypertension during gestation. Diagnosis and treatment of pheochromocytoma must be approached uniquely given the physiologic changes during pregnancy. The standard of care for diagnostic imaging during pregnancy is with magnetic resonance imaging. For these reasons, knowledge of therapy for pheochromocytomas in the pregnant patient is essential for clinical endocrinology practice.

Lithium-associated primary hyperparathyroidism:: An evaluation of screening and referral patterns in a southeastern veteran population.

BACKGROUND: Long-term lithium therapy has a well-established but under-recognized association with primary hyperparathyroidism. Rates of hypercalcemia, screening for primary hyperparathyroidism, and referral for parathyroidectomy were evaluated among United States veterans on long-term lithium therapy. METHODS: Patients undergoing chronic long-term lithium therapy (>12 months) were identified from 1999 to 2022. Demographics, long-term lithium therapy duration, post-treatment calcium, parathyroid hormone, creatinine, and vitamin D levels were abstracted. Rates of screening for hypercalcemia (calcium ≥10.2 mg/dL), primary hyperparathyroidism (parathyroid hormone ≥30 pg/mL in the setting of hypercalcemia), referral for parathyroidectomy, and outcomes were evaluated. RESULTS: A total of 1,356 patients underwent long-term lithium therapy, 514 of whom received chronic long-term lithium therapy. Baseline characteristics of patients with and without post-treatment hypercalcemia were compared. Of 148 patients with post-treatment hypercalcemia, 112 (74.7%) underwent no further evaluation for primary hyperparathyroidism, while 36 (25.3%) patients had a parathyroid hormone level recorded. Although 33 (91.7%) hypercalcemic patients screened positive for primary hyperparathyroidism, only 5 (13%) were referred for parathyroidectomy. Of the 4 patients who underwent parathyroidectomy, mean calcium was 11.2 mg/dL (range 11.1-11.4), and mean parathyroid hormone was 272 pg/mL (range 108-622). Three patients were localized on preoperative imaging, 2 of whom underwent unilateral exploration with cure, with 1 experiencing recurrence at 31 months. The remaining patient who localized preoperatively underwent bilateral exploration and had 2 ipsilateral glands resected and persistence. The patient who did not localize preoperatively underwent bilateral exploration with 3 gland resection and cure. CONCLUSIONS: Screening for primary hyperparathyroidism and referral for parathyroidectomy are underutilized in United States veterans undergoing chronic long-term lithium therapy. Institutional protocols to standardize screening, surveillance, and referrals to endocrinology/endocrine surgery could benefit this population at increased risk for primary hyperparathyroidism.

Recurrent Graves' hyperthyroidism after prolonged radioiodine-induced hypothyroidism.

BACKGROUND: Radioactive iodine (RAI) is the most cost effective therapy for Graves' disease (GD). Patients with GD who have become hypothyroid after therapeutic RAI, rarely develop recurrence of disease. Herein we describe a case of recurrence of thyrotoxicosis after 2 years of hypothyroidism. METHODS: We present the clinical features, laboratory findings, imaging and management of an unusual case of recurrent hyperthyroidism. RESULTS: A 48-year-old male presented to the emergency room with a 2-day history of palpitation, chest discomfort and 30 pounds of weight loss. Examination was remarkable for rapid and irregular pulse, diffuse thyromegaly and brisk deep tendon reflexes but no eye changes or tremors. Laboratory tests showed thyroid-stimulating hormone (TSH) of <0.004 (0.3-5.6 mIU/ml), free thyroxine (FT4) 4.96 (0.9-1.8 ng/dl), free triiodothyronine (FT3) >20 (1.8-4.7 pg/ml), total thyroxine >800 (80-200 ng/dl). Electrocardiogram showed atrial fibrillation with rapid ventricular response. RAI uptake and scan showed a homogenous gland with 54% uptake in 6 h and 45% in 24 h. He was treated with propranolol and propylthiouracil with some clinical improvement. He subsequently underwent RAI therapy and developed hypothyroidism after 8 weeks. Hypothyroidism was treated with levothyroxine. At 2 years after RAI ablation, he again developed symptoms of hyperthyroidism and had suppressed TSH. The levothyroxine dose was stopped, 3 weeks after discontinuing levothyroxine, he remained hyperthyroid with TSH of 0.008 and FT4 of 1.62 and FT3 of 4.8. RAI uptake demonstrated 17% uptake at 24 h. CONCLUSION: Recurrent hyperthyroidism in GD is uncommon after development of post-ablative hypothyroidism. Our case illustrates the need for continued surveillance.

Thyrotoxicosis presenting as hypogonadism: a case of central hyperthyroidism.

Herein, we present a case of central thyrotoxicosis with well-documented serial therapeutic interventions. Thyroid-stimulating hormone (TSH)-secreting pituitary tumors represent a rare cause of hyperthyroidism. It is being diagnosed more frequently with the third-generation TSH assay. Many conditions can produce normal or elevated TSH levels in combination with elevated thyroid hormone levels. The differential diagnosis includes resistance to thyroid hormone (RTH, Refetoff's syndrome), assay interference from anti-T4/T3 and heterophile antibodies, elevated or altered binding proteins, drugs affecting peripheral metabolism, and noncompliance with thyroid replacement therapy. In contrast to RTH, our patient presented had high alpha-subunit-to-TSH molar ratio, failed TSH response to thyrotropin-releasing hormone stimulation, and a large pituitary mass. Normal or high TSH in the presence of elevated T4 or T3 is a fairly common clinical scenario with many etiologic possibilities. This TSH-producing adenoma represents an unusual initial clinical presentation, as hypogonadism appeared before features of thyrotoxicosis were appreciated. This case represents the most modern therapeutic approach to the management of this rare disease. Our patient has done well on octreotide with control of thyrotoxicosis and an additional 30% shrinkage of his tumor mass.