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Parathyroid Adenoma Presenting as Bipolar Affective Disorder

Received August 20, 2006; revised November 14, 2006; accepted November 28, 2006. From the Dept. of Psychiatry; Dept. of General Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Send correspondence and reprint requests to Dr. Pratap Sharan, Dept. of Psychiatry, India Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India. e-mail: drsandeepg2006{at}yahoo.com
© 2007 The Academy of Psychosomatic Medicine

Psychiatric symptoms reported in hyperparathyroidism include depression, anxiety, psychosis, lethargy, apathy, delirium, and dementia.¹ Manic symptoms have been rarely reported.² We report a case of treatment-resistant depression and parathyroid crisis-induced mania with delirium, whose psychiatric symptoms resolved after parathyroid adenomectomy.

A 49-year-old man presented to us in an agitated and confused state. Two weeks before presentation at our center, the patient had developed sudden-onset epigastric and left-subcostal pain that radiated to the back; the pain was aggravated by eating and lying supine and was associated with 2 or 3 episodes of nonbilious, nonprojectile vomiting. Medical records from another center showed that the patient had jaundice, abdominal distention, rigidity in the left hypochondrium, reduced bowel sounds, raised serum bilirubin, leucocytosis, elevated ESR, hypercalcemia (12.7 mg %), abnormalities on urine examination (calcium oxalate crystals, 3–4 RBC, and 4–5 white cells/HPF), mild hepatomegaly with increased echo texture on abdominal ultrasound, and Grade C pancreatitis, along with bilateral basal consolidation on CT abdominal scan. Tests for serum amylase and lipase, hepatitis B and C, and HIV did not reveal any abnormality. His physical condition improved with conservative management over the next 5 days, but his restlessness, disorientation to time and place, forgetfulness, grandiose delusions, irritability, over-talkativeness, pressured speech, overplanning, socially disinhibited behavior, and disturbed sleep persisted. Repeat investigations (renal function test, liver function test, serum amylase, lipase, and magnesium) were essentially normal, except for a raised serum calcium level (13.2 mg %). An ultrasound of the neck suggested a parathyroid adenoma. He was treated with lithium 1,200 mg/day, risperidone 4 mg/day, clonazepam 2 mg/day, amlodipine 5 mg/day, and rabeprazole 40 mg/day for 4 days, after which he was referred to our hospital. At presentation, his score on the Delirium Rating Scale (DRS–R-98) was 16, and his score on the Young Mania Rating Scale was 25.

Evaluation of earlier history revealed that he had had major depression, with significant social and interpersonal dysfunction, for 15 years. The depression had not responded to adequate doses of fluoxetine, sertraline, and citalopram given for an adequate duration of time by previous psychiatrists. He had also had hypertension for 4 years. Family history and premorbid personality were non-contributory.

Physical examination showed a 2- x 2-cm palpable nodule in his neck. Investigations showed hypercalcemia (12.1 mg %), raised serum parathyroid level (1,052 pg/ml [normal levels: 10pg/ml–30pg/ml]), fluctuating blood glucose levels (between 80 and 220 mg %), abnormalities in 24-hour urine analysis (calcium: 260 mg, phosphorus: 605 mg, and creatinine: 594 mg in 2,750 ml of urine), osteopenia on bone-mineral densitometry (0.836; Z score: 1.2), increased tracer concentration in the region of the right thyroid lobe on Technetium scan (which persisted for 2 hours), and a 3x2x2-cm homogenously enhancing nodular, soft-tissue mass posterior to the right thyroid lobe (without calcification or necrosis) on contrast-enhanced CT scan of the neck. Urinary VMA and thyroid-function tests were normal. Lithium and rabeprazole were stopped, and insulin (16 units/day) was started. Psychiatric symptoms and hypercalcemia persisted during the preoperative period (7 days), but resolved completely within 3 days of parathyroid adenectomy. The improvement was maintained over the next 6 months, despite the reduction and discontinuation of his psychotropic medication.

The patient was believed to have hyperparathyroidism-induced depression, despite the onset of depression 15 years before the diagnosis of hyperparathyroidism, because of the absence of personal and family history of affective disorder, non-response to the adequate trials of selective serotonin reuptake inhibitors (SSRIs), amelioration of affective symptoms after parathyroidectomy, and presence of some literature support.^3,4 Authors have suggested that parathyroid-induced depression may be caused by the ability of calcium to enhance release and depletion of norepinephrine and its biosynthetic enzyme, dopamine β-hydroxylase, from neuronal granules,⁵ in which the damage to the blood–brain barrier, as evidenced by the increased cerebrospinal-fluid (CSF) calcium level that occurs in primary hyperparathyroidism, may play a part.⁶ Studies have also shown that improvement in depressive symptoms after parathyroid surgery is accompanied by an increase in CSF concentration of 5-HIAA and HVA.⁷ The onset of mania with delirium during a parathyroid crisis (as evidenced by acute pancreatitis and hypercalcemia) and its rapid resolution postoperatively (along with the correction of hypercalcemia), suggests that the symptom complex was linked to hypercalcemia. The onset of depressive and manic symptoms unresponsive to the short-term use of lithium (<7 days), and a lack of effect on psychiatric symptoms and thyroid functioning suggest that it did not play a role in the development or the resolution of psychiatric symptoms.

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