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To the Editor: Hypophosphatemia is not listed as a symptom of clinical panic disorder in the literature. In experimentally induced panic attacks, low serum phosphate levels have been described (1). In patients with unipolar depression, serum phosphate correlates inversely with measures of anxiety and somatic symptoms (2).
Mr. A, a 31-year-old man with a positive family history of panic disorder and recurrent panic attacks, experienced a recurrence of panic symptoms. His symptom profile was marked by situation-independent panic attacks with concomitant somatic symptoms (continuous hiccups and paresthesia). Under a combined pharmacological treatment plan (mirtazapine and citalopram) in addition to cognitive behavior therapy, remission developed, but he experienced short relapses. A short while later, he was free of panic attacks. His clinical course was mirrored by normalization of his originally high scores on the Body Sensations Questionnaire (3) and the Agoraphobic Cognitions Questionnaire (3) as well as on the somatization, anxiety, and phobic fear dimensions of the SCL-90-R.
Upon routine laboratory testing, marked hypophosphatemia (normal range=2.5–4.5 mg/dl) was observed (1.7 mg/dl, then 1.3 mg/dl), then 1 month later, it was 1.9 mg/dl. His parathormone level was measured as normal: 31.6 pg/dl (normal range: 12–72 pg/dl). The serum phosphate level returned to normal early the next month (2.8 mg/dl), only to fall below the lower limit of normal soon thereafter (2.3 mg/dl). At the next two measurements (2.8 mg/dl) and (3.0 mg/dl), his serum phosphate level again returned to normal.
Our observation of serum phosphate levels correlating inversely with the severity of panic symptoms is not commonly described in the clinical situation. A possible explanation of the occurrence in our patient is the intensity of the panic attacks with a panic state over hours per day. This state was characterized by continuous hiccups and long-lasting paresthesia indicative of hyperventilation. The latter may cause a decrease in serum phosphate as a secondary metabolic acidosis to compensate a primary respiratory alkalosis. An alternative or additive mechanism may be a β-adrenoreceptor-mediated stimulation of muscle glycogenolysis, which depletes intracellular phosphate, causing a transcellular shift of phosphate from plasma into muscle cells. A similar case of hypophosphatemia that was not present past remission of anxiety symptoms was reported by Kligler (4).
Our case thus supports the notion that hypophosphatemia can be observed as a symptom not only directly after experimental panic attacks but also in the clinical course of severe panic disorder. Serum phosphate levels appear to mirror the clinical course of the disorder.
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