Recurrent attacks of vomiting, hypertension and psychotic depression: a syndrome of periodic catecholamine and prostaglandin discharge

Abstract

Abstract. A syndrome of periodic catecholamine and prostaglandin E2 discharge is described in 2 patients aged 17 and 3 years. They had recurrent attacks of vomiting, hypertension and psychotic depression for several years with a fixed periodicity. At initiation of the attack, plasma ACTH, AVP, norepinephrine and prostaglandin E2 were markedly elevated, whereas dopamine was undetectable. This resulted in hypercortisolemia, hyponatremia and oliguria, which were completely normalized when the attack subsided. Dopaminergic inhibition by metoclopramide injection induced a sustained rise in plasma bicyclo-prostaglandin E2 in the patients, a transient rise in 4 controls, and no response in 8 control children. The 4 control responders had significantly higher plasma norepinephrine levels and aldosterone responses than the non-responders (P < 0.001). There was a linear correlation between peak values of bicyclo-prostaglandin E2 and basal norepinephrine levels (r = 0.990, P < 0.001). The patients released bicyclo-prostaglandin E2 and aldosterone more easily than the control responders in terms of plasma norepinephrine and dopamine levels. Treatment of the patient with clonidine was partially effective, whereas administration of indomethacin completely suppressed recurrence of the attacks for 1 year. These results suggest the etiologic possibility that the patients have a decreased dopaminergic inhibition of prostaglandin E2-mediated norepinephrine secretion, which causes periodic discharge of norepinephrine and concomitant release of ACTH and AVP.

Prevalence of Syndrome of ACTH-ADH Discharge in Japan

“…Classified as epilepsy, it may be considered as a periodic partial seizure with autonomic and psychotic symptoms. Although the exact cause of the syndrome is unknown, our previous data indicate that the patients have a decreased dopaminergic inhibition of PGE2-mediated norepinephrine secretion, which may evoke periodic discharge of norepinephrine and concomitant release of ACTH and ADH [3]. This hypothesis remains to be proven.…”

“…These changes in plasma and urinary catecholamines were associated with a parallel change of plasma prostaglandin E2 (PGE2) [3]. By 1984, I had observed another 5 cases of similar periodic attacks.…”

Diabetic Gastroparesis Presenting with a Cyclic Vomiting Pattern

“…Cyclic vomiting, although classically associated with migraine, has also been linked to food allergy and mitochondrial, metabolic, and endocrine disorders, such as overreaction of the hypothalamic pituitary-adrenal (HPA) axis. [18][19][20][21] In terms of the HPA axis, corticotropin releasing factor (CRF) is considered as an importance trigger for the vomiting phase starts, and it stimulates of the hypersecretion of ACTH and cortisol. [21][22][23] The current patient did not show features of migraine and abnormal ACTH and cortisol level.…”

Treatment options for cyclic vomiting syndrome

“…Although the etiopathogenesis of CVS remains unclear, several tenable theories postulated in the last decade help reveal potential pathways involved in this brain-gut disorder: 1) consideration of CVS as a migraine equivalent is based on the homology in patterns and symptoms, positive family histories, and responses to the antimigraine medications [11,12]; 2) involvement of hypothalamic-pituitary-adrenal axis activation as part of the stress response is based on the common stressor trigger, the established role of cortic o t r o p h i n -r e l e a s i n g f a c t o r i n d e l ay i n g u p p e r gastrointestinal (GI) tract motility, and the elevated levels of adrenocorticotrophic hormone and cortisol found in Sato's variant of CVS [13,14]; 3) the role of cellular energy deficits due to mitochondrial DNA mutations is supported by the common response to dextrose, frequent finding of lactic acidosis, and discovery of mitochondrial DNA mutations in the control region [15•]; 4) involvement of autonomic nervous system dysfunction that mediates common symptoms during the episode (pallor, lethargy, hypersalivation, vomiting and diarrhea) is supported by the predominance of sympathetic to parasympathetic tone found in patients with CVS [16,17]. Whether these mechanisms are distinct or overlap, as we suspect, remains unproven.…”