[Panic disorder].

HISTORY AND ADMISSION FINDINGS: After an unremarkable course of her pregnancy a 26-year-old woman was admitted in the 32nd week because of her poor general condition with nausea, vomiting and headache. Her blood pressure was 220/140 mmHg and the pulse irregular with a rate of about 90/min. INVESTIGATIONS: The urine was markedly positive for glucose and protein, the cardiotachogram was unremarkable. DIAGNOSIS, TREATMENT AND COURSE: Antihypertensive treatment was started because pre-eclampsia was suspected. At first the patient's condition improved, but a few hours after admission an emergency section had to be performed for maternal and fetal indications, but the eutrophic male child was dead. Postoperatively the electrocardiogram and increased creatine kinase activity were suspicious of an acute myocardial infarction. Chest radiogram and echocardiography showed signs of marked ventricular dysfunction. Coronary angiography excluded coronary artery disease. The concentrations of catecholamine and its metabolites in 24-hour urine were greatly elevated above normal. Ultrasound and computed tomography demonstrated a tumour in the region of the left adrenal suggesting phaeochromocytoma, a diagnosis that was confirmed when the tumour was resected. CONCLUSIONS: Phaeochromocytoma is a rare cause of toxaemia of pregnancy and presents a high maternal and fetal risk. Its prognosis for both mother and child can be improved only if it is diagnosed and treated prenatally.

Adrenal Gland Neoplasms↗

PubMed1999

Activation of ERK1 and ERK2 is required for manganese-induced neurite outgrowth in rat pheochromocytoma (PC12) cells.

Mn(2+) treatment has been shown to promote neurite outgrowth in rat pheochromocytoma (PC12) cells in a time- and dose-dependent manner. This process is mediated through the interactions of extracellular matrix (ECM) proteins and integrin receptors. Studies were performed to determine whether the phosphorylation of the MAP kinases, ERK1 and 2, is required for Mn(2+)-induced neurite outgrowth. A time- and dose-dependent increase in phosphorylation of both ERK1 and 2 was observed upon treatment of PC12 cells with Mn(2+). Phosphorylation of the ERKs occurred as early as 2 hr after initiating treatment, with a maximum increase occurring at approximately 24 hr. Inhibition of MEK with the specific inhibitor, PD98059, blocked the phosphorylation of ERK1 and 2 and increased Mn(2+) toxicity. When cells were grown in serum-free defined medium, Mn(2+)-induced phosphorylation of ERK1 and ERK2 occurred in cells grown on surfaces treated with growth serum or fibronectin but not on surfaces treated with poly-L-lysine. In addition, the pentapeptide GRGDS, which blocks RGD-mediated interactions, inhibited Mn(2+)-induced phosphorylation of ERK1 and 2. The Mn(2+)-induced increase in phosphorylated ERK1 and 2 was not seen in a PC12 cell line that does not respond to Mn(2+). These data support the hypothesis that integrin-mediated activation of the MAPK signal transduction pathway leading to the activation of ERK1 and 2 is required for Mn(2+)-induced PC12 differentiation and neurite outgrowth.

Adrenal Gland Neoplasms↗