respiratory distress syndrome [3]. Most patients have Predisposing factors such as hematological and solid organ malignancies and chronic renal failure. Pulmonary edema, induced by moderate hypercalcemia, which is associated with primary hyperparathyroidism, has not been reported previously.

In the light of literature, we have discussed a 72-year-old female patient admitted with acute pulmonary edema who had primary hyperparathyroidism.

The 72-year-old female patient was admitted to the emergency service with increasing complaints of shortness of breath, nonproductive cough, difficulty in lying in supine position, and feel of faint for a week. The patient was dyspneic, orthopneic, and sweaty, and the physical exami- nation revealed cyanosis, bilateral rales, and decreased breath sounds in the lung bases. Blood pressure was 140/ 90 mm Hg; heart rate was 112 beats/minute; and arrhythmic

Fig. 1 The posteroanterior lung radiography revealed pulmo- nary edema.

0735-6757/$ - see front matter (C) 2012

512.e2 Case Report

body temperature, 37.2?C. The patient was monitored after starting diuretic infusion, oxygen therapy, and Low Molecular Weight Heparin. History of the patient included type 2 diabetes mellitus for 6 years, hypertension, and warfarin prophylaxis for 3 years because of atrial fibrillation; she was a nonsmoker and had underwent a platinum implant in the left knee 1 month ago. It was learned that the patient had been monitored in intensive care after surgery when she had developed chest pain; afterward, she had been investigated for pulmonary embolism and acute myocardial infarction, but none of them had been detected, and she had been

recommended a Prophylactic treatment. It was learned that the patient received gliclazide, ramipril-hydrochlorothiazide, ASA 300 mg, 5 mg of warfarin, without a history of renal stones, and Ca-D replacement. The pathologic laboratory results of the patient were as follows: serum total Ca: 15.4 mg/dL; corrected Ca level: 15.9 mg/dL; P: 2.8 mg/dL; PTH:

178.8 pg/mL; 25OHvitD3: 8 ug/L; FBG:146 mg/dL; 24- hour urinary Ca: 310 mg/dL; sedimentation: 30 mm/h; and HbA1c: 7.4%.

The posteroanterior lung radiography of the patient was consistent with pulmonary edema (Fig. 1). Electrocardiogram

Fig. 2 Dual phase-setamib parathyroid scintigraphy showed the right inferior adenoma.

Case Report 512.e3

demonstrated AF with slow ventricular response. Dual phase-setamib parathyroid scintigraphy (Fig. 2) was consistent with the right inferior adenoma. The patient’s bone mineral densitometry was consistent with osteoporo- sis. echocardiographic evaluation revealed 55% of EF, hypokinesia, and grade 2 diastolic dysfunction, but akinesia was not detected. Regarding malignancy, abdom- inal ultrasound and lung computed tomography were performed in addition to gynecologic examination and breast ultrasonography. No sign of malignancy was present in the patient. Surgery was recommended because of primary hyperparathyroidism, but the patient refused the intervention. Limited amounts of isotonic saline and furosemide infusions were performed by avoiding fluid overload. Hydrochlorothiazide treatment was discontinued. Parenteral pamidronate 90 mg was slowly infused to the patient with high Ca values. When the Ca value decreased to10.5 mg/dL, dyspnea and orthopnea symptoms signifi- cantly improved (NYHA grade decreased from 4 to 2).

pulmonary infections may lead to cardiogenic and Noncardiogenic pulmonary edema in a patient with endocrine diseases such as hypothyroidism, hyperthyroid- ism, and acute hypocalcemia [4]. Reported cases of acute respiratory distress syndrome in hyperparathyroidism generally occurred during parathyroid crisis at much higher Ca levels coexisting with pancreatitis [3]. The reported cases were pulmonary failures, seen in serious hypercal- cemia, associated with hematologic or solid organ malignancies, accompanied by tertiary hyperparathyroid- ism, which occurred secondary to renal failure. The mechanism of pulmonary edema associated with hypercal- cemia has not been fully understood, and INOS, the increased levels of free radicals and Proinflammatory cytokines, has been thought to induce a clinical presenta- tion pathophysiologically similar to sepsis [5]. Moreover, it is reported that metastatic calcification in lungs, kidneys, and stomach may likely occur in case of long-term hypercalcemia [6]. It is speculated that high Ca-phosphorus formation may cause pulmonary damage by increasing the metastatic calcification [2]. In our case, the matter was the primary hyperparathyroidism with moderate hypercalce- mia. Neither concomitant hypertensive attack nor pancre- atitis was detected. In addition, when the Ca value decreased to10.5 mg/dL, dyspnea and orthopnea symptoms significantly improved.

As a conclusion, moderate hypercalcemia due to hyperparathyroidism may trigger pulmonary edema without parathyroid crisis.

Meral Mert MD Kayseri Training and Research Hospital Endocrinology and Metabolism

Kayseri, Turkey E-mail address: [email protected]

Fatma Betul Uzuncan MD Kayseri Training and Research Hospital Internal Medicine, Kayseri, Turkey

E-mail address: [email protected]

Munevver Mertsoylu Aydin MD Kayseri Training and Research Hospital Pulmonary and Chest Medicine

Kayseri, Turkey E-mail address: [email protected]

Gonenc Kocabay MD

Kartal Kosuyolu Yuksek Ihtisas Heart Education and Research Hospital

Department of Cardiology

Istanbul, Turkey E-mail address: [email protected]

Adile Ortakoylu MD

Kayseri Training and Research Hospital

Internal Medicine Kayseri, Turkey

E-mail address: [email protected] doi:10.1016/j.ajem.2010.12.033

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