Chest Infections |

Shortness of Breath in Association With Pituitary-Dependent Cushing Syndrome FREE TO VIEW

Wilmary Rodriguez-Collado*, MD; Whitney Prince, MD; Shirley Jones, MD
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Scott and White Memorial Hospital, Temple, TX

Chest. 2012;142(4_MeetingAbstracts):166A. doi:10.1378/chest.1388827
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SESSION TYPE: Infectious Disease Case Report Posters II

PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION: Cushing's syndrome is an uncommon disorder of glucocorticoid excess with an estimated annual incidence of 2.3 per million/year. Most cases are adrenocorticotropin hormone (ACTH) dependent; originating either from a pituitary tumor or less frequently, from non-pituitary tumors secreting ectopic ACTH. The clinical manifestations of Cushing’s syndrome are variable and differ in severity depending on the degree and duration of hypercortisolism. The classical presentation including cardiovascular, metabolic, dermatological, musculoskeletal and psychiatric manifestations is generally recognized by clinicians, but in many cases the picture is less clear and diagnostically challenging.

CASE PRESENTATION: A 37 year old male was admitted with complaints of progressive dyspnea, facial swelling and uncontrolled hyperglycemia. Past medical history included hypertension and depression. Physical examination was significant for obesity, moon face, abdominal purple striae and lower extremities bruises. Initial laboratories revealed high cortisol levels and confirmation by inferior petrosal sinus sampling was consistent with pituitary-dependent Cushing's syndrome. Treatment was started with ketoconazole; however he continued to have shortness of breath and hypoxemia. A CT chest showed a cavitary lesion with associated pleural effusion. Pleural fluid cultures grew methicillin sensitive staphylococcus aureus that was felt to be related to bacteremic seeding from septic thrombophlebitis of the right upper extremity. Despite appropriate antibiotics, the patient’s overall condition did not improve with continued hypoxia and dyspnea, necessitating bronchoscopy with bronchoalveolar lavage and transbronchial biopsy. The biopsy was positive for Pneumocystis jiroveci. He was started on trimethoprim-sulfamethoxazole and experienced significant clinical improvement. Repeat cortisol levels were also improved.

DISCUSSION: Patients with endogenous Cushing’s syndrome have impaired immunity and predisposition to infections; hence the recognition that hypercortisolism can attenuate the clinical signs and symptoms of infections is of utmost importance. However, opportunistic infections in these patients are rare. Graham reviewed a total of 23 cases of opportunistic infections in endogenous Cushing's, 14 of whom died of infection (1). Previous studies indicate that opportunistic infections occur less frequently in patients with pituitary forms of Cushing’s syndrome. Our case is unusual given the opportunistic infection in the setting of pituitary-dependent Cushing's syndrome.

CONCLUSIONS: In conclusion, clinical suspicion for opportunistic infection should be maintained along with early control of cortisol levels in Cushing’s patients, otherwise there is significant mortality.

1) Graham BS, et al. Opportunistic Infections in Endogenous Cushing's Syndrome. Annals of Internal Medicine 1984;101:334-338.

DISCLOSURE: The following authors have nothing to disclose: Wilmary Rodriguez-Collado, Whitney Prince, Shirley Jones

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Scott and White Memorial Hospital, Temple, TX




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