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Background— Prolactin is increasingly recognized to play a stimulatory role in the inflammatory response. Because inflammation is considered of crucial importance in the development of atherosclerosis, we aimed to evaluate whether prolactin levels are associated with the occurrence of coronary artery disease (CAD). Methods and Results— We performed a nested case-control study in the prospective EPIC-Norfolk cohort. Cases were apparently healthy men and women, aged 45 to 79 years, who developed fatal or nonfatal CAD (n=882). Controls remained free of CAD (n=1490). Overall, systemic prolactin levels did not differ between cases and controls, and people in the highest prolactin tertile did not have a significantly increased risk of developing future CAD (in men, odds ratio, 1.21; 95% CI, 0.92 to 1.61; in women, odds ratio, 1.12; 95% CI, 0.76 to 1.64). However, in a separate immunohistochemical study, the presence of prolactin receptors could be demonstrated in postmortem human coronary artery plaques (preliminary data). Conclusions— Elevated systemic prolactin levels do not predict CAD in the general population. However, prolactin receptors were found in human coronary artery plaques. This observation may indicate a role of prolactin within atherosclerotic plaques. More studies are needed to define the possible role of prolactin in atherosclerotic plaque development.

In August, 2006, a 75-year-old non-diabetic, non-alcoholic man with hypertension and atrial fi brillation was ad mitted to the Internal Medicine department with low grade fever, increasing otalgia, otorrhoea, dysphagia, and hoarseness. He had suff ered from bilateral tympanic membrane perforation, intermittent otalgia, and otor rhoea for 12 years. In May, 2006, his otolaryngologist had prescribed ofl oxacin ear drops and oral ciprofl oxacin for otalgia and otorrhoea. In June, 2006, he was admitted to the Ear, Nose and Throat department with a 3-week history of left peripheral facial nerve palsy, left trigeminal sensory loss, and general discomfort. He was afebrile, with a serum C-reactive protein concentration of 72 mg/L; other laboratory tests were normal. CT and MRI of the head showed clouding of the left mastoid without intra cranial pathology or menin geal enhancement (fi gure A); chest radiography was normal. A diagnosis of mastoiditis was made, and ceftazidime and fl ucloxacillin were started. Surgical exploration of the left mastoid showed granulation tissue in the external auditory canal and around the ossicles. Microscopically this tissue showed chronic-active necrotising infl ammation; cultures (in cluding those for fungi) were negative. After 2 weeks, the patient was discharged in fair condition. In the current admission, besides earlier described cranial nerve dysfunction, a partial left glossopharyngeal and vagal nerve palsy were diagnosed by the consulting oto laryngologist. C-reactive protein was 57 mg/L with normal white cells. Culture of discharge from the ear grew Pseudomonas aeruginosa, and amoxicillin (empirically started on admission) was replaced by meropenem. 2 weeks later, still in hospital and being treated with meropenem, he developed headache, neck pain, and a left abducens nerve palsy. Repeated chest radiography and MRI of the brain were normal. Cerebrospinal fl uid (CSF) analysis showed only a mild pleocytosis (leucocytes 17×106 per L). The clinical picture suggested a chronic (basal) meningitis, but blood and CSF cultures remained negative. The patient refused meningeal biopsy and further treatment, had progressive diffi culty in swallowing, and died 3 weeks later in hospital from pneumonia. Autopsy showed a focal purulent pre pontine lepto meningeal exudate (fi gure B). Micro scopically, multiple septated and branched hyphae were detected in this exudate and in the left middle and internal ear (fi gure C), combined with chronic-active necrotising infl am mation. The infl ammation extended into the skull base and cranial nerves. A mould cultured from the exudate was characterised as Pseudallescheria boydii by sequence-analysis of parts of the β-tubulin gene. P boydii can cause a wide variety of clinical diseases and is commonly found in soil, polluted water, and manure. P boydii infections of the central nervous system (CNS), meninges, and mastoid are very rare and generally occur in immunocompromised, near drowning, and trauma patients, but have also been reported in patients without one of these risk factors. There was no suspicion of immunocompromise in our patient, and post mortem HIV PCR analysis from lymph node and heart tissues were negative. Diagnosis of CNS involvement by P boydii is often delayed because of non-specifi c clinical presentation, diffi culty in obtaining and culturing appro priate specimens, and because of histological similarity of P boydii to other fungi, such as aspergillus. In our patient the fungus most likely gained access to the ear and CNS through tympanic membrane perforation. In patients with P boydii mastoiditis, surgical intervention, adequate anti-fungal therapy, and identi fi cation and control of underlying immunological conditions are essential. Voriconazole is suggested as the treatment of choice. Awareness of P boydii as a cause of chronic mastoiditis and meningitis may allow early diagnosis and treatment, thereby increasing the chance of resolution.