ABSTRACT
A previously well 59-year-old man presented with paracoccidioidomycosis, more than 15 years after leaving South America. He failed to respond to conventional therapies, first with oral itraconazole and then with amphotericin B plus sulfadiazine, and eventually died of recurrent arterial emboli possibly due to paracoccidioidomycotic aortitis. This patient's presentation demonstrates the difficulties that may be encountered in diagnosing and managing this disease. Paracoccidioidomycosis should be suspected in patients with an appropriate travel history who experience weight loss and have pulmonary, mucosal, and cutaneous lesions. This article comprehensively reviews the literature, with emphasis on epidemiology, clinical presentation, diagnosis, and therapy with imidazole antifungal medications.
Subject(s)
Paracoccidioides/isolation & purification , Paracoccidioidomycosis , Amphotericin B/therapeutic use , Fatal Outcome , Humans , Itraconazole/therapeutic use , Male , Middle Aged , Paracoccidioidomycosis/drug therapy , Paracoccidioidomycosis/pathology , Paracoccidioidomycosis/physiopathology , Sulfadiazine/therapeutic use , Treatment FailureABSTRACT
The concept of the APUD system and the APUDomas associated with it has evolved significantly since Pearse's description in the 1960s. Part of this evolution has been an understanding of the relationships between the APUD system and the central and autonomic nervous systems. The APUD system now referred to as the diffuse neuroendocrine system, can be linked to the central nervous system and autonomic nervous system by genetics, embryology, cellular characteristics, anatomy, interaction of the systems, and the immune system. Awareness of these relationships may enable clinicians to better understand APUDomas and lead to better methods of detection of these tumours and their treatment.
Subject(s)
APUD Cells , Apudoma , Autonomic Nervous System , Central Nervous System , Neuroendocrine Tumors , Neurosecretory Systems , HumansABSTRACT
UNLABELLED: In the syndrome of familial virilization, insulin resistance, and acanthosis nigricans, the interrelationships are not understood. Twin sisters were studied, along with a lesser affected sister and mother. They manifested amenorrhea, hirsutism, masculinization, hypertension, hyperinsulinemia, hypertriglyceridemia, and hyperprolactinemia. Medical therapy with a gonadotropin-releasing hormone agonist plus an antiandrogen resulted in reversal of the hirsutism, yet with preservation of potential fertility. In response to luteinizing hormone (LH) and follicle-stimulating hormone suppression, there was normalization of the serum androgens, but not of the hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, hypertension, or acanthosis nigricans. CONCLUSIONS: (1) This syndrome may be familial. (2) Medical therapy for the virilization is successful. (3) The hyperandrogenemia is primarily LH dependent and not primarily insulin dependent, although insulin may have an amplification effect. (4) Hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, and the hypertension are not androgen dependent.
