4). Due to its rarity, nonspecific Obeticholic Acid molecular weight symptoms and radiological findings, intracranial tuberculomas remain a clinical challenge. Misdiagnosis of tuberculomas as malignant diseases have been described in literature.4, 5, 7 and 8 Our patient was HIV negative, had a medical history

of malignancy and presented with multiple brain lesions so the first suspicion was also metastatic disease. Tuberculomas must however be always included in differential diagnosis of cerebral space occupying lesions. As the patient missed follow-up after his first TB infection this may be the case of a reactivation but reinfection is also a possibility and genotype was not performed. Regarding treatment, the Center for Disease Control and Prevention recommends 12 months of treatment for CNS TB when the MT strain is sensitive to all drugs.9 However numerous variables can affect the response of the disease Entinostat mw to therapy and it has been suggested that treatment duration

should be tailored to the radiological response.6 After 12 months of treatment more than two-thirds of the patients still have contrast enhancing lesions. Although it is not clear if this represents an active lesion or just inflammation, continuing treatment is probably prudent. Total resolution of the tuberculoma is observed when scans demonstrate no enhancing lesions or only an area of calcification.6 Systemic corticosteroids as adjuvant therapy are indicated when there is peri-lesional oedema or paradoxical progression during treatment. Surgical intervention may Sirolimus be necessary in situations with acute complications or when the diagnosis is not ensured.2, 3, 6 and 10 We would like to thank the careful editing of Flávio Monteiro, Papworth Hospital (Cambridge, England). “
“Hermansky–Pudlak syndrome (HPS) is a genetic multisystem disorder characterized by oculocutaneous

albinism, a bleeding tendency secondary to platelet dysfunction, and lysosomal ceroid accumulation.1 Ceroid, which accumulates sporadically and slowly in the lungs, is not crucial for a diagnosis of HPS, but primarily accounts for the significant associated morbidity. Pulmonary fibrosis, usually manifesting in the third and fourth decades of life, accounts for premature death in 50% of HPS patients, which generally occurs by the fifth decade.2 and 3 Nine different genes cause HPS in humans.4 and 5 Among them, the HPS-1 gene shows the highest frequency of mutation. HPS-1 mutation represents the classical disease, which manifests with all the typical complications of HPS. HPS-4 disease is considered to resemble HPS-1, but only a few case of HPS-4 have been reported.6, 7, 8 and 9 HPS-1 and HPS-4 individuals show the greatest degree of pulmonary involvement, with an estimated 80% of HPS-1 subtypes afflicted.6 and 10 Here, we report a case of HPS presenting with interstitial pneumonia and exhibiting a novel HPS-4 gene mutation.