Modification of the course of disease progression in idiopathic pulmonary fibrosis by pirfenidone: evidence of the potential for disease reversal.

Idiopathic pulmonary fibrosis (IPF) is a fibrosing pneumonia of unknown causation with a chronic, progressive course that may be modified by treatment with the antifibrotic agents, pirfenidone and nintedanib. Both drugs have been shown to slow disease progression, but, in rare cases, pirfenidone has been shown to stabilise and even improve lung function. We present a case of a patient whose lung function and pathognomonic features on CT imaging improved significantly on commencement of treatment with pirfenidone.

Hypervitaminosis B12: an indicator of potential significant morbidity.

A woman in her 60s with a history of vitamin B12 deficiency treated with intramuscular hydroxocobalamin was attending a specialist clinic for the management of persisting breathlessness following a previous pulmonary embolism. She reported that a persistently elevated vitamin B12 had been identified several months previously, despite the withdrawal of replacement therapy, and that the cause could not be explained to her by her general practitioner. Recognition of the potentially serious implications of this finding led to the identification of a pancreatic tumour which, by the time of diagnosis, had become too advanced for active management.

Impulsive adolescents exhibit inefficient processing and a low decision threshold when decoding facial expressions of emotions.

Background: Borderline personality disorder (BPD) is a debilitating psychiatric illness whose symptoms frequently emerge during adolescence. Initial studies in adults suggest that the interpersonal difficulties common in BPD may emerge from disrupted processing of social and emotional stimuli. Less is known about these processes in adolescents with BPD symptoms, despite substantial changes in socioemotional processing during this developmental period.

Antitrypsin deficiency: still more to learn about the lung after 60 years.

The past 60 years have seen multiple publications related to lung disease in α-antitrypsin deficiency largely reflecting the pathophysiology, biochemical effect and outcomes of augmentation therapy. However, the complexity of disease phenotype and the impact of the natural history presents problems of patient management, study design and hence interpretation of outcome. Although many national and some international registries exist, the lack of consistent in-depth assessment and importantly, the impact of augmentation therapy likely influences our perception of the true natural history.