Pulmonary Mucormycosis (Zygomycosis) Presenting as an Infective Exacerbation of Chronic Obstructive Pulmonary Disease.

Mucormycosis is a life-threatening fungal infection whose incidence has been rising recently, mainly due to the increasing use of immunosuppressive and corticosteroid treatment. In previous decades, mucormycosis was associated with a very poor prognosis as mortality was approximately 100%. Mortality rates reported in recent literature have only slightly improved despite the availability of targeted therapy with amphotericin B. Pulmonary mucormycosis is characteristically encountered in severely immunocompromised hosts, while rhino-orbital disease is often seen in individuals with diabetes mellitus. We report a rare case of fulminant pulmonary mucormycosis as an exceptionally rare complication of corticosteroid treatment in a 76-year-old patient with chronic obstructive pulmonary disease (COPD) and diabetes. The patient had presented with typical symptoms of an infective COPD exacerbation. The interesting aspects of our case were the absence of malignancy or immunosuppression, the isolation of Rhizomucor species, and the fungal invasion of the pleura and pericardium. Unfortunately, our patient died on the 49th day of hospitalisation, despite appropriate treatment. LEARNING POINTS: Pulmonary mucormycosis in patients with known respiratory disease may mimic an exacerbation of their lung disease, thus delaying diagnosis.Pulmonary mucormycosis can complicate corticosteroid treatment in elderly individuals with other predisposing factors, which is an emerging clinical concern.Pulmonary mucormycosis remains a potentially fatal disease, although early diagnosis and appropriate medical and surgical management can improve outcomes.

Severe asymptomatic non-alcoholic fatty liver disease in routine diabetes care; a multi-disciplinary team approach to diagnosis and management.

OBJECTIVES: To prospectively use a non-invasive algorithm to identify asymptomatic, advanced non-alcoholic fatty liver disease (NAFLD) in a secondary care diabetes clinic and to determine the short-term effect of a multi-disciplinary team (MDT) approach in a liver clinic. RESEARCH DESIGN AND METHODS: NAFLD Fibrosis Score (NFS) was calculated in 64 asymptomatic patients with type 2 diabetes. Advanced fibrosis was identified using transient elastography and confirmed with liver biopsy. In a subsequent retrospective study, 95 patients newly referred to the NAFLD MDT clinic were investigated and the impact of the MDT approach assessed. RESULTS: 25/64 (39.0%) of patients with diabetes had a low NFS (<-1.455). 39/64 (61.0%) patients had a high or indeterminate NFS and were referred for review in the NAFLD MDT clinic, of which 23/39 attended for assessment. 19/23 (82.6%) were diagnosed with NAFLD, of which 6/19 (31.6%) patients had a positive transient elastography (≥8 kPa). Liver biopsy confirmed advanced fibrosis in 5/6 cases, with moderate fibrosis in 1 case. In the retrospective study, 65/95 (68.4%) new referrals to the NAFLD MDT clinic had a diagnosis of NAFLD. Over a median 98 days (IQR 70-182) follow-up, there was a significant improvement in weight (-0.8 kg; P = 0.024), total cholesterol (-0.2 mmol/L; P = 0.044), ALT (alanine transmaminase, -12.5 IU/L; P < 0.001) and GGT (gammu-glutamyl transferase, -13.0 IU/L; P < 0.0001). 7/28 (25%) of patients with diabetes achieved >5% weight loss. CONCLUSIONS: A significant proportion of asymptomatic patients attending type 2 diabetes clinics have undiagnosed advanced NAFLD fibrosis. An MDT approach to NAFLD results in short-term improvements in metabolic and liver parameters.

Acute adrenal insufficiency as a first presentation of myelodysplastic syndrome and sigmoid colon adenocarcinoma: a case report.

Acute adrenal failure due to bilateral adrenal haemorrhage is rare and may initially present with non-specific symptoms. It can rapidly progress into a life-threatening condition if not diagnosed promptly. Both traumatic and non-traumatic conditions have been implicated in the aetiology, with the latter been even rarer. We describe the case of a 57-year-old woman presenting with vomiting and epigastric pain and later developing fever and diarrhoea. The patient then deteriorated into shock and primary adrenal insufficiency was identified. A computed tomography scan noted bilateral adrenal haemorrhage. Further investigations showed a sigmoid colon adenocarcinoma and a myelodysplastic syndrome, with monosomy seven. Bilateral non-traumatic adrenal haemorrhage is an infrequent finding and investigating its aetiology can be challenging. In our patient, two simultaneous underlying diseases were identified. To the best of our knowledge, the combination of these two non-traumatic conditions as a cause of acute bilateral adrenal haemorrhage has not been previously reported.

Cardiovascular effects of tumour necrosis factor α antagonism in patients with acute myocardial infarction: a first in human study.

OBJECTIVE: The inflammatory cytokine, tumour necrosis factor α (TNF-α), exerts deleterious cardiovascular effects. We wished to determine the effects of TNF-α antagonism on endothelial function and platelet activation in patients with acute myocardial infarction. DESIGN AND SETTING AND PATIENTS: A double-blind, parallel group, randomised controlled trial performed in a tertiary referral cardiac centre. 26 patients presenting with acute myocardial infarction randomised to receive an intravenous infusion of etanercept (10 mg) or saline placebo. MAIN OUTCOME MEASURES: Leucocyte count, plasma cytokine concentrations, flow cytometric measures of platelet activation and peripheral vasomotor and fibrinolytic function were determined before and 24 h after study intervention. RESULTS: Consistent with effective conjugation of circulating TNF-α, plasma TNF-α concentrations increased in all patients following etanercept (254 ± 15 vs 0.12 ± 0.02 pg/ml; p < 0.0001), but not saline infusion. Etanercept treatment reduced neutrophil (7.4 ± 0.6 vs 8.8 ± 0.6 × 10(9) cells/l; p = 0.03) and plasma interleukin-6 concentrations (5.8 ± 2.0 vs 10.6 ± 4.0 pg/ml; p = 0.012) at 24 h but increased platelet-monocyte aggregation (30 ± 5 vs 20 ± 3%; p = 0.02). Vasodilatation in response to substance P, acetylcholine and sodium nitroprusside, and acute tissue plasminogen activator release were unaffected by either treatment (p > 0.1 for all). CONCLUSIONS: Following acute myocardial infarction, etanercept reduces systemic inflammation but increases platelet activation without affecting peripheral vasomotor or fibrinolytic function. We conclude that TNF-α antagonism is unlikely to be a beneficial therapeutic strategy in patients with acute myocardial infarction.