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Preview: QJM - current issue

QJM: An International Journal of Medicine Current Issue

Published: Sat, 24 Jun 2017 00:00:00 GMT

Last Build Date: Tue, 27 Jun 2017 09:51:41 GMT


Janeway lesions


This 57-year-old gentleman, with history of diabetes mellitus, but no prior history of heart disease presented with 10 days of fever and generalized weakness. History of a localizing symptom was not forthcoming, but auscultation of the cardiovascular system revealed a systolic murmur of grade 2 intensity in the left parasternal area in the third space. Evaluation revealed leukocytosis (15 300 cell/µl) and raised inflammatory markers (ESR, CRP). Infective endocarditis was considered and multiple sets of blood cultures were sent, however no organism was isolated. An initial trans-thoracic echocardiography did not reveal findings in favor of the diagnosis. Patient was treated symptomatically and evaluation for an alternate etiology was continued. On day 3 of hospital stay, skin lesions were noted over both hands (Figure 1). They were non-tender, non-itchy, erythematous macules, at the base of both palms. Biopsy showed presence of neutrophilic microabscesses. Trans-esophageal echocardiography (TEE) confirmed the diagnosis of native valve, culture-negative endocarditits with a vegetation of 5 × 6 mm on the non-coronary cusp of the aortic valve. Intravenous vancomycin and gentamicin were given for duration of 6 weeks with close watch on renal parameters. Patient’s fever subsided in 10 days and skin lesions resolved completely in 2 weeks.

Acute mesenteric venous thrombosis


A 67-year-old man presented at our emergency department with lower abdominal pain for 1 day. His history revealed deep vein thrombosis of the lower legs without regular medication. His respiratory rate was 26 breaths/min, his heart rate was 112 beats/min, his blood pressure was 90/58 mmHg and his oxygen saturation was 94% when breathing room air.

Sister Mary Joseph node


A previously healthy 66-year-old man presented with a painless, exudative, partly ulcerated nodule on the umbilicus (Figure 1a), which he had noticed after a local trauma occurring 6 weeks before. The patient was otherwise asymptomatic. Systemic antibiotic therapy prescribed by the general practitioner had poor results. The main diagnostic hypotheses were omphalitis, pyogenic granuloma and skin metastasis of internal cancer. Skin biopsy of the nodule revealed dermal infiltration of tubuloglandular neoplastic cells (Figure 1b), which were positive for CK 7 and AE1/AE3, and negative for CK 20, thyroid transcription factor-1 and caudal type homeobox 2. Laboratory tests detected high levels of alkaline phosphatase (242 U/l), gamma glutamyl transferase (487 U/l), alanine aminotransferase (110 U/l), and aspartate aminotransferase (81 U/l), and a remarkable increase in the tumor marker Ca 19-9–75767 U/ml (normal reference: <39 U/ml) and Ca125 to 1549 U/ml (normal reference: <35 U/ml).

Knuckle pigmentation and vitamin B 12 deficiency


A 23-year-old lady presented with fatigue and dyspnea on exertion for 3 months duration. On examination she had severe pallor and pigmentation over the knuckles of both hands (Figure 1). Laboratory investigation showed hemoglobin of 66 g/l, mean corpuscular volume 109 fl, total leucocyte count 3.6 × 109/l and platelet count of 78 × 109/l. Peripheral blood film showed oval macrocytes, marked anisocytosis and poikilocytosis. The serum vitamin B12 level was 59 ng/l (normal > 200 ng/l).

Osteonecrosis, splenic calcification and sickle cell disease


Sickle cell disease (SCD) is a major public health problem. Approximately 300 000 children born annually with the disease. SCD is a chronic condition, and spleen and bone are two commonly affected organs. We recently had the opportunity of observing a girl with deformed femoral head and calcified lesions in spleen, who was initially diagnosed as disseminated tuberculosis, but later a diagnosis of SCD was made on detailed hematological investigations and advanced imaging techniques.

Air embolism and CT-guided lung biopsy


A 74-year-old man underwent computed tomography (CT)-guided percutaneous core needle biopsy of the lung for pulmonary histopathological diagnosis. Ten minutes after the procedure, he experienced chest pain accompanied by sweating. An initial electrocardiogram (ECG) revealed ST-segment elevation in leads II, III, aVF and V1-V3 (Figure 1A). Post-procedural CT images showed a considerable volume of air in the descending aorta, left ventricle and right coronary artery (Figure 1B and C). He was placed in the mild Trendelenburg position to prevent embolization of the air into cerebral circulation. Subsequently, he underwent a coronary angiography (CAG), and received oxygen therapy with FiO2 50% to promote the exchange of oxygen for nitrogen within the air bubbles and accelerate their resorption. CAG revealed no stenosis of the left or right coronary artery (Figure 1D). His chest pain was relieved during CAG. A post-procedural ECG revealed complete resolution of ST-segment elevation, and a subsequent complete blood examination, including blood chemistry and cardiac enzymes levels, was unremarkable. A transthoracic echocardiogram showed left ventricular ejection fraction of 55–60% without valvular disease. The patient was discharged 6 days after lung biopsy. Air embolism is rare but life threatening complication of CT-guided percutaneous lung biopsy. The incidence rate has been reported to be 0.02–0.6%1. The most important thing is that physicians pay attention to this complication in order to recognize it as soon as possible, and are familiar with the appropriate and adequate management for it.

Unilateral Pulmonary Edema, Westermark’s Sign and Palla’s Sign in Pulmonary Embolism


A 54-year-old African American man presented with shortness of breath of two days duration. Physical examination revealed tachycardia with a heart rate of 113 bpm, oxygen saturation at 63% on room air and left sided crackles. Chest radiograph (Figure 1A) showed increased lucency of the right upper and middle lobes (Westermark’s sign, blue arrow), enlarged right descending pulmonary artery (Palla’s sign, red arrow) and left lower zone pulmonary edema (black arrow). Computed tomography (CT) of chest (Figure 1B) with pulmonary angiogram confirmed extensive saddle pulmonary embolism (PE) at the right side with extension into left pulmonary artery branches. 2D echocardiogram revealed elevated right ventricular systolic pressure and a patent foramen ovale with right to left shunting. Hence, catheter directed thrombolysis with tissue-plasminogen activator (t-PA) was performed with significant improvement clinically and radiologically with reperfusion of the right lung lobes evident by restoration of vascular markings on the right and resolution of the left sided pulmonary edema. Here, we can see a perfect example of unilateral pulmonary edema after contralateral embolism and is likely secondary to increased hydrostatic pressure due to interruption of blood flow by PE.2

Lessons learned from a multidisciplinary renal genetics clinic


Background: Inherited renal disorders comprise a significant proportion of cases in both paediatric and adult nephrology services. Genetic advances have advanced rapidly while clinical models of care delivery have remained static.Aim: To describe a cohort of patients attending a multidisciplinary renal genetics clinic and the insights gained from this experience.Design and methods: A retrospective review of clinic cases and their molecular genetic diagnosis over a 5-year period.Results: We report details of 244 individuals including 80 probands who attended the clinic. The commonest reasons for referral was familial haematuria which accounted for 37.5% of cases and cystic kidney disease, accounting for 31% of cases. Eighteen probands had a known molecular genetic diagnosis and were referred for genetic counselling and screening of at risk relatives and management plans. About 62 probands and their families were referred for a precise molecular diagnosis and this was achieved in 26 cases (42%). The most frequent new genetic diagnoses were COL4A5 mutations underlying familial haematuria and familial end stage renal disease. The clinic also allowed for patients with rare renal syndromes to be reviewed, such as ciliopathy syndromes, allowing detailed phenotyping and often a precise molecular genetic diagnosis to be provided.Conclusions: The integration of modern day genetics and genomics into multidisciplinary clinics often allows a precise diagnosis which benefits patients, their relatives and the clinicians providing care and future management.

New-onset atrial fibrillation-related ischemic stroke occurring after hospital discharge in septicemia survivors


Background: Sepsis will induce stroke, new-onset atrial fibrillation (AF) increase ischemic stroke (IS) in in-hospitalization and long-term period after sepsis. Physicians must alert this condition and given suitable treatment.Aim: The associated of IS and new-onset AF in septicemia survivors after discharge have to be evaluated.Design: The inpatient data was used of the Taiwan National Health Insurance Database (NHIRD) in 2010. We identified patients suffered their first occurrence of septicemia (International Classification of Disease, Ninth Revision, Clinical Modification [ICD-9-CM] is 038, 003.1, 036.1) and excluded less than 18 years old. Patients had AF (ICD-9-CM to 427.3×) during the same admission or after septicemia hospitalization discharged were defined as new-onset AF. The outcome was IS happened after septicemia discharge (ICD-9-CM as 433–437).Methods: The factors related to IS after septicemia survival were established using multivariate logistic regression with forward stepwise selection.Results: There were 1286 new-onset AF and 1026 IS happened after septicemia discharge. The crude odds ratio (OR) were 3.88 (95% confidence interval [C.I.]: 1.69–8.89) and 1.62 (95% C.I.: 1.14–2.3) in middle-aged and elderly septicemia survivors with new-onset AF induced IS. The risk of IS after septicemia survivors was noticed adjusted OR 1.74 (95% C.I.: 1.26–2.41) for new-onset AF.Conclusion: The middle-aged and elderly septicemia survivors suffered from new-onset AF had increased incidence of IS within three months. New-onset AF was a mediator factor of IS in septicemia survivors of Asian population.

Asthma–COPD overlap syndrome showed more exacerbations however lower mortality than COPD


Background: Asthma–chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) is a new determinate syndrome whose exact characteristics remain unclear.Aim: The objective of this study is to find more difference between ACOS and COPD.Design: A retrospective study of ACOS and COPD in Chinese.Methods: Data from 65 patients with ACOS and 65 patients with COPD were retrospectively collected and analyzed. The basis of this study was to compare the two groups while ruling out differences in age, sex and smoking history.Results: Patients with ACOS tended to have earlier ages of onset, longer durations of symptoms, better nutritional status, higher single-breath diffusing capacity of carbon monoxide (DLCO) %predicted and airway resistance %predicted, more exacerbations in the preceding 12 months and shorter lengths of hospitalization. DLCO %predicted, airway resistance %predicted, and length of hospitalization were the variables most significantly associated with the presence of ACOS in patients with COPD. ROC correlating airway resistance %predicted value and current ACOS showed an optimal cutoff of airway resistance %predicted of over 296.6. During follow-up (median: 45 months; interquartile range: 6–82 months), 16 patient deaths were recorded (3 patients with ACOS). The risk remained significantly higher in patients with COPD alone than in patients with ACOS (HR 3.932; 95% CI 1.083–19.755; P = 0.046).Conclusion: Patients with ACOS were more likely to have better prognoses and lower mortality than those with COPD alone, though with greater exacerbation frequency.

Monocytes primed with GTS-21/α7 nAChR (nicotinic acetylcholine receptor) agonist develop anti-inflammatory memory


Background: The neural system can finely tune immune system, especially pro- or anti-inflammatory responses of monocytes/macrophages. To maintain immune homeostasis, monocytes/macrophages are supposed to be primed by α7 nAChR agonist to establish anti-inflammatory memory.Aim: To study whether activation of α7 nAChR would elicit anti-inflammatory memory in splenic monocytes in vivo and J774 monocytes in vitro.Design: Laboratory study.Methods: The wildtype mice were sacrificed 4 or 12 h after receiving intravenous injection of GTS-21. The splenocytes were isolated and stimulated with LPS for 4 h to detect Ly6Chi TNF-α+ monocytes by flow cytometry. In the in vitro study, J774 monocytes received priming with GTS-21, washing GTS-21 out and resting, and thereafter stimulating with TLR ligands. The TNF-α protein and Tnfα, Il1β and il6 mRNAs were measured to evaluate anti-inflammatory responses. The H3K9ac, H4K5ac, H4K8ac, Acetyl-CBP, CBP (CREB-binding protein), PCAF (P300/CBP-associated factor) and Acetyl-NF-kB levels were measured in GTS-21-primed monocytes.Results: Activation of α7 nAChR by GTS-21 suppressed TNF-α production in splenic Ly6Chi monocytes. In vivo-GTS-21-primed splenic Ly6Chi monocytes passed on anti-inflammatory feature if stimulated with LPS in vitro. J774 monocytes primed with GTS-21 developed anti-inflammatory trait in response to LPS (TLR4), Poly:IC (TLR3) and R848 (TLR7/8) ligands. In GTS-21-primed monocytes, H3K9ac, H4K5ac, H4K8ac, Acetyl-CBP, CBP, PCAF and Acetyl-NF-kB were reduced 4 h after washing and resting. In the nuclear extract, PCAF, Acetyl-NF-kB, p-NF-kB and p-STAT3 were decreased in LPS-stimulated GTS-21 primed J774 monocytes 4 h after washing and resting.Conclusions: Monocytes primed by α7 nAChR agonist developed anti-inflammatory memory.

Risk of empyema in patients with end-stage renal disease: a nationwide propensity-matched cohort study


Background: Empyema is a rare but important complication among patients with end-stage renal disease (ESRD). However, a nationwide, propensity-matched cohort study has never been performed.Methods: We conducted a retrospective cohort study using data from the National Health Insurance Research Database of Taiwan. The ESRD group consisted of 82 765 patients diagnosed between 2000 and 2008. The comparison group consisted of individuals without kidney disease selected at a 1:1 ratio matched by propensity score estimated with age, gender, year of diagnosis and comorbidities. The occurrence of empyema was monitored until the end of 2011. The hazard ratios (HRs) of empyema were estimated using the Cox proportional hazards model.Results: The incidence of empyema was 2.76-fold higher in the ESRD group than in the comparison group (23.7 vs. 8.19/10 000 person-years, P <0.001), with an adjusted HR of 3.01 [95% confidence interval (CI) = 2.67–3.39]. There was no difference of the incidence of empyema between hemodialysis (HD) and peritoneal dialysis (PD) (adjusted HR = 0.96, 95% CI = 0.75–1.23). In addition, 30-day mortality rate since empyema diagnosis was significantly higher in ESRD group than the comparison group (15.9% vs. 10.9%), with an adjusted OR of 1.69 (95% CI = 1.17–2.44).Conclusion: The risk of empyema was significantly higher in patients with ESRD than in those without kidney disease. The occurrence of empyema was without difference in patients undergoing HD compared to those undergoing PD. The 30-day mortality rate since empyema diagnosis was also significantly higher in patients with ESRD.

Glycaemic control and cardiovascular disease: is there a light at the end of the tunnel?


Patients with type 2 diabetes mellitus (T2DM) have been shown by numerous studies to have a substantially increased risk of cardiovascular disease (CVD), including coronary artery disease, ischemic stroke and heart failure, even after adjusting for other known risk factors.1,2 First reported in the Framingham studies and followed by additional data including a meta-analysis of 102 prospective studies, diabetes confers about a two-fold excess risk for coronary heart disease and ischemic stroke in both men and women, and about a 2-fold and 5-fold excess risk of heart failure in diabetic men and women.1–3 However, there is still a debate as to whether improved glycaemic control reduces the excessive CVD risk of T2DM patients. Large randomised controlled trials (RCTs), aimed at determining the effect of anti-hyperglycaemic agents on CVD, provide a handful of important data, albeit not consistent answers. Nevertheless, looking further into these RCTs provides new perspective on the complex interplay between diabetes treatment and CVD.

RETRACTED: Adjusting for illness severity shows there is no difference in patient mortality at weekends or weekdays for emergency medical admissions


Background: Patients admitted to hospitals over the weekend appear to have a higher risk of death compared to weekday admissions, but the reasons remain unclear. Unlike previous studies, we use a standardised mandated vital signs physiologically based measure of sickness known as the National Early Warning Score (NEWS) to investigate this ‘weekend effect’ for emergency admissions.Aim: To determine if weekend admissions are (i) sicker as measured by their index NEWS, (ii) have an increased risk of death and (iii) have less favourable monitoring of their vital signs compared with weekday admissions.Methods: Analysis of 58 481 emergency adult medical admissions in three acute hospitals with electronic (index) NEWS recorded within 24 h of admission.Results: Admissions over the weekend had higher index NEWS (weekend: 2.24 vs. weekday: 2.05, P < 0.001) with a higher risk of death (weekend: 771/14198 5.43% vs. weekday: 2197//44283 4.96%, Risk Ratio = 1.10, 95% CI: 1.01 to 1.19, P = 0.023) which was no longer seen after adjusting for the index NEWS (Risk Ratio = 1.00, 95% CI 0.92 to 1.08, P = 0.94).The time to index NEWS was earlier (-0.41 h 95% CI -0.47 to -0.35, P < 0.001) for weekend admissions whilst the number of NEWS recorded over their hospital stay was not dissimilar (−0.03 95% CI − 0.39 to 0.34, P = 0.892).Conclusions: Patients who have an acute admission over the weekend with an electronic NEWS recorded within 24 h are sicker, have earlier clinical assessments and after adjusting for their illness severity do not appear to have a higher risk of death compared to weekday admissions.



Acromegaly is a rare, chronic, progressive disease characterized by an excess secretion of growth hormone (GH) and increased circulating insulin-like growth factor 1 (IGF-1) concentrations. It is caused by a pituitary adenoma in the vast majority of cases. The clinical diagnosis, based on symptoms related to GH excess, is often delayed due to the insidious nature of the disease. Consequently, patients often have established systemic complications at diagnosis with increased morbidity and premature mortality. Serum IGF-1 measurement is recommended as the initial screen for patients with suspected acromegaly. The gold standard diagnostic test remains the oral glucose tolerance test with concomitant GH measurement. Therapy for acromegaly is targeted at decreasing GH and IGF-1 levels, ameliorating patients’ symptoms and decreasing any local compressive effects of the pituitary adenoma. The therapeutic options for acromegaly include surgery, medical therapies (such as dopamine agonists, somatostatin receptor agonists and the GH receptor antagonist pegvisomant) and radiotherapy. A multidisciplinary approach is recommended with often a requirement for combined treatment modalities. With disease control, associated morbidity and mortality can be reduced. The recently published evidence-based guidelines by the Endocrine society addressed important clinical issues regarding the evaluation and management of acromegaly. This review discusses advances in our understanding of the pathophysiology of acromegaly, diagnosis of various forms of the disease and focuses on current treatment modalities, and on future pharmacological therapies for patients with acromegaly.