Glucagon role in DM 2 and the actions of drugs that modulate glucagon

Free full text review here.

Tamsulosin and passage of renal stones

No significant benefit in a randomized trial.

Experimental weight gain associated with BP increase

It correlated with visceral fat accumulation.

Drug induced lupus

It used to be procainamide, hydralazine and INH but things have since shifted.

Outcomes after decompression cranieotomy

From a review:

Abstract:

Purpose of review

There is little doubt that decompressive craniectomy can reduce mortality following malignant middle cerebral infarction or severe traumatic brain injury. However, the concern has always been that the reduction in mortality comes at the cost of an increase in the number of survivors with severe neurological disability.

Recent findings

There has been a number of large multicentre randomized trials investigating surgical efficacy of the procedure. These trials have clearly demonstrated a survival benefit in those patients randomized to surgical decompression. However, it is only possible to demonstrate an improvement in outcome if the definition of favourable is changed such that it includes patients with either a modified Rankin score of 4 or upper severe disability. Without this recategorization, the results of these trials have confirmed the ‘Inconvenient truth’ that surgery reduces mortality at the expense of survival with severe disability.

Summary

Given these results, the time may have come for a nuanced examination of the value society places on an individual life, and the acceptability or otherwise of performing a procedure that converts death into survival with severe disability.

Myocardial dysfunction in sepsis

Both systolic and diastolic dysfunction occur. Diastolic dysfunction seems to be more associated with mortality. Ionotropic agents have been disappointing.

Another review on acute pancreatitis

Form the paper:

Purpose of review

Acute pancreatitis is a common condition that affects patients with varying degrees of severity and may lead to significant morbidity and mortality. The present article will review the current paradigm in acute pancreatitis management within the first 72 h of diagnosis.

Recent findings

Patients presenting with acute pancreatitis should be evaluated clinically for signs and symptoms of organ failure in order to appropriately triage. Initial management should focus on fluid resuscitation, with some data to support Ringer's lactate over physiological saline. Routine use of prophylactic antibiotics in acute pancreatitis is not recommended, nor is urgent endoscopic retrograde cholangiopancreatography in the absence of concomitant acute cholangitis. Early oral feeding should be encouraged, not avoided, and use of parenteral nutrition is discouraged. Cholecystectomy during the same admission of biliary pancreatitis should be performed in order to prevent future acute pancreatitis episodes. Patients with acute pancreatitis secondary to alcohol should receive alcohol counseling. Finally, there is ongoing interest in the development of prognostic laboratory tests in acute pancreatitis and pharmacological therapies to reduce the inflammation that occurs in acute pancreatitis.

Summary

Acute pancreatitis is a common and heterogeneous condition with the potential for significant morbidity. Best practices in acute pancreatitis management focus on triage, hydration and enteral feeding.

Concerns about adverse effects of PPIs: current status

From a recent free full text review in Mayo Clinic Proceedings:

First introduced in 1989, proton pump inhibitors (PPIs) are among the most widely utilized medications worldwide, both in the ambulatory and inpatient clinical settings. The PPIs are currently approved by the US Food and Drug Administration for the management of a variety of gastrointestinal disorders including symptomatic peptic ulcer disease, gastroesophageal reflux disease, and nonulcer dyspepsia as well as for prevention of gastrointestinal bleeding in patients receiving antiplatelet therapy. PPIs inhibit gastric acid secretion, and the most commonly associated adverse effects include abdominal pain, diarrhea, and headache. Although PPIs have had an encouraging safety profile, recent studies regarding the long-term use of PPI medications have noted potential adverse effects, including risk of fractures, pneumonia, Clostridium difficile diarrhea, hypomagnesemia, vitamin B12 deficiency, chronic kidney disease, and dementia. These emerging data have led to subsequent investigations to assess these potential risks in patients receiving long-term PPI therapy. However, most of the published evidence is inadequate to establish a definite association between PPI use and the risk for development of serious adverse effects. Hence, when clinically indicated, PPIs can be prescribed at the lowest effective dose for symptom control.

Andexxa approved for reversal of NOACs (direct Xa infibitors)

From Medical Letter cited by JAMA.

Thrombocytopenia does not predict bleeding in cirrhosis

Form the PRO-LIVER study.

The EMR and other “systems improvements”: unfounded optimism

Despite repeated failures, we are on the cusp of positive results according to this piece.

What is the clinical spectrum and what are the mechanisms of thalamic infarct

This free full text review is dated but helpful.

Give doctors tools, not rules

Matthew Hahn on the phony baloney of “value based” care.

Post arrest PCI: the earlier the better

From a recent study:

Background

Timely post-resuscitation coronary reperfusion therapy is recommended; however, the timing of immediate coronary reperfusion for out-of-hospital cardiac arrest (OHCA) has not been established. We studied the effect of the time interval from arrest to percutaneous coronary intervention (PCI) on resuscitated OHCA patients.

Methods

All witnessed OHCA patients with a presumed cardiac etiology received successful PCI at hospitals between 2013 and 2015, excluding cases with unknown information regarding the time from arrest to PCI and survival outcomes. The main exposure of interest was the time interval from arrest to ballooning or stent placement in coronary arteries, and cases were categorized into five groups of 0–90, 90–120, 120–150, and 150–180 min and 3–6 h. The endpoint was survival with good neurological recovery. Multivariable logistic regression analysis was performed, adjusting for patient-community, prehospital, and hospital factors.

Results

A total of 765 patients (24.1% received PCI within 90 min; 31.0% in 90–120 min; 17.8% in 120–150 min; 12.3% in 150–180 min; 14.9% in 3–6 h after arrest) were included. Good neurological recovery was more frequent in the early PCI groups than the delayed PCI group (63.6%, 55.3%, 47.8%, 33.0%, and 42.1%, respectively). The adjusted OR (95% CI) for good neurological recovery compared with the most early PCI group was 0.86 (0.53–1.39) in the PCI group between 90 and 120 min; 0.76 (0.45–1.31) in the PCI group between 120 and 150 min; 0.42 (0.22–0.79) in the PCI group between 150 and 180 min; and 0.53 (0.30–0.93) in PCI group after 3 h.

Conclusions

Among resuscitated OHCA patients with a presumed cardiac etiology and successful PCI, patients who received a delayed coronary intervention after 150 min from arrest were less likely to have neurologically intact survival compared to those who received an early intervention.

UAMS Grand Rounds video archives

For archived events prior to 4/19/18 click here.

8/2/18 Histoplasmosis, blastomycosis. Michael Saccente MD

7/26/18 The Hospitalized Parkinsons patient. Rohit Dhall MD

7/19/18 Cognition, frailty and survivorship: braving the intangibles of critical illness. Emily Kocurek MD

6/24/18 What’s so diff-icult about C diff? Atul Kothari MD

6/21/18 Update in perioperative medicine. Latha Achanta MD

6/14/18 Caring for patients with acute liver failure. Katie Rude MD

6/7/18 iPSC-exosomes for precision medicine for heart failure. Phillip C Yang MD

5/17/18 Alpha-gal red meat allergy: an emerging epidemic of anaphylaxis? Scott P. Commins MD

5/10/18 CAR-T cell therapy toxicity management. Appalla Naidu Sasapu MD

4/26/18 SBE prophylaxis: the myth of sisyphus. What’s the harm? Walter R Wilson MD

4/19/18 Chronic kidney disease mineral and bone disorder (CKD-MBD) originally known as renal osteodystrophy. Robert S Weinstein MD

Update on neurosarcoidosis

From a recent review:

Recent findings

Clinical presentation is heterogeneous with most patients presenting with cranial nerve palsy, headache, or sensory abnormalities. Patients are classified according to probability of the diagnosis with the Zajicek criteria. In these criteria, histopathological confirmation of noncaseating granulomas in affected tissue outside the nervous system is key. Radiological abnormalities on neuroimaging are nonspecific. No biomarkers have been described that adequately identify patients with sarcoidosis. However, soluble interleukin-2 receptor is a relatively novel biomarker that may be useful. In addition to HRCT scan, 18 F-FDG PET-CT scanning can identify occult locations of disease activity and aid in obtaining pathological confirmation. Despite the use of new therapies, still a third of patients remains stable, deteriorate, or die.

Summary

Diagnosing and treating patients with neurosarcoidosis remains a challenge. Long-term prospective studies evaluating patients suspected of neurosarcoidosis are needed to assess sensitivity and specificity of ancillary investigations and diagnostic criteria. Furthermore, future studies are needed to evaluate the prognosis and the optimal treatment strategy.

The neuropsychology of morbid obesity

Several cognitive defects noted in this study.

Neuropsychiatric complications of dopaminergic therapy

As pointed out in this free full text review the neuropsychiatric side effects go beyond impulsive gambling to a variety of impulse control phenomena and other psychiatric disturbances. Moreover, it’s not just in patients treated with Parkinson disease but also some of those treated for restless leg syndrome and prolactinoma. There are a number of poorly understood metabolic effects as well, largely favorable it would seem.

Is there an association between COPD and NAFLD?

From a recent paper:

Abstract

Nonalcoholic fatty liver disease (NAFLD) is independently linked to cardiometabolic morbidity and mortality. Low-grade inflammation, oxidative stress and ectopic fat, common features of chronic obstructive pulmonary disease (COPD), might contribute to the development of NAFLD.

We aimed to investigate the prevalence of NAFLD and to evaluate the relationship between various types of liver damage and COPD severity, comorbidities and circulating inflammatory cytokines. Validated noninvasive tests (FibroMax: SteatoTest, NashTest and FibroTest) were used to assess steatosis, nonalcoholic steatohepatitis (NASH) and liver fibrosis. Patients underwent an objective assessment of COPD comorbidities, including sleep studies. Biological parameters included a complete lipid profile and inflammatory markers.

In COPD patients the prevalence of steatosis, NASH and fibrosis were 41.4%, 36.9% and 61.3%, respectively. In multivariate analysis, SteatoTest and FibroTest were significantly associated with sex, body mass index (BMI), untreated sleep apnoea and insulin resistance, and, in addition, COPD Global Initiative for Chronic Obstructive Lung Disease stage for SteatoTest. Patients with steatosis had higher tumour necrosis factor-α levels and those with NASH or a combination of liver damage types had raised leptin levels after adjustment for age, sex and BMI.

We concluded that NAFLD is highly prevalent in COPD and might contribute to cardiometabolic comorbidities.

Narcolepsy: an autoimmune disease?

From a recent review:

Recent findings
Both genetic and epidemiological evidence point towards an autoimmune mechanism in the destruction of orexin/hypocretin neurons. Recent studies suggest both humoral and cellular immune responses in the disease development.

Summary
Narcolepsy is a severe sleep disorder, in which neurons producing orexin/hypocretin in the hypothalamus are destroyed. The core symptoms of narcolepsy are debilitating, extreme sleepiness, cataplexy, and abnormalities in the structure of sleep. Both genetic and epidemiological evidence point towards an autoimmune mechanism in the destruction of orexin/hypocretin neurons. Importantly, the highest environmental risk is seen with influenza-A infection and immunization. However, how the cells are destroyed is currently unknown. In this review we summarize the disease symptoms, and focus on the immunological findings in narcolepsy. We also discuss the environmental and genetic risk factors as well as propose a model for disease development.