Do Statins Cause Diabetes?

A wealth of evidence has established that cholesterol-lowering statin drugs, widely used for the prevention of cardiovascular disease, do increase the risk of new-onset diabetes, possibly by impairing pancreatic beta cell function and decreasing peripheral insulin sensitivity. Groups at particular risk include the elderly, women, and Asians. The diabetogenic effect of statins appear directly related to statin dose and the degree of attained cholesterol lowering. Statins can cause hyperinsulinemia even in the absence of hyperglycemia and the potential mitogenic effects and implications of prolonged hyperinsulinemia are discussed. Suggestions are made as to how physicians might avert the hyperinsulinemic and diabetogenic effects of statin therapy in clinical practice, and modulate the detrimental effects of these drugs on exercise performance. Finally, long-term studies are needed to determine if the deleterious hyperinsulinemic and diabetogenic effects of statin therapy undermine the beneficial cardiovascular disease risk outcomes in various segments of the population.     

NETT coordinators: researchers, caregivers, or both?

The National Emphysema Treatment Trial (NETT) required the coordinated evaluation and treatment of thousands of patients with emphysema simultaneous with data collection to evaluate the safety and efficacy of surgery versus medical treatment for emphysema. These tasks were performed by a multidisciplinary team led by the clinic coordinator at each NETT center. The clinic coordinators functioned as members of the research team as well as communicators, managers, and members of the patient care team. The clinic coordinators' ability to balance these roles was instrumental to the successful completion of NETT, as evidenced by randomization of 1,218 subjects with only 10 subjects being lost to follow-up. Striving to achieve recruitment goals and working to retain study subjects was very labor intensive. The coordinator role was complicated by the study population's severity of illness combined with the complexity of the NETT protocol. Management of the study subjects' medical condition had to be balanced with the management of a multicenter, randomized clinical trial to ensure quality data collection and protocol adherence.     

Syncope,seizure or both?

Ictal asystole (IA) is a rare phenomenon in patients with seizures with an incidence of 0.27–0.4% and has been proposed as a possible mechanism of sudden unexpected death in epilepsy patients (SUDEP). We present a case of a 53-year-old woman who initially presented with episodes of expressive aphasia and was treated with antiepileptic drugs (AEDs). While on therapy she experienced episodes of syncope. During her hospitalization for tapering of AEDs and 24-hour EEG monitoring, the patient developed a seizure followed by sinus bradycardia and an 18-second sinus pause, resulting in loss of consciousness and slowing of cerebral activity. Ten seconds after the return of cardiac activity, the EEG showed return of cerebral activity. A dual chamber pacemaker was implanted.     

Familial scleroderma: nature,nurture or both?

Background: The aim of the study was to investigate: (i) familial scleroderma (FS) risk factors, (ii) subtype concordance and (iii) relationship between dates (DSO) and ages (ASO) at scleroderma onset. Methods: Forty‐seven cases (23 families; 25 FS pairs) were identified. Scleroderma disease onset was defined by (i) Raynaud’s onset, (ii) first symptom onset (1SxO), (iii) second symptom onset (2SxO) and (iv) scleroderma diagnosis (SDx). Results: Female : male and limited : diffuse (L : D) ratios were 8.4:1 and 3.3:1. The Raynaud’s onset – SDx interval was longer in limited disease (L : D = 14.6:3.1 years; P = 0.01). Raynaud’s first occurred in 36% women ≥50 years. The median differences in ASO between affected family members were 10–12 years. Disease subtype concordance exceeded discordance (16:9 clusters; (P = 0.32) 16:7 families; (P = 0.17)). The observed/expected LL : LD : DD ratios were 14: 8:1/11:7:1 (P = 0.66). FS affected 34% (95% confidence interval 19–50) sister–sister and 44% (95% confidence interval 27–75) mother–daughter pairs. The second family member’s SDx was made at the same (9%) or a younger age (80%) than the first family member. In 14 LL disease families ASO was closer between sisters than mothers–daughters (P = 0.07). There was a trend towards closer ages – than dates – at Raynaud’s and 1SxO in scleroderma‐affected family members (P = 0.054) and closer dates – than ages – at 2SxO (P = 0.02) and SDx. Conclusion: FS showed female predominance, relatively late onset Raynaud’s, subtype ratios similar to idiopathic scleroderma and earlier SDx in younger family members. Familial L scleroderma has a longer prediagnostic latency than familial D scleroderma. FS is likely under‐ascertained. In LL scleroderma, Raynaud’s/1SxO is possibly more genetically determined and 2SxO/SDx more environmentally determined.     

Hot tub lung: infection,inflammation, or both?

Increasing numbers of patients have presented with a hypersensitivity pneumonitis-type course in association with hot tub exposure. Mycobacterium avium complex (MAC) organisms have been isolated from both patient specimens and hot tub water with matching fingerprints by restricted fragment length polymorphism and electrophoresis when performed. Review of the clinical, microbiologic, and radiographic presentations of 9 patients to the Mayo Clinic with this diagnosis are compared with 32 patients in the published literature. The diagnosis, treatment, and prognosis of MAC hot tub lung are reviewed.     

Irritable bowel syndrome or endometriosis, or both?

Both irritable bowel syndrome and endometriosis are common conditions, although symptomatic gastrointestinal endometriosis is extremely rare. We report the case of a patient initially thought to have irritable bowel syndrome, in whom the diagnosis of endometriosis only became clear following a laparotomy for small bowel obstruction. This case highlights the need to question the diagnosis in patients with irritable bowel syndrome when there is any uncertainty, and also to appreciate that other pathology can arise, even when the diagnosis is secure.     

Statins in liver disease: a molehill, an iceberg, or neither?

A growing number of chronic liver disease patients, especially those with metabolic syndrome-associated nonalcoholic fatty liver disease or hepatitis C virus-associated dysmetabolic syndrome, will take statins to prevent cardiovascular disease. As a result, clinicians will weigh complex issues raised by the interaction of statins with liver metabolism in these disorders. In this article, we critically review data concerning statins and liver pathophysiology with an emphasis on nonalcoholic fatty liver disease and hepatitis C virus, while also touching on other chronic liver diseases. Basic research interests include statins' mechanism of action and their effects on cholesterol-related cell signaling pathways and angiogenesis. From the clinical standpoint, many chronic liver diseases increase cardiovascular risk and would undeniably benefit from sustained statin use. The false alarms and security accompanying aminotransferase monitoring, however, are disturbing in light of the scarcity of data on statins' long-term effects on liver histology. Although some actions of statins might eventually prove to be particularly useful in nonalcoholic steatohepatitis, hepatitis C virus, or hepatocellular carcinoma, others may prove harmful. The lack of definitive data makes a fully informed decision impossible. Research using histological endpoints is urgently needed to determine the indications and contraindications of this extraordinary class of agents in patients with chronic liver disease.     

Statins and Renal Disease: Friend or Foe?

The role of statins in the treatment and prevention of cardiovascular diseases, such as coronary artery disease, acute coronary syndromes, diabetes, or stroke, is well established. However, there are still some questions regarding the role of statins in patients with chronic kidney disease (CKD). Dyslipidemia is a known cardiovascular risk factor in individuals without CKD. In these patients, however, the relation of dyslipidemia to cardiovascular risk is complex, and the underlying pathobiological mechanisms are complex. Statins have proven to be highly effective in patients with initial stages of CKD; however, their effects in patients with advanced-stage CKD have been neutral despite a low-density lipoprotein cholesterol–lowering effect. In this review, we summarize the findings of the recent clinical trials of statins in renal disease and make recommendations for our patients.