Accurate documentation, correct coding, and compliance: it's your best defense!

This article focuses on the need for physicians to maintain an awareness of regulatory policy and the law impacting the federal government's medical insurance programs, and to internalize and apply this knowledge in their practices. Basic information concerning selected fraud and abuse statutes and the civil monetary penalties and sanctions for noncompliance is discussed. The application of accurate documentation and correct coding principles, as well as the rationale for implementating an effective compliance plan in order to prevent fraud and abuse and/or minimize disciplinary action from government regulatory agencies, are emphasized.

Diabetes patient education.

Not all medical practices are equipped to provide diabetes self-management training. Physicians can incorporate a team approach in their practice by establishing collaborative relationships with recognized diabetes education programs. The ADA's education recognition program has identified diabetes education programs that meet the National Standards for Diabetes Self-Management Education Programs. This list is available on the ADA's web site at http://www.diabetes.org/recognition and is printed twice a year in Diabetes Forecast. The National Certification Board for Diabetes Educators (NDEA) can provide a list of CDEs in your area. The South Carolina Model Diabetes Patient Education Program of DSC and SCDCP/DHEC is an excellent critical step towards obtaining ADA recognition.

Muscarinic activation of Ca2+/calmodulin-dependent protein kinase II in pancreatic islets. Temporal dissociation of kinase activation and insulin secretion.

We have demonstrated previously that glucose activates the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) in isolated rat pancreatic islets in a manner consistent with a role of this enzyme in the regulation of insulin secretion [Wenham, Landt and Easom (1994) J. Biol. Chem. 269, 4947-4952]. In the current study, the muscarinic agonist, carbachol, has been shown to induce the conversion of CaM kinase II into a Ca(2+)-independent, autonomous form indicative of its activation. Maximal activation (2-fold) was achieved by 15 s, followed by a rapid return to basal levels by 1 min. This response was primarily the result of the mobilization of Ca2+ from intracellular stores since it was not affected by a concentration (20 microM) of verapamil that completely prevented the activation of CaM kinase II by glucose. Surprisingly, carbachol added prior to, or simultaneously with, glucose attenuated nutrient activation of CaM kinase II. This effect was mimicked by cholecystokinin-8 (CCK-8) and thapsigargin, suggesting its mediation by phospholipase C and the mobilization of intracellular Ca2+. In contrast, carbachol, CCK-8 and thapsigargin markedly potentiated glucose (12 mM)-induced insulin secretion. These results suggest that CaM kinase II activation can be temporally dissociated from insulin secretion but do not exclude the potential dependence of insulin exocytosis on CaM kinase II-mediated protein phosphorylation.

Porphyria cutanea tarda (PCT) in a patient with chronic renal failure on haemodialysis.

Porphyria cutanea tarda, diagnosed by reduced levels of red cell uroporphyrin decarboxylase and raised plasma porphyrins, developed in a patient with chronic renal failure due to polycystic kidneys, treated with haemodialysis, who had normal total faecal porphyrins. Haemodialysis did not alter plasma porphyrin levels and we deduced that most of the plasma porphyrins were circulating in high molecular weight protein complexes.