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18% of the world's population lives in India, and many states of India have populations similar to those of large countries. Action to effectively improve population health in India requires availability of reliable and comprehensive state-level estimates of disease burden and risk factors over time. Such comprehensive estimates have not been available so far for all major diseases and risk factors. Thus, we aimed to estimate the disease burden and risk factors in every state of India as part of the Global Burden of Disease (GBD) Study 2016.

Background:Patients with diabetes have increased incidence and severity of periodontal disease not accounted for by differences in the subgingival microbial infection. Poor glycemic control has been consistently associated with periodontal disease severity. Also, recent evidence suggests that hyperglycemia may induce inflammatory cytokine production. Few studies, however, have examined local biochemical measures of periodontal inflammation in patients with type 2 diabetes. The aim of this study was to determine whether glycemic control was related to gingival crevicular fluid (GCF) levels of interleukin‐1β (IL‐1β). Methods:GCF samples were collected from 45 patients with type 2 diabetes and untreated chronic periodontitis. Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and attachment level (AL) were recorded at six sites per tooth. IL‐1β levels were determined from individual GCF samples by enzyme‐linked immunoabsorbent assay (ELISA). Individual site and mean patient values were calculated. Glycated hemoglobin (HbA1c) levels were measured from anticoagulated whole blood using an automated affinity chromatography system. Serum glucose was also determined. Results:Clinical periodontal measures (PD, AL, BOP) and measures of glycemic control (HbA1c, random glucose) were signifi‐ cantly correlated with GCF IL‐1β. Patients with greater than 8% HbA1c had significantly higher mean GCF IL‐1β levels than patients with less than 8% HbA1c. In a multivariate model adjusting for age, gender, PD, AL, BOP, and PI, HbA1c and random glucose were independent predictors of high GCF IL‐1β. Conclusions:Poor glycemic control is associated with elevated GCF IL‐1β. These data are consistent with the hypothesis that hyperglycemia contributes to an heightened inflammatory response, and suggests a mechanism to account for the association between poor glycemic control and periodontal destruction. J Periodontol 2004;75:1203‐1208.

Objective: To present two cases of severe hyperglycemia in patients without diabetes who received gati-floxacin therapy. Methods: We describe the histories, clinical findings, and hospital courses of two women in whom severe hyperglycemia developed after gatifloxacin therapy was initiated. Interacting factors that may result in severe hyperglycemia in patients without diabetes and the literature explaining the mechanism by which gatifloxacin can alter glucose metabolism are reviewed. Results: Our first patient, a 46-year-old woman with end-stage renal disease, presented with a 3-day history of fever, abdominal pain, and hypotension. Admission laboratory data included a fasting plasma glucose level of 72 mg/dL and a glycosylated hemoglobin of 5.3%. She was treated with gatifloxacin for an infected ovarian cyst found on laparotomy. Her subsequent glucose values ranged from 400 to 500 mg/dL and remained high during gati-floxacin therapy. Antibiotic treatment was changed to ciprofloxacin. On outpatient follow-up, the patient's fasting plasma glucose levels had decreased to a range of 87 to 108 mg/dL. Our second patient, a 77-year-old woman with a history of chronic renal failure and congestive heart failure, was hospitalized because of dyspnea and hypotension. She was given gatifloxacin for a urinary tract infection. Her daily fasting plasma glucose value gradually increased from 100 mg/dL on admission to 694 mg/dL on the 6th hospital day. The patient required insulin therapy throughout her hospitalization, and she died on the 12th hospital day. Conclusion: Gatifloxacin therapy may precipitate severe hyperglycemia in patients without diabetes, especially in the elderly population, those with renal insufficiency, and those receiving multiple drugs known to alter glucose metabolism. Discontinuation of gatifloxacin treatment may result in improved glucose homeostasis. (Endocr Pract. 2004;10:40-44)