This article aims to review the physiopathology, diagnosis and treatment of cystic fibrosis-related dyslipidemia (CFD). Bibliographic searches of the Medline and Latin American and Caribbean Health Sciences Literature databases were made (year range, 1987-2007), and the most representative papers on the theme were selected. The characteristic symptoms of CFD are hypertriglyceridemia-with or without hypocholesterolemia-and essential fatty acid deficiency. The principal CFD risk factors are pancreatic insufficiency, high-carbohydrate diet, liver diseases, inflammatory state and corticosteroid therapy. There are no specific recommendations regarding screening, which is typically performed based on the diagnosis, and at regular intervals, and more frequently in individuals belonging to high-risk groups. Treatment includes a balanced diet, micronutrient supplementation, and regular physical exercise according to individual tolerance. In the great majority of the cases, CFD-related hypertriglyceridemia does not reach values for which the use of hypolipidemic drugs is indicated. We conclude that there are few articles in the literature regarding the frequency, etiology and management of CFD. Preventive and therapeutic recommendations for hypertriglyceridemia are extrapolated from studies in individuals without cystic fibrosis. Further research is necessary to investigate the association of essential fatty acid deficiency and the physiopathology of cystic fibrosis. Since hypertriglyceridemia is an important risk factor for coronary artery disease, prospective studies will contribute for a better understanding of the natural history of this condition and define how to prevent and treat it.

Keywords: Cystic fibrosis; Dyslipidemias; Hypertriglyceridemia; Fatty Acids, nonesterified.

Once considered a childhood disease, cystic fibrosis is now also a disease of adults. Increased longevity has resulted in the aging of the cystic fibrosis population. The consequent age-related medical problems among adults with cystic fibrosis have increased medical care needs. These needs are being met by a growing number of non-pediatric pulmonologists and other non-pediatric specialists. The objective of this review was to summarize the current knowledge about diagnosis and treatment in adult cystic fibrosis. In most cases, the diagnosis is suggested by manifestations of chronic sinopulmonary disease and exocrine pancreatic insufficiency. The diagnosis is confirmed by a positive sweat test result. Adult patients may, however, present pancreatic sufficiency and atypical clinical features, sometimes in combination with normal or borderline sweat test results. In such cases, identifying cystic fibrosis mutations and measuring nasal potential difference can have diagnostic utility. The standard therapeutic approach to pulmonary disease includes the use of antibiotics, airway clearance, exercise, mucolytics, bronchodilators, oxygen therapy, anti-inflammatory agents and nutritional support. Appropriate application of these therapies results in most cystic fibrosis patients surviving into adulthood with an acceptable quality of life.

Keywords: Cystic fibrosis; Diagnosis; Therapeutics; Mucoviscidosis.

Cystic fibrosis-related diabetes (CFRD) is the principal extra-pulmonary complication of cystic fibrosis, occurring in 15-30% of adult cystic fibrosis patients. The number of cystic fibrosis patients who develop diabetes is increasing in parallel with increases in life expectancy. The aim of this study was to review the physiopathology, clinical presentation, diagnosis and treatment of CFRD. A bibliographic search of the Medline and Latin American and Caribbean Health Sciences Literature databases was made. Articles were selected from among those published in the last twenty years. Insulin deficiency, caused by reduced β-cell mass, is the main etiologic mechanism, although insulin resistance also plays a role. Presenting features of type 1 and type 2 diabetes, CFRD typically affects individuals of approximately 20 years of age. It can also be accompanied by fasting, non-fasting or intermittent hyperglycemia. Glucose intolerance is associated with worsening of nutritional status, increased morbidity, decreased survival and reduced pulmonary function. Microvascular complications are always present, although macrovascular complications are rarely seen. An oral glucose tolerance test is recommended annually for patients ≥ 10 years of age and for any patients presenting unexplained weight loss or symptoms of diabetes. Patients hospitalized with severe diseases should also be screened. If fasting hyperglycemia persists for more than 48 h, insulin therapy is recommended. Insulin administration remains the treatment of choice for diabetes and fasting hyperglycemia. Calories should not be restricted, and patients with CFRD should be managed by a multidisciplinary team.

Keywords: Cystic fibrosis; Diabetes mellitus.

Diabetes mellitus is an endocrine/metabolic disorder characterized by hyperglycemia. Its impact on the respiratory system is characterized by functional changes and alterations in gas exchange. The objective of this study was to evaluate the increase in oxidative stress and the potential damages to the lung structure in an experimental model of streptozotocin-induced diabetes. We conducted histological, biochemical and blood gas analyses in the lungs of diabetic rats. We concluded that the effects of experimental diabetes mellitus include oxidative stress, structural changes in the lung tissue and altered gas exchange.

Keywords: Lung; Diabetes mellitus; Oxidative stress; Diabetes mellitus, experimental; Free radicals.

Objective: To evaluate structural alterations of the lung in rats with diabetes mellitus (DM), by quantifying oxidative stress and DNA damage, as well as to determine the effects that exogenous superoxide dismutase (SOD) has on such alterations. Methods: A controlled experimental study involving 40 male Wistar rats, divided into four groups (10 animals each): control; SOD-only (without DM but treated with SOD); IDM-only (with streptozotocin-induced DM but untreated); and IDM+SOD (with streptozotocin-induced DM, treated with SOD). The animals were evaluated over a 60-day period, day 0 being defined as the day on which the streptozotocin-injected animals presented glycemia > 250 mg/dL. The SOD was administered for the last 7 days of that period. At the end of the study period, samples of lung tissue were collected for histopathological analysis, evaluation of tissue oxidative stress, and assessment of DNA damage. Results: There were no significant differences among the groups regarding DNA damage. In the IDM-only group, there was a significant increase in the extracellular matrix and significantly greater hyperplasia of the capillary endothelium than in the SOD-only and control groups. In addition, there were significant changes in type II pneumocytes and macrophages, suggesting an inflammatory process, in the IDM-only group. However, in the IDM+SOD group, there was a reduction in the extracellular matrix, as well as normalization of the capillary endothelium and of the type II pneumocytes. Conclusions: Exogenous SOD can reverse changes in the lungs of animals with induced DM.

Keywords: Diabetes mellitus, experimental; Oxidative stress; Lung; DNA damage.

We evaluated the effect of aminoguanidine on pulmonary oxidative stress and lung structure in an experimental model of diabetes mellitus. Thiobarbituric acid reactive substances (TBARS), histology and arterial blood gases were evaluated in animals with diabetes mellitus (DM group), animals with diabetes mellitus treated with aminoguanidine (DM+AG group), and controls. The TBARS levels were significantly higher in the DM group than in the control and DM+AG groups (2.90 ± 1.12 vs. 1.62 ± 0.28 and 1.68 ± 0.04 nmol/mg protein, respectively), as was PaCO2 when compared with that of the control group (49.2 ± 1.65 vs. 38.12 ± 4.85 mmHg), and PaO2 was significantly higher in the control group (104.5 ± 6.3 vs. 16.30 ± 69.48 and 97.05±14.02 mmHg, respectively). In this experimental model of diabetes mellitus, aminoguanidine reduced oxidative stress, structural tissue alterations, and gas exchange.

Keywords: Oxidative stress; Diabetes mellitus, experimental; Lung.

Tuberculosis continues to be a major public health problem. Although efforts to control the epidemic have reduced mortality and incidence, there are several predisposing factors that should be modified in order to reduce the burden of the disease. This review article will address some of the risk factors associated with tuberculosis infection and active tuberculosis, including diabetes, smoking, alcohol use, and the use of other drugs, all of which can also contribute to poor tuberculosis treatment results. Tuberculosis can also lead to complications in the course and management of other diseases, such as diabetes. It is therefore important to identify these comorbidities in tuberculosis patients in order to ensure adequate management of both conditions.

Keywords: Tuberculosis/epidemiology; Tuberculosis/prevention & control; Diabetes mellitus/prevention & control; Smoking/adverse effects; Alcohol drinking/adverse effects; Street drugs/adverse effects.

Objective: To determine whether abnormal continuous glucose monitoring (CGM) readings (hypoglycemia/hyperglycemia) can predict the onset of cystic fibrosis-related diabetes (CFRD) and/or clinical impairment (decline in BMI and/or FEV1) in pediatric patients with cystic fibrosis (CF). Methods: This was a longitudinal prospective cohort study involving CF patients without diabetes at baseline. The mean follow-up period was 3.1 years. The patients underwent 3-day CGM, performed oral glucose tolerance test (OGTT), and had FEV1 and BMI determined at baseline. OGTT, FEV1, and BMI were reassessed at the end of the follow-up period. Results: Thirty-nine CF patients (10-19 years of age) had valid CGM readings at baseline, and 34 completed the follow-up period (mean = 3.1 ± 0.5 years). None of the study variables predicted progression to CFRD or were associated with hypoglycemic events. CGM could detect glucose abnormalities not revealed by OGTT. Patients with glucose levels = 140 mg/dL, as compared with those with lower levels, on CGM showed lower BMI values and z-scores at baseline-17.30 ± 3.91 kg/m2 vs. 19.42 ± 2.07 kg/m2; p = 0.043; and -1.55 ± 1.68 vs. -0.17 ± 0.88; p = 0.02, respectively-and at the end of follow-up-17.88 ± 3.63 kg/m2 vs. 19.95 ± 2.56 kg/m2; p = 0.039; and -1.65 ± 1.55 vs. -0.42 ± 1.08; p = 0.039. When comparing patients with and without CFRD, the former were found to have worse FEV1 (in % of predicted)-22.67 ± 5.03 vs. 59.58 ± 28.92; p = 0.041-and a greater decline in FEV1 (-36.00 ± 23.52 vs. -8.13 ± 17.18; p = 0.041) at the end of follow-up. Conclusions: CGM was able to identify glucose abnormalities not detected by OGTT that were related to early-stage decreases in BMI. CGM was ineffective in predicting the onset of diabetes in this CF population. Different diagnostic criteria for diabetes may be required for individuals with CF.

Keywords: Cystic fibrosis; Glucose intolerance; Glucose tolerance test; Diabetes mellitus.