Abstract:

AIM: To report the first fatal case of a toxin A positive toxin B gene positive strain of Clostridium difficile that caused pseudomembraneous colitis in a patient living in Trinidad & Tobago.

Presentation of case: Patients admitted in a tertiary hospital with history of diarrhea were being investigated and reviewed. A case of a 47-year old Trinidadian of African descent presenting with diarrheal stool at a public hospital in Trinidad and Tobago. The identified patient had his stool sample analyzed using conventional and molecular microbiology procedures to identify the bacteria, toxins and genes produced by the microorganism. The antimicrobial susceptibility was also determined using agar dilutions according to CLSI guidelines.

DISCUSSION: The patient‘s stool sample produced positive results for Clostridium difficile toxin. The Quick Check Complete® kit demonstrated the production of toxin and the glutamate dehydrogenase enzyme. This strain exhibits the toxin A and B gene.

CONCLUSION: Clostridium difficile isolated from this patient revealed the presence of toxin A and B gene. This gave a 1266bp and 204bp DNA fragment corresponding to the toxin A and B gene respectively, based on the primers used. The isolated strain was resistant to meropenem, ampicillin, ceftriaxone, cefotaxime and ciprofloxacin. This organism seems to have been responsible for the formation of psuedomembranous colitis in the studied patient. Further research is needed on similarly detected strains, to better understand their significance in Inflammatory Bowel Diseases and their prevalence in our geographical location. 

References:

[1.] Alonso, R., Martin, A., Pelaez, T., Marin, M,, Rodriguez-Creixems, M., Bouza, E(2005). Toxigenic status of Clostridium difficile in a large Spanish teaching hospital. J Medical Microbiol; 54(2), 159-162

[2.] Bauer, M,, Kuijper, E,, Van, Dissel, J(2009). European Society of Clinical Microbiology and Infectious Diseases (ESCMID): treatment guidance document for Clostridium difficile infection (CDI). Clin Microbiol Infect; 15(12), 1067-1079.

[3.] Bartlett, J.,G., Chang, T.W., Gurwith, M., Gorbach, S,L,, Onderdonk, A.B (1979). Antibiotic-Associated Pseudomembranous Colitis Due to Toxin-Producing Clostridia. N Engl J Med; 298(10), 531-534. doi

[4.] Borriello, S. (1998). Pathogenesis of Clostridium difficile infection. J Antimicro Chemo; 41(suppl 3), 13-19.

[5.] Cleary, R.K.(1998). Clostridium difficile-associated diarrhea and colitis. Dis Colon Rectum; 41(11), 1435-1449.

[6.] Cohen, S.H., Gerding, D.N., Johnson, S., Kelly, C.P., Loo, V.G., L. Clifford, McDonald, M., Wilcox, M.H. (2010). Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA). Infect Control Hosp Epidemiol; 31(5), 431-455.

[7.] Clinical and Laboratory Standard Institute (CLSI). Performance Standards for Antimicrobial Susceptibility Testing; Twenty-Second Information Supplement 2012; M100-S22; Vol 31 No.1

[8.] Figueroa, I., Johnson, S,, Sambol, S.P., Goldstein, E.J., Citron, D.M., Gerding, D.N(2012). Relapse versus reinfection: Recurrent Clostridium difficile infection following treatment with fidaxomicin or vancomycin. Clinical Infectious Diseases; 55(suppl 2), S104-S10

[9.] Gebhard, R.L., Gerding, D.N., Olson, M.M., Peterson, L.R., McClain, C.J., Ansel, H.J., Schwartz, M.L(1985). Clinical and endoscopic findings in patients early in the course of Clostridium difficile-associated pseudomembranous colitis. American J Med; 78(1), 45-48.

[10.]   Hassett, J., Meyers, S., McFarland, L., Mulligan, M.E.( 1995). Recurrent Clostridium difficile infection in a patient with selective IgG1 deficiency treated with intravenous immune globulin and Saccharomyces boulardii. Clin Infect Dis;20 (Supplement 2):S266-S8.

[11.]   Higazi, T.B., Mohannad, A.S., Burkett, M., Pusok, R(2011). PCR Detection of Clostridium difficile and its Toxigenic Strains in Public Places in Southeast Ohio. Intl. J; 2(2), 105-111.

[12.]   Johnson, S., Samore, M.H., Farrow, K.A., Killgore, G.E., Tenover, F.C., Lyras, D., Rafferty, M. E. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. N Engl J Med 1999; 341(22), 1645-1651.

[13.]   Kato, H., Kato, N., Watanabe, K., Iwai, N., Nakamura, H., Yamamoto, T., et a (1998)l. Identification of toxin A-negative, toxin B-positive Clostridium difficile by PCR. J Clin Microbiol; 36(8):2178-82

[14.]   Kelly, C.P., Pothoulakis, C., LaMont, J.T. Clostridium difficile colitis(1994). N Engl J Med;330(4):257-62.

[15.]   Koss, K., Clark, M., Sanders, D., Morton, D., Keighley, M., Goh, J (2006). The outcome of surgery in fulminant Clostridium difficile colitis. Colorectal Dis; 8(2), 149-154.

[16.]   Lemee, L., Dhalluin, A., Testelin, S., Mattrat, M.A., Maillard, K., Lemeland, J.F., Pons J.L (2004). Multiplex PCR targeting tpi (triose phosphate isomerase), tcdA (Toxin A), and tcdB (Toxin B) genes for toxigenic culture of Clostridium difficile. J Clin Microbiol; 42(12), 5710­5714.

[17.]   Loo VG, Bourgault AM, Poirier L, Lamothe F, Michaud S, Turgeon N, Gilca R. Host and pathogen factors for Clostridium difficile infection and colonization. N Engl J  Med 2011; 365(18), 1693-1703.

[18.]   McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial acquisition of Clostridium difficile infection. N Engl J Med 1989;320(4):204-10.

[19.]   McDonald LC, Killgore GE, Thompson A, Owens JrRC, Kazakova SV, Sambol SP, Gerding DN. An epidemic, toxin gene–variant strain of Clostridium difficile. N Engl J Med 2005; 353(23), 2433-2441.

[20.]   Poutanen SM, Simor AE. Clostridium difficile-associated diarrhea in adults. Can Med Assoc J 2004;171(1):51-8.

[21.]   Price, A., Davies D. Pseudomembranous colitis. J Clin Pathol 1977;30(1):1-12

[22.]   Persson S, Torpdahl M, Olsen K. New multiplex PCR method for the detection of Clostridium difficile toxin A (tcdA) and toxin B (tcdB) and the binary toxin (cdtA/cdtB) genes applied to a Danish strain collection. Clin Microbiol Infect 2008; 14(11), 1057-1064.

[23.]   Samie A, Obi CL, Franasiak J, Archbald-Pannone L, Bessong PO, Alcantara-Warren C., & Guerrant, R. L. PCR detection of Clostridium difficile triose phosphate isomerase (tpi), Toxin A (tcdA), Toxin B (tcdB), Binary Toxin (cdtA, cdtB), and tcdC genes in Vhembe District, South Africa. Am J Trop Med Hyg 2008; 78(4), 577-585.

[24.]   Sharp SE, Ruden LO, Pohl JC, Hatcher PA, Jayne LM, Ivie WM. Evaluation of the C. Diff Quik Chek Complete Assay, a new glutamate dehydrogenase and A/B toxin combination lateral flow assay for use in rapid, simple diagnosis of Clostridium difficile disease. J Clin Microbiol 2010; 48(6) 2082-2086.

[25.]   Surawicz CM, Brandt LJ, Binion DG, Ananthakrishnan AN, Curry SR, Gilligan PH, et al. Guidelines for diagnosis, treatment, and prevention of Clostridium difficile infections. Am J Gastroenterol 2013;108(4):478-98.

[26.]   Voth, D.E., Ballard, J.D (2005). Clostridium difficile toxins: mechanism of action and role in disease. Clin Microbiol Rev ;18(2):247-63

[27.]   Wang, Q., Garrity, G.M., Tiedje, J.M., Cole, J.R. (2007). Naive Bayesian classifier for rapid assignment of rRNA sequences into the new bacterial taxonomy. Appl Environ Microbiol; 73(16), 5261-5267 

Abstract:

The Insulin reistent triggered by high proinsulin to insulin ratio which is associated with NIDDM( 1 ). Elevated intact proinsulin seems to indicate an advanced stage of β-cell exhaustion and is a highly specific marker for insulin resistance. It might be used as arbitrary marker for the therapeutic decision between secretagogue, sensitizer, or insulin therapy in type 2 diabetes( 2 ). In DM2, insulin processing deficient. There is an increased proinsulin:insulin ratio( 3 ). Changes in proinsulin levels are associated with diabetes.

Random proinsulin levels and the proinsulin-to-C-peptide ratio represent dynamic markers of the state of β-cell function that complement immune markers in identifying relatives who are at high risk of contracting type 1 diabetes( 4 ). Proinsulin is a very sensitive marker of beta cell exhaustion and may therefore be useful for therapeutic decision-making in type 2 diabetes ( 5 ). IDDM in humans and in non-obese diabetic (NOD) mice is a T-cell–dependent autoimmune disease in which the β-cells of the pancreatic islets are destroyed.

Several putative β-cell auto antigens have been identified, but insulin and its precursor, proinsulin, are the only ones that are β-cell specific.(6), his assay allows for a pathophysiological staging of type 2 diabetes based on beta-cell secretion. It could be confirmed by a large epidemiological study (IRIS-2, 4,265 patients) that intact proinsulin is a highly specific marker for insulin resistance. It could also be shown in other studies that successful resistance treatment with insulin or glitazones led to a decrease in elevated proinsulin levels and, thus, to a decrease of cardiovascular risk, while the levels remained high during sulfonylurea therapy.

Therefore, patients with increased fasting intact proinsulin values should be treated with a therapy focusing on insulin resistance. Assessment of beta-cell function by determination of intact proinsulin may facilitate the selection of the most promising therapy and may also serve to monitor treatment success in the further course of the disease.( 7). 

References:

[1.] Michelle, B. French (1997). Transgenic Expression of Mouse Proinsulin II Prevents Diabetes in Nonobese Diabetic Mice, Diabetes January vol. 46 no. 1 34-39,Retrieved from, http://diabetes.diabetesjournals.org/content/46/1/34.short,

[2.] Mykkänen, L.(1997). The relation of proinsulin, insulin, and proinsulin-to-insulin ratio to insulin sensitivity and acute insulin response in normoglycemic subjects. Diabetes. Dec;46(12):1990-5.Retrieved from ,diabetes.diabetesjournals.org/content/46/12/1990.full.pdf.

[3.] Pfützner, A.(2004). Fasting intact proinsulin is a highly specific predictor of insulin resistance in type 2 diabetes.Diabetes Care. Mar;27(3):682-7.Retrieved   from,www.ncbi.nlm.nih.gov/pubmed/14988285

[4.] Pfützner, A.( 2004), Role of intact proinsulin in diagnosis and treatment of type 2 diabetes mellitus, Diabetes Technol Ther. Jun;6(3):405-12.Retrieved by http://www.ncbi.nlm.nih.gov/pubmed/15198846

[5.] http://care.diabetesjournals.org/content/27/3/682.abstra

[6.] www.raymondcheong.com/.../DB33%20-%20Diabetes,%20Insulin%20A

[7.] http://www.alpco.com/pdfs/ALPCO_Proinsulin_ELISA_and_Diabetes_Research.pdf 

Abstract:

Lactation breast abscess is a painful, debilitating condition that if inappropriately managed, may lead women to discontinue breastfeeding prematurely. This study assessed the rate and predisposing factors to development of breast abscesses among 100 women in the Batibo Health District.

A structured questionnaire was used to collect socio-demographic and other data which was analyzed using the Statistical Package for Social Sciences (SPSS), version 16.0; SPSS inc. 38 of the 100 women were found to have had breast abscess giving a rate of 38%. Premature cessation of breastfeeding, refusal to breastfeed, excessive weight gain during pregnancy, and abrupt method of weaning were the major predisposing factors identified. Thus, breast abscesses occur among lactating mothers in the Batibo Health District. 

References:

[1.] Bernaix, L. (2000). Nurses attitudes, subjective norms and behavioral intentions towards supports of breastfeeding mothers. Journal of Human Lactation. 16(3); 202-209.

[2.] Black, A., Renfrew, M., Dykes, F., Burt, S. (1994). Assessing learning needs for breastfeeding; setting the scene. Maternal and Child Nutrition 2(4); 196-203.

[3.] Brosco, S. (1999).Knowledge, attitude and practice of breastfeeding. European Journal of Scientific Research. 4 (2): 404-422.

[4.] Chan, S.M., Nelson, E.A., Leung, B.S. (2000). ‗Breastfeeding in a longitudinal post-partum material nutrition study. Journal of Hong Kong Paediatrics.  5:466-71.

[5.] Cunningham, F.G., Macdonald P.C., Grant, N.F.(1997). Williams Obstetrics. Conn Appleton and Lange. 20:564-565.

[6.] Devareux, W. P. (1970). The adequate puerperal mastitis: Evolution of its management. American Journal of Obstetrics and Gynecology: 20(8);78-81.

[7.] Efem, S. E. (1995). Breast Abscess in Nigeria Lactational versus Non-lactational. Quarterly Journal of Medicine  40(1);25-27.

[8.] Eskstrom, A., Nissen, E. (2006). A mothers‘s feeding for her infant as strengthened by excellent breastfeeding, councelling and continuity of care. Journal of  Pediatrics., 18(2): e309­e314.

[9.] Evans, M. (1995). Incidence, prevalence and cost. Heads Journal of Mastitis: 3:65-71.

[10.]   Fetherson, C. (1998). Risk factors for lactation mastitis. Journal of Human Lactation. 14:101-109.

[11.]   Fetherson, C. (2001). Mastitis in lactating women: physiology or pathology? Breastfeeding Review. 9(1):5-12.

[12.]   Fildes, F. (1986). The education of health practitioners supporting breastfeeding women; time for critical thinking/reflection. Maternal/ Child Nutrition. 2(4); 204-216.

[13.]   Foxman, B., D‘Arcy, H., Bobo, J.K., Schwartz, F. (2002).Lactation mastitis: occurrence and medical management among 946 breastfeeding women in the United States. American Journal of Epidemiology. 155:103-114.

[14.]   Hartmann, J.R., O‘Connell, D.L., Kinlay, S. (1985). Risk facrors for masttis in breastfeeding women: results of a prospective cohort study. Australian  Journal of  Public Health 25:115-120.

[15.]   Hilson J. A., Rasmussen, K. M. (2006). Excessive weight gain during pregnancy is associated with early termination of breastfeeding. Journal ofAmerical Nutrition. 136(6);140.

[16.]   James, S.S., Dobson, P.D. (2005). Breast engorgement: patterns and selected outcomes. Journal of  Human Lactation, 10:87-93.

[17.]   Jonsson, S.,Pulkkinen, M.O. (1994). Mastitis today: incidence, prevention and treatment. Annals of Gynaecology: 208:84-87.

[18.]   Kaufmann, R., Foxman, B. (1991). Mastitis among lactating women: occurrence and risk factors. Social Science Medicine.33:701-705.

[19.]   Kjorup, S., Torhell, J. (1999).Accurate puerperal breast abscess. Journal of Obstetrics and Gynecology. 188:807-809.

[20.]   Labbok, C., Krsovec, A. (1990). Breast Abscesses in Lactating women. World Journal of Surgery. 27:130-133.

[21.]   Lowe, T. (1990). Breastfeeding; attitudes and knowledge of health practitioners. Australian Fan Physician. 19(3):392-396.

[22.]   Linda, J. H. (1995). ‗Factors related to breast abscess after delivery‘. Journal of Obstetrics and Gynaecology. 40(3):297-8.

[23.]   Mather, G.P. (1992). Lactation failure. Journal of Indian Pediatrics. 21:1541-44.

[24.]   Mathur, G. P., Chitrasonhi, S., Singh, S. B. (1992). Lactation failure. Journal of Pediatrics. 29(12);1541-4.

[25.]   McMukin, S., Malone, R. (1994). Breastfeeding; midwives personal experience. Med Midwives. 4 (5):10-12.

[26.]   Palma, E. R (2004).Common problems during Lactation and their Management. Journal of PediatricS. 80s: 1452-54.

[27.]   Sajeewa, A. (2006). Incidence of breast and nipple abnormalities among primigravid women. Sri Lanka Journal of Child Health. 35:51-4.

[28.]   Schwartz, K., D‘Arcy, H.J., Gillespi, B., Bobo, J.,Longeway, M.,Foxman, B. (2002). ―Factors associated with weaning in the first three months post-partum. Journal of Family practice. 51:439-444.

[29.]   Spock, M.D., Lowenberg, K. (1955). ‗Inadequate Brest Milk Production. Journal of Obstetrics and Gynaecolody. 870-877.

[30.]   Udani, P. M. (1979).  Researches on human milk and infant nutrition. Indian Journal of Pediatrics. 12:593:611.

[31.]   Vogel, A., Hutchison, L., Mitchell, E.A. (1999). Mastitis in the first year post-partum. International Breastfeeding Journal. 26:218-225.

[32.]   WHO Global strategy on infant feeding, 2002.

[33.]   Weighert, L.J., Wilde, L. B., Hall-Lord, M.L., Rydhstroem, H. (2005). Effects of acupuncture and care interventions on the outcome of inflammatory sypmtoms of the breast in lactating women. International Nurses Review 51:56-64. 

Abstract:

Schools are ideal setting to implement screening services for eye healthcare program. We conducted a study in schools around the Primary Health Centre Sampaje which is under the KVG Medical College, Sullia with objectives of appraising various ocular symptoms in the children and studying the prevalence of refractive errors, squint, vitamin A deficiency, conjunctivitis and color blindness among the children.

This was a cross sectional study conducted between July and October 2009 using a predesigned structured questionnaire and ocular examination on a total number of 1938 students attending 30 schools in the Sampaje Primary Health Centre (PHC) area. Prevalence of total ocular morbidity was 20.12% of which Refractive errors constituted 17.1%. (Myopia 16.9% and Hyperopia 0.20%), Squint 2.1%, Vitamin A deficiency 0.6%, Conjunctivitis and Color blindness 0.5%. An alarming prevalence of ocular morbidity of about 20% was demonstrated in the present study.

Also, since majority of children (76%) with ocular morbidity in the present study were asymptomatic, the need for active screening of all school going children for the various ocular morbidities is imperative. 

References:

[1.] Chaturvedi, S., Aggarwal, O.P.( 1999). Pattern and distribution of ocular morbidity in primary school children of rural Delhi. Asia Pac J Public Health.; 11(1):30-3.

[2.] Dandona, L., Williams, J.D., Williams, B.C, Rao, G.N (1998). Population based assessmentof childhood blindness in southern India. Arch Ophthalmol.; 116: 545-546.

[3.] Datta, A., Choudhury, N., Kundu, K(1983). An epidemiological study of ocular condition among primary school children of Calcutta Corporation. Indian J Ophthalmol; 31:505-10.

[4.] Desai, S., Desai, R., Desai, N.C., Lohiya, S., Bhargava, G., Kumar, K (1989). School eye health appraisal. Indian J Ophthalmol; 37:173-5.

[5.] Gilbert, C. E.(1999). Anderton L, Dandona L, Foster A. Prevalence of visual impairment in children: a review of available data. Ophthalmic epidemiol; 6: 73-82

[6.] Gupta, M., Gupta, B., Chauhan, A., Bharadwaj, A (2009). Ocular morbidity prevalence among school children in Shimla, Himachal, North India. Indian J Ophthalmo:; 57:133-138.

[7.] Kuruvilla, J., Srinivasa, Rao, P.N(1978). Ocular morbidity in school children in rural coastal area of Karnataka. Indian J Ophthalmol [serial online] [cited 2009 Oct 2]; 26: 9-12. Available http://www.ijo.in/text.asp?1978/26/2/9/31464.

[8.] Lions Aravind Institute of Community Ophthalmology, Madurai. Childhood blindness.[cited 2010 Mar 23] Available from URL: http://laico.org/v2020resource/files/Childhood_Blindness_final.pdf

[9.] Rahi, J.S., Sripathi, S., Gilbert, C.E., & Foster, A (1995). Childhood Blindness in India: causes in 1318 blind school studies in nine states. Eye.; 9: 545-550.

[10.]   Registrar General & Census Commissioner, Government of India. Provisional Population Total Paper 1 of 2011 India series 1:98, Census India 2011. [cited 2011 Jun 6]  Available from URL:http://censusindia.gov.in/2011-prov results/data_files/karnataka/7PPT%20Paper%201%202011%20Karnataka-literacy85_98.pdf

[11.]   Registrar General and Census Commissioner. Census of India 2001.

[12.]   Singh S, Singh H, Joshi VS. Eye diseases among primary school children. Indian J Ophthalmol 1974; 22:1-3.

[13.]   Smith JS. Childhood Blindness in India (editorial). Eye. 1995; 9:543-544.

[14.]   Sethi S, Kartha GP. Prevalence of refractive errors in school children (12-17 years) of Ahmedabad city. Indian Journal of Community Medicine. 2000; 25(4):181-3.

[15.]   Vision screening in children. Training module. Danish assistance to the national programme for control of blindness. New Delhi, India: 1.

[16.]   World Health Organization. Global Initiative for the Elimination of Avoidable Blindness. Geneva: WHO; 1997. PBL97.61. 

Abstract:

The review is a critical analysis of the article‖ Improvement of Eustachian Tube Function by Tissue-Engineered Regeneration of Mastoid Air Cells‖ published in the Laryngoscope.

In the review of this article, first to summarize it, then to analyze its print structure, keeping in view its layout and reader friendly ease. Lastly the review aims towards a critique analysis of the article evaluating its authority, currency, accuracy, objectivity and coverage. Any tables, graphs, diagrams and illustrations will also be analyzed. 

References:

[1.] Development of a porous poly(DL-lactic acid-co-glycolic acid)-based scaffold for mastoid air-cell regeneration. Gould TW, Birchall JP, Mallick AS, Alliston T, Lustig LR, Shakesheff KM, Rahman CV. Laryngoscope. 2013 Dec;123(12):3156-61.

[2.] Kanemaru, S., Nakamura, T., Omori, K., et al (2004). Regeneration of mastoid air cells; clinical applications. Acta Otolaryngol;(suppl 551):80–84.[PubMed]

[3.] Koc, A., Ekinci, G., Bilgili, A.M., Akpinar, I.N., Yakut, H., Han, T(2003). Evaluation of the mastoid air cell system by high resolution computed tomography: three-dimensional multiplanar volume rendering technique. J Laryngol Otol.;117:595–598.[PubMed]

[4.] Kanemaru, S., Nakamura, T., Omori, K., Magrufov, A., Yamashita, M., Ito, J (2005). Regeneration of mastoid air cells in clinical applications by in situ tissue engineering. Laryngoscope.;115:253–258.[PubMed]

[5.] Magrufov, A., Kanemaru, S., Nakamura, T., et al(2004). Tissue engineering for the regeneration of the mastoid air cells: a preliminary in vitro study. Acta Otolaryngol.;124(suppl 551):75–79.[PubMed]

[6.] Monasta, L., Ronfani, L., Marchetti, F., et al(2012). Burden of disease caused by otitis media: systematic review and global estimates. PLoS One.;7(4):e36226. [PMC free article][PubMed]

[7.] en.wikipedia.org/wiki/Prospective_cohort_study

[8.] www. laryngoscope.com

[9.] www.ncbi.nlm.nih.gov/…erm=Laryngoscope%5BJournal%5D 

Abstract:

I shall review this article mainly for its action on blood glucose levels and the cardiovascular system. In this article the author has elaborated only on three drugs namely Sitagliptin, Saxagliptin, and Vildagliptin.

Saxagliptin, Vildagliptin and Sitaglitins are different in their metabolism (Saxagliptin and Vildagliptin are metabolized in the liver while Sitagliptin is not metabolised in liver) their recommended dosage, excretion, and the daily dosage for effective treatment. But when compared to their efficacy regarding lowering the safety of the drug its HBA1c lowering effect and patient tolerance, all are almost same.

I shall look into the different studies which the author has taken as references to impress the usefulness of DPP-4 inhibitors in not only influencing the glycemic cycle but also the cardiovascular system and the weight neutrality.

I shall look into the different studies used as references by the author to prove his point.

A study done by Hsieh et al showed that inhibition of DPP-4, or increasing of GLP-1 receptor (GLP-1R) signaling, causes a decrease dintestinal secretion of triacylglycerol, apolipprotein B-48 and cholesterol. Further the endogenous GLP-1R signaling is required for the control of secretion and biosynthesis of intestinal lipoprotein.

These studies with other similar ongoing studies used by the author have impressed that the DPP-4 inhibitors group of drugs will has a beneficial effect not only on the glycemic control but also on cardiovascular system. 

References:

[1.] Dror, Dicker,M.D.(2011). Impact on glycemic control and cardiovascular risk factors DPP-4 Inhibitors, Diabetes care, volume 34, supplement 2 may 2011. Page:S276 –S278 care.diabetesjournals.org

[2.] Lisa, Nainggolan, (2013). DPP-4 Inhibitors and Heart Failure in Diabetes: Be Vigilant,http://www.medscape.com/viewarticle/817543

[3.] Sell, Henrike, et al titled(2013): Adipose Dipeptidyl Peptidase-4 and Obesity, Diabetes Care Issue: Volume 36(12), , p 4083–4090, care.diabetesjournals.org 

Abstract:

Proposal mainly concentrates on the core problem on the early screening of cardiovascular diseases. With presently available instruments diagnosis of the heart diseases is possible, but the constraint that idea is focusing on, is the cost-effective method to be implemented in rural sector. The diagnosis method presently available is ECG, which cannot give the prior information of the disease but only depicts the present status and also for the analysis of the ECG signal a specialized doctor is required. Taking into consideration of disadvantages in the current instruments, a new proposal of module, which can overcome these problems being portrayed. 

References:

[1.] Aleksandar Milenković, Chris Otto, Emil Jovanov (2006). ―Wireless sensor networks for personal health monitoring: Issues and an implementation‖ Computer communications Journal (Elsevier) (Volume: 29, Issue: 13-14), pp. 2521 -2313

[2.] Helen, M., Colhoun, etal (2004). ―Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicenter randomized placebo-controlled trial‖. The Lancet journal, Volume 364, Issue 9435, August 2004, pp. 685–696.

[3.] Ian graham etal (2007) ―European guidelines on cardio vascular disease prevention in clinical practice‖, European heart journal (Elsevier), pp. 2375-2414.

[4.] Mark Espeland (2003). ―Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes‖, Controlled Clinical Trials (Elsevier) Volume 24, Issue 5,  pp. 610–628.

[5.] Pantelopoulos, A., Dayton (2010). ―A Survey on Wearable Sensor-Based Systems for Health Monitoring and Prognosis Systems, Man, and Cybernetics‖, Part C: Applications and Reviews, IEEE Transactions on (Volume: 40, Issue: 1), pp. 1 – 12.

[6.] Yong Gyu Lim, Ko Keun Kim, Suk Park (2006) .―ECG measurement on a chair without conductive contact‖, Biomedical Engineering, IEEE Transactions on (Volume: 53, Issue: 5), pp. 956 – 959. 

Abstract:

AIM: This research is aimed at assessing the level of threat measles infection has on child development in northern region of Ghana and its impact on child health in recent times.

METHODS AND SAMPLING: A sample size of 20 health professionals, comprising 15 Public Health Nurses and 5 Family Physicians were used. A convenient and purposive sampling method was used to gather data through interviews and from primary information sources. Data was analysed using Microsoft excel and word processing.

RESULTS/FINDINGS: The results show that the threat of measles infection in northern region is significantly reduced, recording three confirmed cases in 2011. The diminishing trend was

acclaimed to be attributable to high level of cooperation from parents‘ willingness to send their

children out for vaccination and improved living standards of many Ghanaians, among others. These reasons notwithstanding, measles infection is still fluctuating from year to year.

CONCLUSION: Though the disease is fast diminishing, it still has a potential to escalate given that it shot from zero confirmed cases from 2010 to three confirmed cases in 2011. 

References:

[1.] CDC (2013). Measles case definition index. http://wwwn.cdc.gov/NNDSS/script/casedef.aspx?CondYrID=908. Downloaded. 15/07/2014

[2.] Ghana Health Service, (2005). Annual report.

[3.] Ghana health service,(2011). Gushegudistrict health management team annual report northern region Ghana.

[4.] Ghana health service,(2011). Yendi municipal annual report 2010 northern region, Ghana.

[5.] Ghana health service (2011). TolonKumbungu district health management team annual report northern region.

[6.] Ghana health service (2011).Kpandai district health management team annual report northern region.

[7.] Ghana health service (2011). West Mamprusidistrict health management team annual report, northern region

[8.] 8. Mohammed I (2013): Northern region records 51 maternal deaths. Tamale. 99.3 FM Zaa. http://www.zaaradio.com/?q=articles/2013/08/05/northern-region-records-51-maternal­deaths-january-july-2013. Downloaded. 14/08/2013

[9.] Paget,B. et al, (2003): Disease of children in the sub-tropics and tropics 4th Edition. London. Educational Low Priced Books Scheme (pages 497-501).

[10.]   WHO (2004): Report on supplemental measles immunization activities in Ghana. Accra. WHO

[11.]   WHO (2001-2005). EPI 5-Year strategic plan for measles immunization in Ghana. Accra. WHO

[12.]   WHO (2014). Measles disease surveillance. http://www.emro.who.int/health­topics/measles/disease-surveillance.html. Downloaded. 15/07/2014 

Abstract:

BACKGROUND: Globally, the oral health care for pregnant women is inadequate relating to education and health promotion sectors along with disparities in socio-economy and ethnicity. Neglected oral care often has long-term effects on our overall health, including the health of the baby during pregnancy. Serious problems like gingivitis and periodontal disease may also occur during this period as a result of neglected oral hygiene.

OBJECTIVE: This descriptive type of cross sectional study was carried out to assess the pattern of common oral and dental diseases among pregnant women.

MATERIALS AND METHODS: A total 147 pregnant women attended at the selected hospital and healthcare centre of Dhaka city for routine checkup over a period of five months from September 2013 to January 2014 fulfilled the eligibility criteria were selected consecutively. Pre­tested semi structured interviewer administrated questionnaires were used to collect the information.

RESULTS: The study shows that most of the pregnant women (72%) age ranged from 20-24 years. Also, majority (88%) of them were housewives while only 11% were service holders with monthly family income of BDT≤10000 of more than half of the respondents (52%). Oral complaints found from the study were bleeding gums (78%), sensitive tooth (52%) and cavities (35%) respectively. In addition, 63% never access to their dentists throughout their whole life and only 6% visited their dentists at the time of pregnancy. Lastly, the frequency of oral diseases revealed in this study was gingivitis (100%), dental caries (54%), dental erosion (52%), periodontitis (27%) and apthous ulcer (16%) respectively.

CONCLUSION: It can be said from the study that educational and occupational statuses of pregnant women in Bangladesh were not satisfactory. An extensive number of pregnant women did not seek oral health care during pregnancy. There is a need for further study on oral health status of the pregnant women to formulate appropriate oral health guidelines for better oral and dental health outcome. 

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Abstract:

Pharmacovigilance (PV), defined by the world health organization (WHO) as the science and activities relating to the detection, assessment, understanding and prevention of adverse effects or any other drug-related problem. Emergence of PV activities and the awareness would play a vital role in ensuring that doctors, healthcare professional, together with the patient, have enough information to make an educated decision when it comes to choosing a drug for treatment and eventually achieving the patient safety in large. 

References:

[1.] Adis International. The Erice Manifesto: for global reform of the safety of medicines in patient care. Drug Saf 2007; 30:187-90.

[2.] Assessment of the European Community System of Pharmacovigilance. European Medicines Agency 2006. Available via http://www.cbg-meb.nl/NL/docs/nieuws/rapp-fraunhofer.pdf Accessed March 1, 2012.

[3.] Biswas P, Biswas AK. Setting standards for proactive pharmacovigilance in India. Indian J Pharmacol. 2007;39:124–8.

[4.] Chapter 6 of The SAFETY of MEDICINES IN PUBLIC HEALTH PROGRAMMES: Pharmacovigilance an essential tool. WHO book.

[5.] Coombes R. FDA tightens its grip on drug regulation. BMJ 2007; 334:290-1.

[6.] Directive 2010/84/EU. Official Journal of the European Union 2010, Dec 31,L. 348/74-99.

[7.] European Medicine Agency Updates on RMP: EMA website http://www.ema.europa.eu/ema/index.jsp?curl=pages/regulation/document_listing/document_list ing_000360.jsp

[8.] European Risk management Strategy: Achievements to date. European Medicines Agency 2007. Available via http://www.emea.europa.eu/pdfs/human/phv/30816707en.pdf Accessed Dec 18 2007.

[9.] Good Pharmacovigilance Practices. European medicines Agency 2012. Available via http:// www.ema.europa.eu/ema/index.jsp?curl=pages/regulation/document_listing/document_listing_0 00345.jsp&mid=#section1 Accessed March 1, 2012.

[10.]   Heath G, Colburn WA. An evolution of drug development and clinical pharmacology during the 20th century. J ClinPharmacol 2000; 40:918-29.

[11.]   Hugman B. The Ericedeclaration : the critical role of communication in drug safety. Drug Saf 2006; 29:91-3.

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[15.]   Nair MD. Pharmacovigilance: the need for a formal system in India. 2001. Available at the site of Pharmabiz www.pharmabiz.com http://www.pharmabiz.com/article/detnews.asp?articleid = 11329&sectionid = 46 .

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[17.]   Raine JM. Risk management -a European Regulatory View. In: Mann R, Andrews E (eds) Pharmacovigilance.2nd edn 2007. Wiley, Chichester.

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Abstract:

In this article review, I will outline and discuss in different paragraphs, significance of the article, whether this fit to the existing literature; its accuracy, article structure, its objectivity, and we will briefly analyzed different figures and tabulations by reporting types of analysis performed, and I will assess whether the author‘s analysis support reasoning and claims. I will examine whether the analysis support the main findings in this study. I will suggest new information, methodology and other approaches that might bring contributions to the scope or the principal idea of this work. I will compare ideas in this study with other‘s opinions, of course related to the topic. 

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Abstract:

There are conflicting reports regarding menstrual irregularities and HIV infection in women. Varying degrees of menstrual abnormalities have been reported with prolonged ARV use, and these have implications for drug adherence. The objective of this study was to assess the effect of ARV drugs on menstrual pattern among HIV positive women in South-western Nigeria. It was a descriptive cross-sectional survey among 238 HIV positive women on anti-retroviral therapy randomly selected after excluding for co-morbidities. Research instrument was semi structured interviewer administered questionnaires, and data was analyzed using the SPSS software. Level of significance for statistic test was p ≤ 0.05

Mean age of respondents was 38.6±2.3 years and 205(86.1%) had commenced ART for a period of 1-5 years mostly 1st line ART, 45(18.9%) have missed their ARVs at one time or the other in the last 1year. Self reported adherence was good among 227(95.4%), calculated adherence was above 95% among 185(77.7%) with a mean calculated adherence of 93.0±3.6% and a median of 95.0%. About 167(70.2%) of respondents reported a change in their menstrual pattern.

Different patterns of menstrual changes reported were changes in number of days, interval between menstruations and flow of menstrual blood, 52(73.2%) believed that use of ART caused these menstrual changes, only 36(50.7%) reported these changes to the doctor. Predictors of having menstrual disturbances include missing pills, poor adherence and use of ARVs for period longer than 5years. ARVs were found to be common causes of menstrual irregularities. Thus, clients‘ concerns should always be addressed most especially issues that may compromise ARV adherence 

References:

[1.] Abularach, Silvia, and Jean Anderson. 2005. ―Gynecologic Problems.‖ In A Guide to the Clinical Care of Women with HIV, U.S. Department of Health and Human Services, Health Resources and Services Administration, HIV/AIDS Bureau, 177–230.

[2.] Bach, Xuan Tran, Thanh Nguyen Long, Hoang Nguyen Nga, Van Hoang Quynh, and Hwang Jongnam. 2013. ―Determinants of Antiretroviral Treatment Adherence among HIV/AIDS Patients: A Multi Study.‖ Global Health Action 6.

[3.] Chirgwin, KD, J Feldman, O Muneyyirci-Delale, S Landesman, and H Minkoff. 1996. ―Menstrual Function in Human Immunodeficiency Virus-Infected Women without Acquired Immunodeficiency Syndrome.‖ Journal of Acquired Immune Deficiency Syndrome 12(5): 489–94.

[4.] Ellerbrock, TV, TC Wright, TJ Bush, P Dole, K Brudney, and MA Chiasson. 1996. “Characteristics of Menstruation in Women Infected with Human Immunodeficiency Virus.‖ Obstet Gynecol 87(6): 1030–34.

[5.] Harlow SD, Schuman P, Cohen, M, SE Ohmit, S Cu-Uvin, X Lin, K Anastos, D Burns, R Greenblatt, H Minkoff, L Muderspach, A Rompalo, D Warren, MA Young, and RS Klein. 2000. “Effect of HIV Infection on Menstrual Cycle Length”.‖ Journal of Acquired Immune Deficiency Syndrome 24(1): 68–75.

[6.] Hoytt, Mary Jo. 1998. Menstrual Symptoms in HIV Positive Women.

[7.] Maclean, Deirdre. 2000. Menstrual Problems and HIV. Canada.

[8.] New York State Department of Health AIDS Institute. 2011. New York Menstrual Disorders in HIV-Infected Women.

[9.] Nielsen, H. 1999. ―Hypermenorrhea Associated with Ritonavir.‖ Lancet 353: 811–12.

[10.]   Ogundahunsi, O A, M O Ogundipe, N O Akinola, O O Soyinka, A O Odewabi, and Oyegunle V A. 2011. ―The Effect of HIV and Antiretroviral Therapy on Fertility Hormones in Amenorrheic HIV-Positive Women.‖ African Scientist 11(3): 143–46.

[11.]   Okochi, C. A., O. Oladepo, and A. J. Ajuwon. 2000. ―Knowledge about Aids and Sexual Behaviors of Inmates of Agodi Prison in Ibadan, Nigeria.‖ International Quarterly of Community Health Education 19(4): 353–62.

[12.]   Okonko, I O, P O Okerentuga, and Akinpelu A O. 2012. ―Prevalence of HIV among Attendees of ARFH Centre in Ibadan , Southwestern Nigeria.‖ Middle-East Journal of Scientific Research 11(1): 7–12.

[13.]   Olugbenga-Bello, A I, O A Adeoye, and K G Osagbemi. 2013. ―Assessment of the Reproductive Health Status of Adult Prison Inmates in Osun State , Nigeria.‖ International Journal of Reproductive Medicine: 1–9.

[14.]   Omoyeni, Sunday T, Akanni I Akinyemi, and Adesegun Fatusi. 2012. ―Adolescents and HIV-Related Behaviour in Nigeria : Does Knowledge of HIV/AIDS Promote Protective Sexual Behaviour among Sexually Active Adolescents?‖ In Population Association of America Annual Meeting, California, 1–19.

[15.]   Paterson, DL, S Swindells, J Mohr, M Brester, and EN Vergis. 2000. ―Adherence to Protease Inhibitor Therapy and Outcomes in Patients with HIV Infection.‖ Annals of Internal Medicine 133(1): 21–30.

[16.]   Sethi, Ajay K, David D Celentano, Stephen J Gange, Richard D Moore, and Joel E Gallant. 2003. “Association between Adherence to Antiretroviral Therapy and Human Immunodeficiency Virus Drug Resistance.” Clinical Infectious Diseases 37: 1112–18.

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[19.]   Wasti, Sharada P., Padam Simkhada, Julian Randall, Jennifer V. Freeman, and Edwin van Teijlingen. 2012. ―Factors Influencing Adherence to Antiretroviral Treatment in Nepal: A Mixed-Methods Study.‖ PLoS ONE 7(5).

[20.]   Wasti, SP, E Van Teijlingen, P Simkhada, J Randall, and S Baxter. 2011. ―Factors Influencing Adherence to Antiretroviral Treatment in Asian Developing Countries: A Systematic Review.‖ Trop Med Int Health 17: 71–81. 

Abstract:

Human epidermal growth factor receptor -2 (HER-2) is a member of EGFR (epidermal growth factor receptor) family, plays a very significant role in cell growth and proliferation [1] HER – 2 protein is over expressed in 20% of breast cancer and is associated within aggressive course , poor prognosis and response to treatment [2-3]. The introduction of transtuzumab, a monoclonal antibody directed against, the extra cellular domain of HER -2 receptor, has revolutionized the treatment of HER – 2 positive early breast cancer and has led to significant improvement in disease free survival and overall survival over chemotherapy alone. 

In randomized multicenter trials with HER – 2 over expressing metastatic breast cancer patients, addition of transtuzumab to first line chemotherapy has improved objective response rate, the time to disease progression and overall survival over chemotherapy alone [4,5]. Hence transtummab is now considered as the standard of care for all patients who over amplify HER – 2 neu receptors.

These benefits have come with the cost of increased risk of cardiotoxicity. Transtuzumab related cardiotoxicity is mediated by interruption of normal HER – 2 signaling pathway in the heart, which is responsible for maintenance of normal growth, repair and survival of cardiomyocytes. Cardiotoxicity related to transtuzumab is different from that of anthracyclins as it is not dose related and appears to be largely reversible on discontinuation of therapy. There is no alteration is ultra structural abnormalities where as that due to anthracyclins are caused by free radical induced oxidative stress to cardiac muscles cells [12]. 

References:

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[2.] Cardinale D, Colombo A, Torrisi R et al. Transtuzumab induced cardiotoxicity: Clinical and Prognostic implications of troponin I evaluation J Clin Oncol 2010; 28: 3910-3916.

[3.] Cardinale D, Sandri MT. Role of Biomarkers in Chemotherapy induced cardio toxicity Prog Cardiovasc. Dis 2010; 53: 121 – 129.

[4.] Carlson RW, Allred DC, Anderson BO et al. Breast Cancer Clinical practice guidelines in oncology J Natt Compr Cane Netw 2009; 7: 122-192.

[5.] Ewer MS,Vooletich MT,Durand JB et al. Reversibility of Transtuzumab – Related Cardiotoxicity: New Insights Based on Clinical Course and Response to Medical Treatment .J Clinoncol 2005;23:7820-7826.

[6.] Force T.Krause DS, Van Etten A. Molecular mechanisms of cardio toxicity of tyrosine kinase inhibition. Nat Rev Cancer 2007; 7; 332-344.

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[8.] Goldhrisch A, Ingle JN, Gelber RD et al. Thresholds for therapies: highlights of St Gallen International Expert consensus on primary therapy of early breast cancer 2009. Ann Oncol 2009, 20: 1319-1329.

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[10.]   Halyard MY, Pisanoky TM, Ducck AC et al. Radiotherapy and adjuvant transtuzumab in operable breast cancer, tolerability and adverse event data from the NCCTG phase III trail N 9831. J Clin Oncol 2009; 27: 2638 – 2644.

[11.]   Hunt SA. Acc/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to update the 2001 Guidelines for the Evaluation and Management of Heart Failure) J. Am Coll Cardiol 2005; 4b: el – e 82.

[12.]   Hutchins LF, Unger JM, Crowley J J et al. Underreparesentation of patients 65 years of age or older in cancer-treatment trials. N Engl J Med 1999; 341: 2061-2067

[13.]   Ky B, Putt M, SawayaH, French B, Januzzi JL, Sebag IA, Plana JC, Cohen V ,Banchs J, Carver JR, Wiegers SE ,Martin RP, Picard MH, Gerszten RE, Halpern EF ,Passeri J, Kuter I, Scherrer-Crosbie M.. Early increases in multiple Biomarkers Predict Subsequent cardiotoxicity in Breast Cancer patients treated with Doxorubicin, Taxanes and transtuzumab

[14.]   L.Tarantini,S.Gori,P.Faggiano et al.Adjuvant transtuzumab cardiotoxicity in patients over 60 yrs of age with early breast cancer:a multicentric cohort study.Annals of oncology Vol 23 no 12 Dec. 2012

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Abstract:

Enterocutaneous fistula (ECF) is a rare and late complication following mesh repair for incisional hernias. This report is a case series of two patients reporting ECF following 10 and 13 years after open surgery for the incisional hernia. Laparotomy was performed in both and the defect was repaired by anatomical closure without a mesh. This case report emphasizes that although polypropylene mesh has been shown to be relatively safe in many studies, it can at times be associated with long-term ECF. 

References:

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Abstract:

BACKGROUND

Despite the modifications on Oral Contraceptive Pills (OCPs) in term of content and dosage to lessen their side effect, paucity of information existed on the effect of COCP on kidney function.

AIM OF STUDY

Hence, this study investigates the effect of COCP containing 0.15mg levonorgestrel (a progestogen) and 0.03mg ethinylestradiol (an estrogen) on kidney biochemical parameters and electrolytes.

METHODS

The study involves 15 female rabbits divided into three groups (A, B and C). Group A served as the control, while B and C served as the test groups and were administered the COCP per body weight human doses for 7 days and 14 days respectively. At the end of the study, blood sample was obtained for the determination of plasma creatinine, urea, Na, Cl and K using standard laboratory procedures.

RESULTS

Results showed significant increase (p<0.05) in plasma creatinine, urea and K+ but a decreases in plasma Na+ and Cl-in the tests compared to the control.

CONCLUSION

Considering the observed changes in the parameters herein studied, COCPs usage is not without impact on kidney function and may cause homeostasis dysfunction and hence the need for further studies. 

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