Willingness of Family Caregivers to Consent to Relative's Postmortem Examination that Die Suddenly in a Nigerian Tertiary Hospital.

BACKGROUND: Postmortem examination is necessary to diagnose the cause of sudden death, and family caregivers are expected to consent to this examination. This study assessed knowledge, attitude, practices and willingness of family caregivers to consent to postmortem examination of their relative if they die suddenly in a Nigerian tertiary hospital. METHODS: Descriptive cross-sectional study of family caregivers of our patients that completed an interviewer administered semistructured questionnaire assessing their knowledge, attitude, practices and willingness to consent to postmortem examination of their relative if they die suddenly. Data were analyzed using descriptive and inferential statistics. RESULTS: A total of 224 caregivers were interviewed. The mean age (SD) was 34.95 (11.74), ranging 22-75 years. They were parents (32.6%), siblings (37.9%), spouses (11.2%) and other relatives (18.3%). Only 17% had adequate knowledge, 44.6% positive attitude and 11.2% good practices to postmortem examination of sudden death. The majority (75.9%) would consent to postmortem examination of their relatives if they die suddenly. Sociodemographic variables associated with willingness to consent to postmortem examination after relative's sudden death include being male (AOR 3.61; 95%CI 3.09-8.92; p=0.001), having tertiary education (AOR 4.83; 95%CI 1.01-8.29; p=0.034), Christianity (AOR 2.59; 95%CI 1.25-5.35; p=0.010) and skilled worker (AOR 1.43; 95%CI 1.33-3.80; p=0.020). CONCLUSION: Some family caregivers would not consent to postmortem examination of their relatives when they die suddenly. Sensitization programs targeting family caregivers are necessary to increase knowledge and enhance prevention of sudden death as well as improve willingness to consent to postmortem examination when their relatives die suddenly.

Protective Effect of Kolaviron on Cyclophosphamide-Induced Cardiac Toxicity in Rats.

BACKGROUND: Cyclophosphamide (CP) is a nitrogen mustard alkylating drug used for the treatment of chronic and acute malignant lymphomas, myeloma, leukemia, neuroblastoma, adenocarcinoma, retinoblastoma, breast carcinoma, and immunosuppressive therapy. Despite its vast therapeutic uses, it is known to cause severe cardiac toxicity. Kolaviron (KV), a Garcinia kola seed extract containing a mixture of flavonoids, is reputed for its antioxidant and membrane stabilizing properties. OBJECTIVE: This study investigated the protective effect of KV on CP-induced cardiotoxicity in rats. METHODS: Thirty rats were used, and they were divided into 6 groups of 5 rats each. Group I received 2 mL/kg propylene glycol orally for 14 days; group II received CP (50 mg/kg/d, intraperitoneally [i.p.]) for 3 days; groups III and IV received 200 and 400 mg/kg/d KV, respectively, orally for 14 days and groups V and VI were pretreated with 200 and 400 mg/kg/d KV, respectively, orally for 14 days followed by CP (50 mg/kg/d, i.p.) for 3 days. RESULTS: CP treatment resulted in a significantly lower food consumption and body weight in rats. The lactate dehydrogenase and creatine kinase enzymes in cardiac tissues of rats treated with CP were significantly higher. In cardiac tissues, 3-day doses of CP resulted in significantly higher heart weight, cardiac troponin I, myeloperoxidase, malondialdehyde, hydrogen peroxide and lower superoxide dismutase, catalase, glutathione peroxidase activities, and reduced glutathione levels. Histological examination of cardiac tissues showed sign of necrosis of myocardium after CP treatment. However, administration of KV at 200 and 400 mg/kg for 14 days prior to CP treatment, increase food consumption, body weight, and attenuates the biochemical and histological changes induced by CP. CONCLUSIONS: These results revealed that KV attenuates CP-induced cardiotoxicity by inhibiting oxidative stress and preserving the activity of antioxidant enzymes.

Combined Administration of l-Carnitine and Ascorbic Acid Ameliorates Cisplatin-Induced Nephrotoxicity in Rats.

OBJECTIVES: Cisplatin (CIS) is an effective antitumor drug. However, its clinical use is limited due to nephrotoxicity. l-Carnitine and vitamin C are both natural antioxidant that can be obtained from diets. This study investigated the effects of l-carnitine and/or vitamin C in rats against cisplatin-induced nephrotoxicity. METHODS: Twenty-five male Wistar rats were divided into 5 groups of 5 rats each. Group 1, normal control. Group 2, positive control, received cisplatin (10 mg/kg/day intraperitoneally [i.p.]) for 3 days. Groups 3, 4, and 5 received cisplatin for 3 days and thereafter l-carnitine (50 mg/kg/day), vitamin C (100 mg/kg/day), or their combination, respectively, for 28 days. At the end of the study, a biochemical study was carried out in which nephrotoxicity markers, electrolytes, hematological indices, oxidative stress biomarkers, and renal histopathological alterations were evaluated. RESULTS: CIS-treated rats developed significant polyuria, increase in the plasma levels of creatinine, urea, and inorganic phosphate (Pi), alteration in hematological parameters, and decrease in plasma levels of Na+, Cl-, K+, Ca2+, and Mg2+. Measurements of 24-hour urine output demonstrated markedly decreased creatinine and urea and increased Na+, Cl-, K+, Ca2+, and Mg2+ levels in the CIS-treated group, whereas Pi levels were not changed. It also caused significantly decreased catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) levels in the rats' kidneys. Histopathological scores revealed renal tubular damage in CIS-treated rats. However, l-carnitine, vitamin C, or their combination significantly attenuated the alterations caused by CIS in the plasma and kidneys of the rats. CONCLUSION: l-Carnitine and vitamin C administration ameliorated CIS-induced nephrotoxicity due to their antioxidant and anti-inflammatory effects.

The Garcinia kola biflavonoid kolaviron attenuates experimental hepatotoxicity induced by diclofenac.

This study sought to investigate the effects of kolaviron on diclofenac-induced hepatotoxicity in rats. Sixty male Wistar rats were divided into 6 groups of 10 rats each as follows: a control group that received oral propylene glycol and treatment groups that received diclofenac alone, diclofenac followed by Livolin Forte (a reference drug), or diclofenac followed by kolaviron at three different doses. At the end of the study period, five rats per group were sacrificed under ketamine hydrochloride anesthetic, 24h after treatment, while the other 5 rats in the group were allowed to recover for 2 weeks before being sacrificed. Liver enzyme activities, total bilirubin levels, and the concentrations of several pro-inflammatory cytokines were determined using plasma samples, while liver tissue samples were used for antioxidant analysis and histopathological examination. Compared with the control group, plasma liver enzyme activities, along with bilirubin levels, were higher in the groups that received diclofenac alone or diclofenac+the highest dose of kolaviron, respectively. These groups had higher plasma concentrations of pro-inflammatory cytokines than did the control group. However, the administration of Livolin Forte and kolaviron (at the lower doses) ameliorated diclofenac-induced hepatic injury by improving antioxidant status, preventing an increase in inflammatory mediators, decreasing malondialdehyde, and attenuating the adverse effect of diclofenac on hepatic tissues. In addition, there was a significant difference in the histological scores between the groups that received either diclofenac alone or diclofenac followed by the highest dose of kolaviron when compared with the other three groups (Livolin Forte or lower doses of kolaviron). In conclusion, kolaviron appears to be as effective as Livolin in attenuating DCLF-induced hepatotoxicity in rats. However, high doses of kolaviron seem to cause damage to the liver.