Background: Tetralogy of Fallot (TOF) is a very common cyanotic congenital heart disease presenting early at birth with various degrees of cyanosis. If left uncorrected surgically, can lead to death.
Objectives: This study is aimed at determining pattern and surgical outcome of children with teratology of Fallot in a budding health facility in India over a year period.
Result: A total of 51 children were diagnosed of TOF over the period, of which 66.7% were males with mean age of 48.14 ± 45.36 months.
The surgical outcome showed only 3.9% mortality. The death was among children >1 to 5 years. The mean number of days in intensive care unit (ICU) was 5.8 ± 11.2 days. 82.4% of the patients were off-pump post-operatively, compared to 17.6% with re-pump. Among those who had re-pump, 77.8% were males and among those without re-pump, 64.3% were likewise males (χ2 = 0.6, p = 0.41). About 92.2% (47/51) of patients had pulmonary regurgitation post-op, ranging from mild to moderate regurgitation. 51.1% of the regurgitations were mild while 25.5% and 23.4% were moderate and severe regurgitations respectively.
Post-operative VSD was detected in 51% (26/51) of the patients. The post-op right ventricular pressure (RVOT) was significantly lower than that of pre-op pressure, 10.8 ± 1.5 mmHg vs. 31.7 ± 4.5 mmHg (pair t test = 8.7, p < 0.001).
Conclusion: Timely surgical repair is crucial in alleviating several morbidity and mortality associated with teratology of fallot. Pulmonary regurgitation is a very common sequel after surgery and can result in death.
With the discovery by Calghatgi (2013) that three common antibiotics (Abs) increased mitochondrial reactive oxygen (ROS) and lipid peroxide (LP) and depleted their natural absorbant glutathione led me to investigate further the potential impacts of these genotoxic substances on carcinogenesis. The range of impacts on mitochondria and cellular DNA varied by antibiotic to those consistent with known prior contributions to carcinogenesis. Specific cancers probably increased by these changes were HCC, RCC (KCC), CRC, cancer of the esophagus. Tumor suppressor gene mutations resulting from LP were noteworthy in this regard and mutations induced in CRC were consistent with those found in carcinogenesis of CRC. In addition depression of short chain fatty acids in microbiomes were found which depress the immune system increasing risk of all cancers. Many cancers were increased according to epidemiological studies linking Abs with elevated odds ratios, with one concern in particular, fatal breast cancer. The impact of loss of functionality of the mitochondria was also linked to depression of the citric acid cycle and therefore ATP which deflected metabolism to glycolysis, the Warburg mechanism also increasing risk of all cancers, favoured by cancer cells. In conclusion, some portion of many cancer types are probably increased in likelihood by number, type and frequency of Abs treatment and chronic residue exposure which varies from individual to individual. This led me to propose a three pronged carcinogenesis mechanism for Abs. 1. Cancer critical mutations 2. Immune depression 3. loss of mitochondrial functionality leading to Warburg effects. Damage to mitochondria were also noted by common pesticides tested in China and cancer associations were also found for many pesticides supporting a similar contributory etiology. Heart health concerns were raised by these findings because of the myriad mitochondria in the heart and because of long term reliability needs. Studies suggesting hearts were affected by Abs and pesticide exposure were presented. Because of their geographical ubiquitousness and the huge range of diseases associated with mitochondrial dysfunction, antibiotics and pesticides and bacteriocidal biocides are of concern for biodiversity and life in general. I propose research steps to evaluate Abs safety and suggest directions for further research and make suggestions on ways to ameliorate Abs toxicity.
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