ABSTRACT
Purpose: Chronic rhinosinusitis (CRS) is a widely prevalent condition globally as well as in India. The spectrum of fungal involvement in CRS runs from benign colonisation to potentially life-threatening invasive disease. Successful treatment of such mycotic infections largely depends on the accurate identification of the pathogen, early and appropriate intervention by surgical clearance, supported with antifungal medication as per standard regimen. Thus, this study was undertaken to determine the prevalence of fungal rhinosinusitis (FRS), and to analyse its clinicomycological profile. Materials and Methods: Fifty-two patients with clinical suspicion of CRS attending a tertiary care hospital during a one-year period were included in this retrospective analysis. The sinonasal specimens were subjected to microscopy by KOH mount and fungal culture as per standard mycological technique. Tissue specimens were also subjected to histopathological examination. Results: Male to female ratio was 1.25:1; age varied from 14 years to 62 years with majority of patients (37%) belonging to age group 21-40 years. The prevalence of FRS was 44%, and 74% of it was caused by Aspergillus sp. Aspergillus flavus (A. flavus) (52%) was the most prevalent fungus isolated. Allergic fungal rhinosinusitis (AFRS) was the most common presentation (79%). Conclusion: FRS is a continuous spectrum of disease varying in presentation, treatment and long-term sequelae. Correct identification of the fungus remains essential for appropriate treatment.
ABSTRACT
The amino acid homocysteine (Hcy), formed from methionine has profound importance in health and diseases. In normal circumstances, it is converted to cysteine and partly remethylated to methionine with the help of vit B12 and folate. However, when normal metabolism is disturbed, due to deficiency of cystathionine-beta-synthase, which requires vit B6 for activation, Hcy is accumulated in the blood with an increase of methionine, resulting into mental retardation (homocystinuria type I). A decrease of cysteine may cause eye diseases, due to decrease in the synthesis of glutathione (antioxidant). In homocystinurias type II, III and IV, there is accumulation of Hcy, but a decrease of methionine, thus, there is no mental retardation. Homocysteinemia is found in Marfan syndrome, some cases of type I diabetes and is also linked to smoking and has genetic basis too. In hyperhomocysteinemias (HHcys), clinical manifestations are mental retardation and seizures (type I only), ectopia lentis, secondary glaucoma, optic atrophy, retinal detachment, skeletal abnormalities, osteoporosis, vascular changes, neurological dysfunction and psychiatric symptoms. Thrombotic and cardiovascular diseases may also be encountered. The harmful effects of homocysteinemias are due to (i) production of oxidants (reactive oxygen species) generated during oxidation of Hcy to homocystine and disulphides in the blood. These could oxidize membrane lipids and proteins. (ii) Hcy can react with proteins with their thiols and form disulphides (thiolation), (iii) it can also be converted to highly reactive thiolactone which could react with the proteins forming -NH-CO- adducts, thus affecting the body proteins and enzymes. Homocystinuria type I is very rare (1 in 12 lakhs only) and is treated with supplementation of vit B6 and cystine. Others are more common and are treated with folate, vit B12 and in selected cases as in methionine synthase deficiency, methionine, avoiding excess. In this review, the role of elevated Hcy levels in cardiovascular, ocular, neurologial and other diseases and the possible therapeutic measures, in addition to the molecular mechanisms involved in deleterious manifestations of homocysteinemia, have been discussed.