Over-the-Counter Medication Use among Parents in Saudi Arabia.

Introduction: Self-medication is a growing public health concern worldwide. Studies have shown a gap between best practice and the current practice of using over-the-counter (OTC) medications. Despite being a well-recognised problem in Saudi Arabia, few studies have investigated OTC medication use in Saudi Arabia. Therefore, this study aimed to investigate the attitudes and knowledge of parents regarding OTC medication use in the Jeddah region, Saudi Arabia. Method: A cross-sectional study was carried out via an electronic questionnaire sent randomly to parents over four months, from 1 January to 30 April 2022. The participants' characteristics and categorical variables were represented descriptively by frequency and percentage. A Chi-square test was used to test the relationship between the variables. Results: In total, 211 questionnaires were included in this study. Females represented 54.5% of the participants included in the study. Parents belonging to the 18-to-30-year-old group comprised the highest percentage (37.9%), and most of the parents (72.9%) had received an undergraduate education. Family physicians were the most common source (37.3%) of information about OTC medications, whereas more than half of parents purchased OTC medications from the community pharmacy (58.8%). While almost half of the parents (52.1%) visited a family physician when side effects of OTC medications appeared in their children, only (33.6%) stopped giving their children the OTC medicine. The relationship between the sociodemographic characteristics (including educational level, marital status, and employment status) and OTC drug consumption was significant (p < 0.001). Conclusion: Educational campaigns are needed to guide patients about the proper use of OTC medications. Studies on OTC medication use are lacking in Saudi Arabia in terms of its frequency, reasons for use, type of self-medication, and contributing factors.

Comparing the renoprotective effects of the antioxidants melatonin, vitamin D and vitamin E in diabetic rats.

OBJECTIVES: Diabetes mellitus is associated with oxidative stress that leads to inflammation and diabetic nephropathy. This study aimed to determine the possible renoprotective effects of the antioxidants melatonin, vitamin D and vitamin E in diabetic rats. METHODS: We divided 108 albino rats into 12 groups. G1 group was fed a normal diet and did not receive any medication. G2 to G4 consisted of non-diabetic rats that were treated as follows: G2 with melatonin; G3 with vitamin E; G4 with vitamin D. Groups G5 to G12 consisted of diabetic rats that were treated as follows: G5 received no medication; G6 treated with insulin; G7 treated with melatonin; G8 treated with melatonin and insulin; G9 treated with vitamin E; G10 treated with vitamin E and insulin; G11 treated with vitamin D and G12 treated with vitamin D and insulin. Two months after treatment commenced, histological and biochemical examinations of glucose profile, oxidative stress status, renal function, homocysteine and TNF-α were performed. RESULTS: Total antioxidant capacity (TAC) increased significantly in groups G2, 7, 8, 10 and 11. TNF-α significantly increased in G2, but decreased in all other groups. Creatinine increased significantly in groups G5, 6, 7, 8, 9, 11 and 12. In the kidneys of the diabetic rats, thickened capillary basement membrane, diffuse mesangial sclerosis and nodular glomerulosclerosis was observed. Rats treated with melatonin showed marked improvement in these symptoms. However, in those treated with vitamin D and E, thickened capillary basement membrane and mesangial sclerosis was still present. CONCLUSIONS: Melatonin, administered either with or without insulin had a significant biochemical antioxidant effect and histological renoprotective effect. Conversely, vitamin D and E did not appear to have any effects on the parameters measured.

Effect of melatonin versus vitamin D as antioxidant and Hepatoprotective agents in STZ-induced diabetic rats.

BACKGROUND: Diabetes mellitus (DM) is a serious chronic disease, with multiple complications including hepatopathy associated with imbalance of the oxidative status. The purpose of this study is to observe possible protective effects of vitamin-D and melatonin on glucose profile, antioxidant-oxidant status, lipid peroxidation, and histopathological protection of the liver in streptozotocin-induced diabetic rats. METHODS: Eighty three male albino rats were divided into nine groups as follows: G1 (n = 10) Normal control rats; G2 (n = 8) were normal rats treated with melatonin only; G3 (n = 10) were normal rats treated with vitamin D only; G4 (n = 9) were diabetic rats, which received no medications; G5 (n = 8) were diabetic rat treated with insulin only; G6 (n = 10) were diabetic rats treated with melatonin only; G7 (n = 9) were diabetic rats treated with melatonin and insulin; G8 (n = 9) were diabetic rats treated with vitamin D only; G9 (n = 10) were diabetic rats treated with vitamin D and insulin. Two months post treatment, blood was collected to measure: Fasting blood sugar (FBS), glycosylated hemoglobin (HbA1c), fructosamine (FA), total antioxidant capacity (TAC), malondialdahyde (MDA). livers were isolated for histopathological study. RESULTS: As compared to normal rats, our results demonstrate that glucose, fructosamine and HbA1c levels is increased in diabetic groups and declined to lesser levels in treated groups. TAC level of diabetic rats is not significantly changed. Vitamin D administration significantly increased TAC while it is not changed with melatonin either in treated or non-treated groups. The liver of diabetic rats shows only mild focal microvesicular fatty degeneration. The liver of diabetic rats treated with insulin shows degeneration of cell edema in the stroma. The liver of diabetic rats treated with melatonin with or without insulin, exhibited marked improvement. The liver of diabetic rats treated with vitamin D with or without insulin, shows degeneration of cells and edema in the stroma. CONCLUSION: Our results demonstrated the beneficial antioxidant effect of vitamin D administration to normal and diabetic rats as compared to melatonin. Nevertheless, melatonin still shows more therapeutic effect on liver cell injury induced by induction of diabetes.

Comparative immunohistochemical expression of ß-catenin, EGFR, ErbB2, and p63 in adamantinomatous and papillary craniopharyngiomas.

UNLABELLED: Craniopharyngiomas (CPs) are rare epithelial tumors located mainly in the sellar/parasellar region. CPs have been classified into histopathologically, genetically, clinically and prognostically two distinctive subtypes: adamantinomatous and papillary variants. AIM: To determine the immunohistochemical expression of ß-catenin, EGFR, ErbB2, and p63 in adamantinomatous and papillary CPs. MATERIALS AND METHODS: ß-Catenin, EGFR, ErbB2, and p63 immunostaining was performed on paraffin embedded tissue sections of 25 CPs including 18 adamantinomatous craniopharyngioma (ACP) and 7 cases of papillary craniopharyngiomas (PCPs). RESULTS: 17 cases (94%) of ACP exhibited strong nuclear/cytoplasmic expression of ß-catenin. On the contrary, all cases of PCP showed exclusively membranous expression (P value<0.0001). Regarding EGFR, 15 (83%) and 5 cases (71%) of APC and PCP respectively were positive. On the other hand, only 3 cases (17%) of APC and none of PCP exhibited positivity for ErbB2. p63 over-expression was observed in 16 cases of ACP (89%) and 6 cases of PCP (86%). However, the distribution of p63 staining was diffuse in ACP, while in PCP; the staining was mainly restricted to the basal cell layer. CONCLUSION: Nuclear accumulation of ß-catenin is a diagnostic hallmark of the ACP and is very helpful in the differential diagnosis between both ACP and PCP in the setting of small biopsies. Moreover, the restricted nuclear ß-catenin accumulation in the cohesive cell clusters within the whorl-like areas supports that aberrant ß-catenin expression may play a role in the morphogenesis of ACP.

Integrative bioinformatics links HNF1B with clear cell carcinoma and tumor-associated thrombosis.

Clear cell carcinoma (CCC) is a histologically distinct carcinoma subtype that arises in several organ systems and is marked by cytoplasmic clearing, attributed to abundant intracellular glycogen. Previously, transcription factor hepatocyte nuclear factor 1-beta (HNF1B) was identified as a biomarker of ovarian CCC. Here, we set out to explore more broadly the relation between HNF1B and carcinomas with clear cell histology. HNF1B expression, evaluated by immunohistochemistry, was significantly associated with clear cell histology across diverse gynecologic and renal carcinomas (P<0.001), as was hypomethylation of the HNF1B promoter (P<0.001). From microarray analysis, an empirically-derived HNF1B signature was significantly enriched for computationally-predicted targets (with HNF1 binding sites) (P<0.03), as well as genes associated with glycogen metabolism, including glucose-6-phophatase, and strikingly the blood clotting cascade, including fibrinogen, prothrombin and factor XIII. Enrichment of the clotting cascade was also evident in microarray data from ovarian CCC versus other histotypes (P<0.01), and HNF1B-associated prothrombin expression was verified by immunohistochemistry (P = 0.015). Finally, among gynecologic carcinomas with cytoplasmic clearing, HNF1B immunostaining was linked to a 3.0-fold increased risk of clinically-significant venous thrombosis (P = 0.043), and with a 2.3-fold increased risk (P = 0.011) in a combined gynecologic and renal carcinoma cohort. Our results define HNF1B as a broad marker of clear cell phenotype, and support a mechanistic link to glycogen accumulation and thrombosis, possibly reflecting (for gynecologic CCC) derivation from secretory endometrium. Our findings also implicate a novel mechanism of tumor-associated thrombosis (a major cause of cancer mortality), based on the direct production of clotting factors by cancer cells.

ProExC is a novel marker for distinguishing between primary endometrial and endocervical adenocarcinomas.

BACKGROUND: Distinguishing endocervical adenocarcinoma (ECA) from endometrial adenocarcinoma (EMA) is clinically significant and cannot always be made on the basis of morphology alone or clinical findings. The aim of this study was to study the potential utility of ProExC as a new marker for cervical adenocarcinoma, and to evaluate a panel of monoclonal antibodies composed of p16, ER, PR, and vimentin, and assess their diagnostic value in distinguishing between ECA and EMA. METHODS: Immunohistochemistry using monoclonal antibodies to ProExC, p16, estrogen receptor (ER), progesterone receptor (PR), and vimentin, was performed to examine 30 cases, including 10 ECAs and 20 EMAs. RESULTS: Eight out of 10 cases (80%) of ECA were positive for ProExC, whereas only 2 cases of EMA (10%) were positive. The difference of ProExC expression in the two groups of malignancy was statistically significant (p=0.003). P16 was positive in 8 cases (80%) of ECAs and in 4 cases (20%) of EMAs. Estrogen receptor was negative in all cases of ECA, while it was positive in 95% of EMA. Progesterone receptor was positive in 2 cases (20%) of ECA and in 16 cases (80%) of EMA. Vimentin was positive in only one case (10%) of ECA, and in 16 cases (80%) of EMA. CONCLUSION: ProExC is a novel immunohistochemical marker for differentiating ECA from EMA and its inclusion in a panel of immunohistochemical markers including p16, ER, PR, and vimentin is recommended when there is morphological and clinical doubt as to the primary site of endocervical or endometrial origin.

Expression of the urothelial differentiation markers GATA3 and placental S100 (S100P) in female genital tract transitional cell proliferations.

The degree of urothelial differentiation in putative transitional (urothelial) proliferations in the female genital tract is still controversial. To further investigate the similarities (or dissimilarities) between female genital tract transitional proliferations and bladder urothelium, we evaluated the expression of S100P and GATA3, 2 proteins that we previously found to be strongly expressed in bladder urothelial tumors, in 25 benign ovarian Brenner tumors, 19 Walthard cell nests (17 tubal and 2 ovarian hilus), 1 mature teratoma with a benign urothelial proliferation, 2 proliferating (borderline) ovarian Brenner tumors, 1 malignant Brenner tumor, and 12 ovarian transitional cell carcinomas (TCC). Each lesion was also evaluated for p63 expression by immunohistochemistry. Immunostaining was performed on formalin-fixed, paraffin-embedded tissue sections using the avidin-biotin-peroxidase complex method. Eighty-eight percent of Brenner tumors were positive for S100P, whereas 96% and 100% were positive for GATA3 and p63, respectively. One of 2 proliferating Brenner tumors was positive for S100P, whereas both cases were positive for GATA3 and p63; the malignant Brenner tumor was positive for S100P and p63, but negative for GATA3. Only 17% of TCC were positive for S100p, whereas 33% and 50% of TCC were positive for GATA3 and p63, respectively. Tubal Walthard cell nests were either completely negative or showed only scattered positive staining for S100P; in contrast, 89.5% and 100% of Walthard nests, including the 2 ovarian cases were positive for GATA3 and p63. The teratoma-associated benign urothelial proliferation was also negative for S100P, but positive for GATA3 and p63. Although proliferating and malignant Brenner tumors may exhibit a more intermediate immunoprofile, expression of S100P, GATA3, and p63 by a majority of ovarian Brenner tumors underscores the similarity between these neoplasms and urothelial proliferations of bladder origin. The indeterminate phenotype seen in Walthard nests and ovarian TCC suggests that these proliferations may represent an incomplete or alternate form of differentiation.

Oncofetal protein glypican-3 distinguishes yolk sac tumor from clear cell carcinoma of the ovary.

Clear cell carcinoma (CCC) of the ovary is the surface epithelial neoplasm most often confused with primitive germ cell tumors, particularly yolk sac tumor (YST) and dysgerminoma. OCT3/4 has proven to be a sensitive and relatively specific marker for the latter entity, but existing markers for YST are limited. Recent studies suggest that glypican-3 (GPC3), an oncofetal protein expressed in fetal liver and malignant tumors of hepatocytic lineage, is also expressed in germ cell tumors, particularly YST. To investigate whether GPC3 is useful in distinguishing YST from ovarian CCC, we studied the expression of GPC3 in a large series of ovarian neoplasms and compared it to the expression profiles of CK7 and alpha-fetoprotein. Tissue microarrays containing over 400 benign and malignant ovarian neoplasms, including 34 CCCs were stained with monoclonal GPC3 (clone 1G12, Biomosaics, Burlington, VT). These arrays contained a wide assortment of ovarian surface epithelial neoplasms and sex cord stromal neoplasms, as well as germ cell tumors. Full paraffin tissue sections from 32 YSTs and 10 CCCs were also assessed. All but one YST (97%), including those associated with mixed germ cell tumor were positive for GPC3, whereas all teratomas and embryonal carcinomas were negative. Both cytoplasmic and membrane staining were present in the positive cases, with no background staining. The syncytiotrophoblastic cells in the germ cell tumors and placental villi included in the arrays were also positive for GPC3. Most CCCs (83%) were completely negative for GPC3, as were 99% serous, 94% endometrioid, and 100% mucinous tumors. Five CCCs exhibited focal, moderate to strong GPC3 expression and in 2 the expression was focal and weak. All other tissues, including normal ovary were negative for GPC3. GPC3 seems to be a promising diagnostic marker for differentiating YST from ovarian CCC (P < 0.0001). Because GPC3 may be associated with alpha-fetoprotein expression, further studies are required to determine the utility of GPC3 in differentiating YST from CCC with hepatoid differentiation.