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The aim of work is description of new observations related to the participation of demodex in tumor morphogenesis with goal to study the example of eyelid papilloma, imagine the connection between the presence of the demodex mite and certain changes in the typical histomorphological picture of the neoplasm.

Materials and methods: Histomorphological examination covers biopsy and operative material of eye pathology with diagnosis of neoplasm (eyelid papilloma and actinic keratosis (senile keratosis, senile keratoma, solar keratosis)) were selected, with special attention paid to the presence of horn cysts. Agile methodologies were employed to manage the research workflow effectively.

Results: As a result of the conducted histomorphological examination, in 24 cases (48%), patterns pathognomonic for demodectic infection were found. Such patterns, which could indicate the presence of a demodex mite, were cystic formations, as well as fragments of a dead parasite. We noted their presence not only in the tumor tissue, but also in the adjacent hair follicles, sebaceous glands, and subepidermal stroma. It is no coincidence that the authors who previously noted the presence of pigmented elements in keratopapillomas or seborrheic keratomas could not explain their origin, resorting to putting forward such fantastic assumptions as the presence of "symbiosis of melanoblasts and epithelial cells, which ensures the transfer of pigment from the first to the second".

Conclusions: Histomorphological study of serial sections allows us to see the successive stages of transformation of cavity intratissue defects created by the activity of the mite into horn cysts. Cavity defects are the main evidence of demodectic infestation. They occur in basal cell and squamous cell carcinomas, xanthomas, sebaceous adenomas, etc. tumors of the eyelids, but only in keratoacanthomas and senile keratomas they can turn into corneal cysts, which can be assumed to be due to the differentiating potential of these neoplasms.

The incidence of hyperlipidemic acute pancreatitis (HLAP) has been increasing annually. However, it is unclear whether there is a correlation between serum inflammatory factors and HLAP. This study aimed to explore the relationship between serum inflammatory factors and HLAP.

Methods: In this study, sixty patients with hyperlipidemic severe acute pancreatitis were registered from January 2020 to December 2024 at our hospital. Sixty healthy volunteers who underwent physical examination at the hospital physical examination center during the same period were selected as controls. Th1/Th2 cells, high-sensitivity C-reactive protein (hs-CRP), interleukin-17 (IL-17), tumor necrosis factor-alpha (TNF-α) were compared between two groups.

Results: The BMI level of the HLAP group was higher than that of the control group. The levels of hs-CRP, IL-17, and TNF-α in the HLAP group were higher than those in the control group.

Conclusion: High BMI, hs-CRP, IL-17, and TNF-α levels may be risk factors for HLAP.

The study was carried out electrophysiological effects of hydrocortisone for protection on the prelimbic cortex (PrL) neurons in rats, particularly in response to high-frequency stimulation (HFS) of the Caudate-Putamen nuclear complex (CPu) on the models of Parkinson's disease (PD). The study involved 19 rats of the Albino line, each weighing 250 gr. The rats were divided into three experimental groups: intact, rotenone model of Parkinson's disease (PD), and rats with PD but treated with hydrocortisone for protection. Extracellular recording was conducted to measure the impulse activity of single neurons in the prelimbic cortex (PrL) particularly in response to high-frequency stimulation (HFS) of the Caudate-Putamen nuclear complex (CPu) on the models of PD and PD treated with hydrocortisone for protection. In rats with the PD model, there was a decrease in post-stimulus synaptic depressor tetanic effects compared to the norm. This means that the ability of synapses to depress their activity after stimulation was reduced in PD. Conversely, excitatory effects increased in PD rats compared to the norm. This indicates an increase in the excitatory response of neurons in the PD model. When hydrocortisone was applied in PD rats, the frequency of impulse activity dropped sharply, even falling below the levels observed in the normal condition. This indicates that hydrocortisone treatment mitigated the heightened neural activity induced by PD, possibly returning it to a more normal state. Overall, these findings suggest that PD alters synaptic responses and neural activity in the PrL, and hydrocortisone treatment seems to reverse some of these effects.

The aim of the study was to investigate the value of intravitreal injection conbercept on the best-corrected visual acuity in patients with age-related macular edema.

Methods: In this study, 114 patients (114 eyes) were treated with intravitreal injection of Conbercept in our hospital from August 2020 to January 2022. According to the clinical effect after treatment, they were divided into effective group (78 cases, 78 eyes) and ineffective group (36 cases, 36 eyes). All patients were continuously treated with intravitreal injection of Conbercept. The best corrected visual acuity (BCVA) was compared between the two groups.

Results: Before treatment, the BCVA was compared between the effective group and the ineffective group (P>0.05). After 1, 2, and 3 times of treatment, the BCVA values of the effective group were lower than those of the ineffective group, and the BCVA changes of the effective group before and after treatment were greater than those of the ineffective group (P<0.05).

Conclusion: The BCVA values of the effective group were lower than those of the ineffective group, and the BCVA changes of the effective group before and after treatment were greater than those of the ineffective group, suggesting that conbercept can improve the visual acuity of patients with macular edema caused by wet age-related macular degeneration.

Modern skin cancer pathogenesis includes new concepts such as nitroso photocarcinogenesis and nitroso-mediated photosensitivity. The above 2 new concepts are in all likelihood also modeled/determined by photocarcinogens known as nitrosamines and/or NDSRIs available as contaminants in many drugs worldwide. The phototoxicity of nitrosamines is a known nonspecific property of them, for which evidence exists as far back as 1972. Current data from 2023/2024 are completely supportive of nitrosamines identified in drugs, with genotoxicity and phototoxicity proven once again. Regulators' data on polycontamination of a drug with up to several nitrosamines at the same time are of concern. The carcinogens/mutagens in question could also act as bi-/polycarcinogens depending on whether they are metabolized or not. Permanent combined intake of potentially/actually nitrosamine-contaminated drugs appears to be key in the subsequent development of multiple cutaneous tumours, according to new findings in the literature. The localization of these tumours in areas exposed to intense solar radiation could also be seen as indirectly pointing to the presence of certain photosensitisers in the human body. Some of these nitrosamines are photocarcinogens and human carcinogens at the same time. The identification and specification of each of these genotoxic photosensitizers in drugs has yet to be further investigated in detail. The FDA identifies them currently as substances with carcinogenic potency. The clinicopathologic correlations published to date within the intake of potentially contaminated drugs are indicative of 1) the need to redefine skin cancer pathogenesis and 2) the subsequent possible introduction of complete elimination regimens against nitrosamines. We inform about another polymedication intake in a patient with arterial hypertension and diabetes mellitus, which includes the following medications: gliclazide 60 mg once daily and metformin hydrochloride 850 mg once daily, both since 24 years ; sotalol hydrochloride 80 mg since 2 years; bisoprolol fumarate 5 mg since 17 years; candesartan cilexetil/hydrochlorothiazide 16 mg/ 12.5 mg since 2 years; and lercanidipine hydrochloride 20 mg also since 2 years. Within this intake, it is notable that 1) all 6 of these drugs appear in the databases for possible availability as nitroso compounds, and that 2) this is the seventh consecutive keratinocyte tumor treated surgically (in this period). In the presented patient, surgical treatment was performed using a shark pedicle island flap for BCC of the nose, which is an ideal option for tumors with location in the alar or periralar area. An optimal postoperative outcome was achieved. This article focuses on the possible role of drug-mediated photo nitrosogenesis/ carcinogenesis of skin cancer by briefly reviewing and analyzing the available literature to date.

Clinical practice guidelines aim to facilitate early diagnosis, implement early treatment and minimise gaps in care regardless of physician expertise or level of seniority. Consensus guidelines must be adapted to meet local and regional differences allowing for optimum benefit with what is available in terms of diagnostics and treatments. Childhood and adolescent obesity are no exception to this. In this survey we aim to understand practice variation and gaps to better advocate for a regional and local care plan for obesity care in the young.

Methods: A questionnaire was conducted between July 2024 and August 2024, aimed at healthcare professionals of all medical specialties. It consisted of 104 questions.

Results: Family medicine consultants treat most obese youth in Jordan. Several gaps were identified in the assessment and care of patients, including but not limited to psychosocial effects of obesity and efficient multidisciplinary teamwork.

Conclusion: Clear consensus guidelines are necessary to tackle childhood and adolescent obesity in Jordan.

Linear scleroderma of head and face (LSH) in children is a severe disorder, that results in hemiatrophy of skin, subcutaneuse tissue, bones with functional disabilities, neurologic disorders and uveal involvement. The aim of the research was to establish uveal involvement in children with hemifacial scleroderma. Materials and methods: A retrospective analysis was done in a group of 110 children with hemifacial scleroderma. A comprehensive clinical, laboratory and instrumental examination was performed, including MRI of the brain, EEG, and an ophthalmologist's examination, which included visometry, biomicroscopy, and ophthalmoscopy. Results: 10 cases of uveal involvement were detected (9% of 110 pt). 9 patients had anterior segment inflammation (iridocyclitis), in 2 iridocyclitis was combined with retinal changes (in 1- peripheral focal chorioretinitis, in 1- iridocyclitis and central focal chorioretinitis). In one case, iridocyclitis was combined with optic neuropathy. In 3 children uveitis appeared at the disease debute, in the others 3-10 years later. Uveal inflammation in all cases was on the side of scleroderma skin involvement. In 3 children uveitis was bilateral. Seizures and concomittant foci in white matter of the brain were detected in 2 children with uveitis. 90% of the group had positive antinuclear factor. Persistent decrease in visual acuity developed in 3 patients. Соnclusion: Patients with LSH must undergo routine eye examination using basic ophthalmological techniques (visometry, biomicroscopy, ophthalmoscopy) every 6 months and highly necessary in case of relapse of scleroderma We assume that patients with UI in LSH must be defined as patients with JSS and treated intensively with systemicglucocorticoids, cytostatics and even biologics in case of resistance.

A high level of hemoglobin and hematocrit is one of the most important laboratory indicators of polycythemia vera (PV). Nevertheless, in some cases, these indicators may be normal or below the norm. This form of the disease is called latent or masked PV (LPV). It has been found that thrombohemorrhagic complications (THC) are more common in LPV patients than in classic PV (CPV) patients. The relationship between JAK2 gene mutation allele burden, thrombocytosis, leukocytosis level and the occurrence of thrombosis during LPV was analysed in different studies. The results some of them were conflicted. It is also possible that this situation occurs due to the delay in diagnosis and treatment of patients with LPV.

Aim: investigate the laboratory and clinical features of the latent form of PV.

Materials and methods: An analysis of PV patients registered in 2019-2020 was conducted. Out of them patients with LPV were distinguished. During diagnosis of the disease, general blood analysis, trepanobiopsy and histological examination of bone marrow, molecular genetic examination of peripheral blood and bone marrow were performed. All numerical indicators obtained in the course of the research were statistically analyzed taking according to the modern recommendations. Indicators in the groups were arranged in the order of variation, and the average indicator, standard error of this indicator, confidence interval for the 95% confidence level (CI-confidence interval) were calculated for each order. For comparing the groups, the integrity criterion p was taken into account. Calculations were performed using ONE-WAY-ANOVA calculation software.

Results: We study 101 patients. Out of them 36 patients with latent polycythemia were identified. The clinical and laboratory parameters of patients with LPV and CPV were compared. In latent PV the complaints of patients were less intense; the size of the spleen was smaller; thrombotic complications were more often; hemoglobin, hematocrit, erythrocytes count was lower; the number of platelets was higher; leukocytes count and JAK2М617F gene allel burden were not statistically different. The most part of LPV patients, in contrast to CPV patients, was in a high-risk group of THC.

Conclusion: According to the obtained results, it can be concluded that timely and correct diagnosis of LPV is very important. Despite the fact that disease passes in a latent, masked form, THC are more likely to occur. This can be attributed to the high platelet count in the blood and the lack of timely treatment of the disease.

In recent years, the prevalence of thoracic aortic aneurysm has increased, and in most cases this pathological condition is diagnosed accidentally. The aim of the current study was to determine the relationship of clinical, laboratory and morphological data with the presence of aorta wall dissection in patients with thoracic aortic aneurysm to reveal factors associated with aorta dissection.

Materials and methods: The following data of 109 patients mean aged of 53 years with thoracic aortic aneurysm (43 patients with aortic dissection) were analyzed: presence/absence of arterial hypertension, indicators of general blood analysis and blood biochemistry, immunomorphological characteristics of the expression of Von Willebrand factor.

Results: Statistically significant differences were found between the incidence of arterial hypertension with respect to the presence or absence of aortic dissection (p=0.002), the relationship between the content of lymphocytes (p=0.021), segmented neutrophils (p=0.001) and the presence of Von Willebrand factor in the medial layer of the aorta, i.e., the prevalence of vasa vasorum (p=0.018), with aortic dissection. The average expression area of Willebrand factor in the medial layer of the aorta during dissection was 3.6 (1.5)%, and in patients without aortic dissection - 0.8 (0.3)%.

Conclusion: The results of the study indicate that aortic dissection in patients with thoracic aortic aneurysm is associated with high blood pressure and is accompanied by the development of an inflammatory reaction.

The present study meticulously delineates the biochemical alterations in serine protease activity and various life variables in patients with kidney failure compared to a control group. By evaluating 160 samples, comprising 80 from individuals with renal failure and 80 from healthy controls, the researchers observed a significant elevation in serine protease activity among kidney failure patients (274.38 ± 1.55 U/L) relative to the control group (173.78 ±1.49 U/L). Beyond serine protease, other enzymes such as lactate dehydrogenase, basal phosphatase, myeloperoxidase, peroxidase, and aspartate aminotransferase also showed heightened activities in renal failure patients; alanine aminotransferase similarly exhibited a notable increase. Conversely, catalase and arylesterase activities were markedly reduced in these patients compared to controls. The mineral profile revealed substantial decrements in calcium, iron, copper concentrations alongside potassium levels in kidney failure sufferers while showing pronounced increments in phosphate, zinc, and sodium concentrations. Furthermore, protein profiles indicated a stark decrease in total protein, albumin levels along with triglycerides and various cholesterol forms except for high-density lipoprotein cholesterol which increased significantly alongside urea, creatinine and glucose levels; globulin and uric acid also saw considerable elevations when contrasted with the control group's data. These comprehensive findings underscore the profound metabolic disruptions inherent to kidney failure while providing pivotal insights into enzyme activities and mineral imbalances associated with this condition.