Generalized Papulovesicular Eruption as a Side Effect of the Pfizer-BioNTech COVID-19 Vaccine.

COVID-19 is inflicted by SARS-CoV-2 and resulted in a global health crisis that necessitated the urgency of vaccine development to prevent its spreading among the public. Pfizer-BioNTech COVID-19 is one of the emergency use authorized (EUA) vaccines. This vaccine is efficacious against the SARS-CoV-2 virus; nonetheless, recipients have frequently reported side effects. Recipients of this vaccine experienced miscellaneous side effects like fatigue and headache. However, cutaneous eruptions of varying degrees of severity and involvements have been manifesting post-vaccination. Dermatological eruptions following vaccination against COVID-19 disease are poorly recognized. Dermatological manifestations triggered post-vaccination differ in the clinical context and patient's demographic features. The only constant factor is various clinical and histopathological relations to establish the diagnosis of cutaneous eruption post-vaccination. Herein, we report a case of an 18-year-old male with T-cell acute lymphocytic lymphoma (ALL) in remission since August 2018 and other comorbidities. After the administration of the first dose of the Pfizer-BioNTech COVID-19 vaccine, the patient developed pruritic eczematous eruption presenting as grouped erythematous-violaceous papulovesicular lesions with fine scales over his upper and lower extremities. These eruptions started two days after the administration of the vaccine. This eruption became generalized 21 days after receiving the second dose of the Pfizer-BioNTech COVID-19 vaccine. Clinical suspicion of the drug-induced vesicular eruption was suspected; thus, a biopsy was obtained and showed erosions and mixed inflammatory cell infiltrate. From a clinical and histopathological correlation, vesicular eruption following vaccination with Pfizer-BioNTech COVID-19 was confirmed. Nevertheless, other diagnoses cannot be ruled out, but from the clinical-histopathological association, the vaccine-inflicted eruption is the likely culprit. Reports are crucial to understanding the nature of such dermatological manifestation after emerging diseases and counteractions like vaccinations. The dermatological manifestations are vaguely recognized; thus, by reporting on the cases similar to the case in this report, more data will be available to understand the nature and underlying cause of such eruptions.

Serum sTWEAK and FGF-23 Levels in Hemodialysis and Renal Transplant Patients.

BACKGROUND: Kidney transplantation is the treatment of choice for patients with end-stage renal disease. OBJECTIVE: To evaluate the changes in serum soluble TNF-like weak inducer of apoptosis (sTWEAK) and fibroblast growth factor 23 (FGF-23) in hemodialysis (HD) patients and renal transplant recipients (RTR). METHODS: Serum samples were obtained from 30 patients on chronic HD, 30 RTRs, and 30 normal controls. Biochemical factors, sTWEAK, FGF-23, and interlukin-6 (IL-6) were measured by standard methods. RESULTS: Serum levels of sTWEAK in RTRs were significantly higher than those in the HD patients (p=0.025); RTR and HD patients had significantly lower sTWEAK levels than the controls (p=0.001 and p= 0.038, respectively). Serum levels of FGF-23 in HD patients were significantly (p=0.001) higher than those in the RTR; the level was higher in both studied groups compared to that in the controls (p=0.001 for both groups). The mean serum level of IL-6 in HD was significantly higher than that in RTR patients (p=0.013). IL-6 levels in both groups were significantly higher than those in controls (p=0.001 and p= 0.012, respectively). In HD group a negative correlation was found between FGF-23 and sTWEAK (r= 0.375, p=0.041); there were also a significant correlation between FGF-23 and IL-6 (r= 0.480, p= 0.007) and between IL-6 and sTWEAK (r= 0.409, p=0.025). CONCLUSION: We found that serum sTWEAK is decreased and FGF-23 is increased in HD and RTR groups comparing with the control group. However, further studies are needed to shed light over their direct role on atherosclerosis and cardiovascular outcomes.

Effect of isoproterenol on cyclosporine-induced nephrotoxicity in rat.

BACKGROUND: Oxidative stress is the main mechanism resulting in cyclosporine-induced nephrotoxicity. Because of its ability to stimulate endogenous melatonin production, isoproterenol is one of the most powerful antioxidant drugs. In this study, we sought to determine the effect of isoproterenol on cyclosporine-induced nephrotoxicity in rats. MATERIALS AND METHODS: Thirty two young male Wistar rats were divided into four groups: of group A were controls that received placebo; group B, received intraperitoneal isoproterenol (20 mg/kg/d) alone; group C, intravenous cyclosporine (15 mg/kg/d) alone; and group D, both drugs simultaneously at the same doses and durations namely cyclosporine 1 week after administration of isoproterenol. Blood samples to measure serum urea, creatinine, and melatonin levels were drawn four times for each group: before injection, at the mid period of treatment, at the end of treatment, and 1 week after the last injections. RESULTS: Isoproterenol increased mean serum melatonin level in groups B and D rats (P < .05). With regard to deteriorated renal function [DRF = (urea + creatinine)/2], administration of cyclosporine with (group D) or without (group C) isoproterenol was associated with decreased renal function (P < .05), although it was more perturbed in the latter instance. Measured DRF at the middle and the end of drug administration periods of A and B (revealed significant differences compared with groups C and D; P < .05). DISCUSSION: Although cyclosporine-induced nephrotoxicity is not completely eliminated by isoproterenol, the latter showed some protective effects.

Effects of losartan and enalapril on high-sensitivity C-reactive protein and total antioxidant in renal transplant recipients with Renin-Angiotensin system polymorphisms.

BACKGROUND: As renin-angiotensin system (RAS) activity may affect the severity of oxidative stress and inflammatory markers, we assessed the effects of enalapril (E) and/or losartan (L) on these markers in renal transplant recipients with RAS polymorphisms. PATIENTS AND METHODS: After determination by PCR of RAS genotypes, consisting of the angiotensin-converting enzymes (ACE I/D), angiotensinogens (AGT M235T) and angiotensin II type 1 receptors (ATR1 A1166C), 76 recipients were recruited randomly and assigned 4 groups. The first (n = 17) and second (n = 24) groups were treated with E (E(+): 10 mg/d) and L (L(+): 50 mg/d) alone, respectively. The third positive control group (n = 17) received E + L (E(+)L(+): 10 mg/d + 50 mg/d) and the fourth negative control group (n = 18) received no medication (E(-):L(-)). High-sensitivity C-reactive protein (hs-CRP) and total antioxidant (TA) inflammatory and antioxidative markers were measured after 2 months. After a 2-week washout period, the E(+) group was changed to L(+) and vice versa in a crossover design. They were followed for another 8 weeks before retesting hs-CRP and TA. A value of P < or = .05 was considered significant. RESULTS: After 2 and 4 months of treatment with the drug regimen, hs-CRP and TA levels were significantly decreased and consequently increased among the E(+)L(+), L(+) and E(+) groups (P < .05). On analyzing the relationship between RAS polymorphisms and baseline hs-CRP or TA levels, CC genotype of ATR1 showed lower hs-CRP levels (P = .04). However, none of the RAS polymorphisms predicted the antioxidant and anti-inflammatory response rates to the drugs (P > .05). CONCLUSION: Although hs-CRP was lower in the CC genotype patients of ATR1 polymorphisms E and/or L reduced hs-CRP and increased TA regardless of the RAS genotype.

Kidney transplantation candidates and cardiovascular risk factors.

OBJECTIVE: We sought to determine the prevalence of cardiovascular disease and risk factors among chronic renal failure (CRF) patients on the transplantation waiting list. METHODS: Fifty CRF patients on chronic hemodialysis who underwent evaluation for transplantation were compared with 60 hypertensive patients matched for age. We used Framingham scoring to calculate the absolute risk; relative risk was calculated based on the low-risk Framingham cohort. RESULTS: According to traditional risk factors, a significant difference was observed in systolic blood pressure and total cholesterol (greater in the hypertensive group), and in the prevalence of the male gender, smoking, and diabetes, which were greater in the CRF group. The latter had a greater degree of left ventricular hypertrophy, lower diastolic blood pressure, and a lower prevalence of familial history of cardiovascular disease and obesity. Patients with CRF had a greater relative risk compared with the Framingham control population, but it did not differ from that observed in the group of hypertensive individuals. CONCLUSION: The prevalence of cardiovascular disease and traditional risk factors is high among renal transplantation candidates. The Framingham equations do not adequately quantify the real cardiovascular risk; other risk factors specific for that population probably contribute to their greater cardiovascular risk.