P086 Kawasaki syndrome and Epstein Barr virus: a case report (again!)

Background Kawasaki disease (kDa), also known as mucocutaneous lymph node syndrome, is always updating. We present the case of a toddler boy with concomitant positive EBV serology. Material The infant is referred to the pediatric ward for stomatitis with cheilitis, fever> 40 ° C, asthenia, irritability evolving for 4–5 days. In addition, clinical examination revealed multiple, small cervical lymph nodes, < 1 cm. There is no conjunctivitis, no skin rash, nor reactivation of the BCG scar. Biology reveals hyperleukocytosis with very high ESR and CRP. ECG and Echo-heart, requested for suspicion of Kawasaki syndrome, are normal. Results Empirical treatment with Aciclovir—Cefalexin with topical care was started. Viral serologies return HSV (-), CMV (-), but EBV (+). Clinical improvement was noted within 36 h. However, inflammatory markers improve within 2–3 days. At 15 days, the child presents with typical convalescent peeling of the fingers and toes; associated with marked thrombocytosis. The diagnosis of Kawasaki Syndrome is definitively confirmed. Discussion The exact aetiology of Kawasaki syndrome remains unclear. Among the factors frequently encountered, the Epstein Barr Virus is reported for almost 30 years. The syndrome frequency is highest before the age of 5 years; similar to Infectious Mono-Nucleosis (due to EBV…). Our case depicts a concomitant Kawaski syndrome and positive EBV serology; without any detectable coronary artery abnormality. Conclusion Kawasaki syndrome is a real “chameleon” condition with possible cardiovascular complications. The viral aetiology springs up through “an old friend”: the Epstein Barr Virus ...Even without any aneurysm (also associated with EBV), the American Heart Association recommends long-term monitoring for all Kawasaki syndromes.

Therapeutic management of a symptomatic Kaposi’s sarcoma patient with renal failure undergoing haemodialysis: A case report

Kaposi’s sarcoma (KS) is a rare inflammation-based vascular cancer involving the skin. The viral aetiology of KS is the human herpesvirus 8 (HHV-8). KS may be frequently diagnosed in immunosuppressed kidney-transplanted patients, while is less common in patients with dialysis. It is known that various immunological abnormalities can lead to impaired immune status in uremic patients. It is noteworthy that despite the incidence of KS in patients with renal impairment, only few cases have reported efficacy and safety profile of KS targeting anti-cancer drugs in this kidney disease population. Herein, we report the first case of a symptomatic KS patient with renal disease in haemodialysis and focus on its therapeutic management. We also review the main data available from literature regarding the safety of KS therapy in dialysis patients.

Sulfasalazine-induced drug reaction with eosinophilia and systemic symptoms (DRESS) with concomitant acute chikungunya virus infection: possible role of new viral trigger

Drug reaction with eosinophilia and systemic symptoms (DRESS) is designated as a potentially lethal adverse drug effect with characteristic signs and symptoms such as skin rash, fever, leucocytosis with eosinophilia or atypical lymphocytes, lymphadenopathy and liver or renal dysfunction. In addition to most commonly implicated drug category (aromatic anticonvulsants), lamotrigine, sulfonamides, dapsone and abacavir may also induce this syndrome. We describe here a case a sulfasalazine-induced DRESS with coexisting chikungunya fever. The shared presentation of fever with rash in both conditions made it a challenging diagnosis. Sulfasalazine hypersensitivity manifesting as DRESS has rarely been reported. Furthermore, we document chikungunya virus (CV) as a possible triggering agent for DRESS. To the best of our knowledge, CV as a viral aetiology in DRESS has not been reported previously in the literature.

Alpha-1 Antitrypsin and Hepatocellular Carcinoma in Liver Cirrhosis: SERPINA1 MZ or MS Genotype Carriage Decreases the Risk

Heterozygotes for Z or S alleles of alpha-1-antrypsin (AAT) have low serum AAT levels. Our aim was to compare the risk of hepatocellular carcinoma (HCC) in patients with liver cirrhosis carrying the SERPINA1 MM, MZ and MS genotypes. The study groups consisted of 1119 patients with liver cirrhosis of various aetiologies, and 3240 healthy individuals served as population controls. The MZ genotype was significantly more frequent in the study group (55/1119 vs. 87/3240, p < 0.0001). The MS genotype frequency was comparable in controls (32/119 vs. 101/3240, p = 0.84). MZ and MS heterozygotes had lower serum AAT level than MM homozygotes (medians: 0.90 g/L; 1.40 g/L and 1.67 g/L; p < 0.001 for both). There were significantly fewer patients with HCC in the cirrhosis group among MZ and MS heterozygotes than in MM homozygotes (5/55 and 1/32 respectively, vs. 243/1022, p < 0.01 for both). The risk of HCC was lower in MZ and MS heterozygotes than in MM homozygotes (OR 0.3202; 95% CI 0.1361–0.7719 and OR 0.1522; 95% CI 0.02941–0.7882, respectively). Multivariate analysis of HCC risk factors identified MZ or MS genotype carriage as a protective factor, whereas age, male sex, BMI and viral aetiology of cirrhosis increased HCC risk.

ETIOPATHOGENETIC MECHANISMS OF PERIODONTAL DISEASES AGAINST THE BACKGROUND OF VIRAL LIVER DISSEASES

The article presents a review and analysis of relevant available literature sources on etiopathogenetic mechanisms of periodontal disease and liver diseases of viral aetiology, and, in particular, hepatitis B and C viruses. Significant prevalence, pronounced polymorphism of clinical hepatic and extrahepatic manifestations, the incidence rate of liver cirrhosis and hepatocellular carcinoma allows us to consider hepatitis of viral aetiology as a medical and social challenge. Multi-vector liver dysfunctions can cause oral presentations in this group of patients, and in particular, in their periodontal tissues. Viral liver damage is associated with significant impairment of the microbiocenosis in gingival sulcus and periodontal pockets. Dysbiotic changes are characterized by an increase in the number of opportunistic pathogens and anaerobic periodontal pathogens. Exacerbation of dysbiosis along with deterioration of oral hygiene occurs as a consequence of reduced local resistance and hyposalivation due to the sialotropic properties of hepatitis C virus. Significant pathogenetic role in the development of periodontal disease is played by disorders of metabolic and synthetic functions of the liver, as well as hormonal imbalance, metabolic disorders, immune-mediated damage, induction of autoimmune mechanisms and cytokine imbalance. The formation of hepatogenic osteopenia and osteoporosis enhances the loss of bone mass of the alveolar processes in the jaws and, accordingly, the resorption of bone tissue with the further progression of more aggressive forms of generalized periodontitis.

Acute interface fluid syndrome after laser in situ keratomileusis in a case of cytomegalovirus (CMV) endotheliitis and secondary glaucoma

Cytomegalovirus (CMV) can cause recalcitrant recurrent keratouveitis and secondary glaucoma. We report a case of chronic recurrent anterior uveitis with secondary glaucoma presenting with acute visual loss and interface fluid 9 years after laser in situ keratomileusis. Based on clinical presentation, a viral aetiology was suspected. Aqueous tap was positive for CMV-DNA by real-time quantitative PCR of the aqueous humour. The patient was treated with systemic antivirals, topical corticosteroids and antiglaucoma medications. The interface fluid resorbed rapidly. The intraocular pressure (IOP) was controlled by trabeculectomy. There was no further corneal deterioration at 7-month follow-up and the IOP had also stabilised. We believe this is only the third reported case of CMV-related interface fluid syndrome. This case highlights the role of quantitative PCR analysis for establishing viral aetiology in recurrent unilateral hypertensive anterior uveitis and reports the unusual finding of interface fluid which resolved after starting systemic antiviral therapy.

SEROLOGICAL EVIDENCE OF AVIAN INFECTIOUS BRONCHITIS IN NIGERIA

Avian infectious bronchitis is an acute rapidly spreading viral respira­tory disease of chickens characterized by tracheal rales, coughing and sneezing. In adult laying flocks it causes a drastic drop in egg production — most of which are malformed.The disease was first described in the U.S.A. by Schalk and Hawn (1931) and its viral aetiology was confirmed 5 years later (Beach and Schalm, 1936). It is now report­ed to be world-wide in distribution (Estola, 1966).However, the F.A.O. Animal Health Year Books do not .list AIB as being present in Nigeria. Similarly, a recent compilation of Nigeria Veterinary bibliography (1970-1983) did not include AIB and the disease until a previous report (Komolafe and Erojikwe, 1985) has not been described in Nigeria.In the present communication, a serological evidence based on the detection of AIR virus specific preci­pitating antibody in the sera of sufs­pected cases is reported.