Tibial tubercle avulsion fracture during sport activities in adolescent: a case report.

BACKGROUND AND AIM OF WORK: Tibial tubercle avulsion fractures (TTAF) are uncommon condition in children and adolescents. These lesions may be misdiagnosed and consequently not properly treated. Reduction and fixation is indicated if displacement is higher than 2mm or if the extensor apparatus is damaged. Authors present a case of a TTAF associated with a complete lateral patellar retinaculum lesion in a 13-year-old male adolescent non-professional basketball player. METHODS: Surgery consisted of reduction and fixation with 2 half threaded cancellous and washers; TTA was then basted and reinforced with a non absorbable suture according to Krachow technique and finally the patellar lateral retinaculum through a direct repair with absorbable material. RESULTS: Clinical evaluation after 3 years showed bone healing, a complete resolution of pain, complete range of motion, good strength and complete functionality of the operated limb. CONCLUSIONS: Misdiagnosis or delayed treatment of TTAF can often result in nonunion, functional impairment, and persistent pain. For these reasons, authors believe that a stable and quick fixation associated to specialized rehabilitation are crucial for recovery. (www.actabiomedica.it).

[Hepatitis-associated aplastic anemia: description of a new case]. / Epatite acuta associata ad anemia aplastica: descrizione di un caso.

Hepatitis-associated aplastic anemia is an only recently recognised syndrome. We present a case whereby a month after an episode of fever, a 17-year-old boy was recovered with liver enzyme elevation and circulating platelet reduction. All the acute viral hepatitis markers were negative. After bone marrow aspiration a severe aplastic anemia was diagnosed and all the findings were consistent with hepatitis-associated aplastic anemia. The disorder was initially treated with glucocorticoids and platelet transfusion, obtaining the normalization of the liver enzymes but worsening of the aplastic anemia. An HLA-identical related marrow donor was not found. The patient responded to immunosuppressive treatment but died of multi-organ failure due to severe sepsis.

Hyperhomocysteinemia and the MTHFR C677T polymorphism promote steatosis and fibrosis in chronic hepatitis C patients.

The factors and mechanisms implicated in the development of hepatitis C virus (HCV)-related steatosis are unknown. Hyperhomocysteinemia causes steatosis, and the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism induces hyperhomocysteinemia. We investigated the role of these factors in the development of HCV-related steatosis and in the progression of chronic hepatitis C (CHC). One hundred sixteen CHC patients were evaluated for HAI, fibrosis and steatosis grades, body mass index, HCV genotypes, HCV RNA levels, homocysteinemia, and the MTHFR C677T polymorphism. Hyperhomocysteinemia was associated with the TT genotype of MTHFR (r = 0.367; P = .001). Median values of homocysteine in the CC, CT, and TT genotypes of the MTHFR gene were 9.3, 12.2, and 18.6 micromol/L, respectively (P = .006). Steatosis correlated with the MTHFR polymorphism, homocysteinemia, HAI and fibrosis. Steatosis above 20% was significantly associated with fibrosis. Prevalence and high grade (>20%) of steatosis were 41% and 11% in CC, 61% and 49% in CT, and 79% and 64% in TT, respectively (P = .01). Relative risk of developing high levels of steatosis was 20 times higher for TT genotypes than CC genotypes. According to multivariate analysis, steatosis was independently associated with hyperhomocysteinemia (OR = 7.1), HAI (OR = 3.8), liver fibrosis (OR = 4.0), and HCV genotype 3 (OR = 4.6). On univariate analysis, fibrosis was associated with age, steatosis, MTHFR, homocysteinemia and HAI; however, on multivariate analysis, liver fibrosis was independently associated with age (P = .03), HAI (P = .0001), and steatosis (P = .007). In conclusion, a genetic background such as the MTHFR C677T polymorphism responsible for hyperhomocysteinemia plays a role in the development of higher degree of steatosis, which in turn accelerates the progression of liver fibrosis in CHC.

Silent celiac disease in chronic hepatitis C: impact of interferon treatment on the disease onset and clinical outcome.

GOALS: To assess the impact of interferon treatment on celiac disease onset in hepatitis C patients and to clarify its clinical relevance and outcome. BACKGROUND: Hepatitis C is associated with autoimmunity, which can be exacerbated by interferon treatment. Cases of celiac disease activation during interferon treatment have been reported. STUDY: Retrospective evaluation of 534 hepatitis C patients with or without symptoms compatible with celiac disease onset during interferon treatment and 225 controls. Anti-transglutaminase antibodies were assayed. HLA-DQA1 and -B1 loci were typed. Upper gastrointestinal endoscopy was applied to confirm the diagnosis in antibody-positive patients. RESULTS: Anti-transglutaminase antibodies were detected before treatment in 1.3% of hepatitis C patients and in 0.4% of controls (not significant). Eighty-six percent of patients with anti-transglutaminase antibodies showed activation of celiac disease while on interferon. Symptoms ranged from mild to severe, and interferon had to be discontinued in 2 of 7 (29%) patients. Symptoms disappeared in 6 of 7 patients after interferon withdrawal. Onset of symptoms compatible with celiac disease during interferon therapy was significantly associated with the presence of anti-transglutaminase antibodies (OR 53). CONCLUSIONS: In hepatitis C patients, the activation of silent celiac disease during interferon treatment is almost universal and should be suspected, but it uncommonly requires interferon treatment discontinuation. Symptoms subside after interferon withdrawal.