The incidence of nausea and vomiting in cancer patients in Greek clinical practice: A longitudinal study.

AIM OF THE STUDY: To assess nausea and vomiting in cancer patients during two cycles of chemotherapy, and the impact on their quality of life. MATERIAL AND METHODS: A longitudinal study was conducted in an oncology department of a large general public hospital in Northern Greece. The sample consisted of 200 cancer patients. Data were collected with the MASCC-Antiemesis Tool and FACT-G questionnaire and specific demographic and clinical characteristics. RESULTS: In cycle 2, acute vomiting was experienced by 16% of the patients and delayed vomiting by 14%; acute nausea was experienced by 27.5% and delayed nausea by 38%. In cycle 3, acute and delayed vomiting were experienced by 17.5% and 15% of the patients, respectively, acute nausea by 29.5%, and delayed nausea by 36.5%. The comparison of severity in acute vomiting between cycle 2 and cycle 3 yielded a statistically significant (p = 0.003) difference; similar results were obtained in the comparison of severity of acute nausea (p < 0.001). The correlation of severity of acute nausea with physical, emotional, and functional well-being as well as the total score of quality of life in two measurement points was statistically significant (p < 0.005). Multiple forward linear regression analysis showed that the total score of quality of life was significantly associated with age, gender, educational status, occupational status, type of cancer, family status, and diet. CONCLUSIONS: Our study confirms that nausea and vomiting are significant clinical problems that influence quality of life. Further research is needed to evaluate the predictors of acute and delayed nausea and vomiting during chemotherapy.

Combined GSTP1 and NQO1 germline polymorphisms in the susceptibility to Multiple Sclerosis.

Germline polymorphisms of detoxification genes could influence susceptibility to Multiple Sclerosis (MS). Glutathione-S-transferases (GSTs) and NAD(P)H: quinone oxidoreductase 1 (NQO1) are detoxifying enzymes involved in biotransformation of metabolites preventing cells from oxidative damage. In order to evaluate the possible contribution of the A313G GSTP1 inactivating polymorphism, alone and in combination with the C609T NQO1 genetic variant in MS susceptibility, we performed a case-control study consisting of 254 MS patients and 370 healthy donors. Genotypes were investigated using a new Real-Time PCR and PCR-RFLP assays. The GSTP1 polymorphism was evaluated in relation to patients' characteristics (clinical subtypes, age and gender) and the NQO1 gene status. GSTP1 genotype distribution was similar between cases and controls. Higher frequency of GSTP1 heterozygotes was observed in patients with relapsing remitting disease (RRMS) (p = 0.019), especially in those presenting a benign form (EDSS ≤ 2 after 10-15 years from the disease onset). Interestingly, genotype distribution analysis of combined GSTP1 and NQO1 polymorphisms revealed significantly higher frequency of GSTP1 heterozygous (A/G) and NQO1 variant genotypes (C/T and T/T) in patients as compared to the controls (p = 0.031). The increased incidence of combined GSTP1 and NQO1 variant genotypes in MS patients may suggest that defective function of detoxification enzymes might be an important determinant of susceptibility and clinical manifestation of the disease. Moreover, the results suggest a possible role for the GSTP1 heterozygous background in the development of RRMS.

Oculomotor nerve palsy as an extraintestinal manifestation of Crohn's disease.

Patients with inflammatory bowel disease (IBD) may present with extraintestinal manifestations. Neurological symptoms associated with IBD are infrequent. Thus, any unexplained neurological symptom that occurs in patients with IBD should raise the suspicion of a link between the two disorders. We report a case of a man in his 60s, who was diagnosed with Crohn's disease and developed ptosis and diplopia. Neurological examination revealed oculomotor nerve palsy, sparing the pupil. MRI and magnetic resonance angiography of the brain were insignificant and no other cause was determined. He was treated with oral corticosteroids and symptoms gradually subsided. Cranial nerve palsies associated with IBD have been rarely reported. They usually involve the optic and acoustic nerve and are attributed to a common dysimmune base. This is the first reported case of oculomotor nerve palsy (III cranial nerve) associated with IBD. Clinicians treating patients with IBD should be alert for unusual neurological complications and treat them appropriately.

Association of Psychometric Indices and Normal Electrodiagnostic Studies in Referral for Suspected Carpal Tunnel Syndrome.

BACKGROUND/AIM: The aim of this study was to investigate psychometric indices and their association with electrodiagnostic studies (EDX). PATIENTS AND METHODS: A total of 100 patients referred for EDX testing of the upper limbs were prospectively enrolled. Demographic data, laboratory test results, referral physician specialty, main symptom, WHODAS 2.0-12 item version, Hospital Anxiety and Depression Scale (HADS), Boston Carpal Tunnel Questionnaire (BCTQ) and a Numeric Rating Scale (NRS) indicating the extent of their discomfort were collected. RESULTS: Normal EDX results were elicited from 56% of patients. Only the presence of numbness in the right hand, pain in the left hand and older age were significantly associated with an abnormal EDX result. The more depressed and anxious the patients were, the more they scored on psychometric scales. CONCLUSION: The large prevalence of normal EDX studies raises the issue of unnecessary referrals. A proportion of patients are referred only according to their reported symptoms. Psychological factors affect the way a person expresses physical discomfort, leading to unnecessary EDX referrals and inevitably with normal results.

Antibodies to inositol 1,4,5-triphosphate receptor 1 in patients with cerebellar disease.

OBJECTIVE: To describe newly identified autoantibodies associated with cerebellar disorders. DESIGN/METHODS: We first screened the sera of 15 patients with cerebellar ataxia, without any known associated autoantibodies, with immunocytochemistry on mouse brain. After characterization and validation of a newly identified antibody, 85 additional patients with suspected autoimmune cerebellar disease were screened using a cell-based assay. RESULTS: Immunoglobulin G from one of the first 15 patients demonstrated a distinct staining pattern on Purkinje neurons. This autoantibody, as characterized further by immunoprecipitation and mass spectrometry, was binding inositol 1,4,5-triphosphate receptor 1 (IP3R1), an intracellular channel that mediates the release of Ca2+ from intracellular stores. Anti-IP3R1 specificity was then validated with a cell-based assay. On this basis, screening of 85 other patients with cerebellar disease revealed 2 additional IP3R1-positive patients. All 3 patients presented with cerebellar ataxia; the first was eventually diagnosed with primary progressive multiple sclerosis, the second had a homozygous CAG insertion at the gene TBP, and the third was thought to have a neurodegenerative disease. CONCLUSIONS: We independently identified an autoantibody against IP3R1, a protein highly expressed in Purkinje neurons, confirming an earlier report. Because a mouse knockout model for IP3R1 exhibits ataxia and epilepsy, this autoantibody may have a functional role. The heterogeneity of the antibody-positive patients suggests that this antibody may either have a direct involvement in disease pathogenesis or it is a surrogate marker secondary to cerebellar injury. Anti-IP3R1 antibodies should be further explored in various ataxic and epileptic syndromes as they may denote a marker of response to immunotherapies.

The C609T inborn polymorphism in NAD(P)H:quinone oxidoreductase 1 is associated with susceptibility to multiple sclerosis and affects the risk of development of the primary progressive form of the disease.

Oxidative stress plays a pivotal role in the pathogenesis of multiple sclerosis (MS). Inactivating polymorphisms of genes encoding detoxification enzymes, such as NAD(P)H:quinone oxidoreductase 1 (NQO1), could influence susceptibility to MS. To test this hypothesis we performed a case-control study in which we compared the distribution of NQO1 genotypes between 231 MS patients and 380 controls, using both PCR-RFLP and real-time PCR assays. Correlations with MS clinical subtype classification and gender were also evaluated. A significantly higher frequency of the homozygous (T/T) and heterozygous (C/T) NQO1 C(609)T variant genotypes was observed among MS patients compared to controls (P=0.01), with MS patients showing a 1.5-fold increased risk of carrying at least one variant T allele (P=0.009). Interestingly, patients belonging to the primary progressive subgroup exhibited a significantly higher incidence of the heterozygous C/T variant genotype, compared to the other forms of MS (P=0.019). There was no correlation of the NQO1 polymorphism with gender. These results provide the first evidence for a pathogenetic role for the NQO1 C(609)T polymorphism in MS susceptibility and suggest a possible role for the NQO1 genetic background in the development of primary progressive MS.