ABSTRACT
In B-cell chronic lymphocytic leukaemia (B-CLL), cutaneous infiltration is far less common than in T-cell CLL. However, the effect of fludarabine on cutaneous infiltration in patients with B-CLL is uncertain. We describe a 63-year-old man with B-CLL presenting with cutaneous lesions, who was treated successfully with oral fludarabine. Skin biopsy of one of these lesions revealed diffuse infiltration of uniform lymphocytes. Using PCR analysis, the same immunoglobulin heavy-chain gene rearrangement was found in lymphocytes in all samples (peripheral blood, bone marrow and skin lesion). The patient received four courses of oral fludarabine. Simultaneously with the normalization of the peripheral blood lymphocytosis, the patient became free of the cutaneous infiltration of CLL after four courses of oral fludarabine. Skin lesions had not recurred by the 12-month follow-up examination. To our knowledge, this is the first case of B-CLL leukaemia cutis treated with oral fludarabine. The introduction of fludarabine may contribute to a better outlook for these patients in the future.
Subject(s)
Antineoplastic Agents/therapeutic use , Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy , Leukemic Infiltration/pathology , Skin/pathology , Vidarabine/analogs & derivatives , Administration, Oral , Aged , Humans , Leukemia, Lymphocytic, Chronic, B-Cell/pathology , Leukemic Infiltration/drug therapy , Male , Treatment Outcome , Vidarabine/therapeutic useABSTRACT
Li-Fraumeni syndrome is a familial cancer syndrome characterized by different tumors and hereditary p53 mutations. Here, a chronic myeloid leukemia-like syndrome case in a Li-Fraumeni syndrome family with del (12) (p12) cytogenetic abnormality was presented. A hereditary p53 mutation (pro309ser) supported the Li-Fraumeni syndrome diagnosis in this family. This syndrome was characterized by the clonal myeloproliferative accumulation in bone marrow and peripheral blood with negative bcr/abl gene rearrangement finding. The etiology of this rare syndrome is still unclear. This is the only chronic myeloid leukemia-like syndrome case reported in a Li-Fraumeni syndrome family. Del (12)(p12) was observed in leukemias except chronic myeloid leukemia-like syndrome. The deletion in chromosome 12p12 with hereditary p53 mutation should have a critical role in chronic myeloid leukemia-like syndrome etiology in our case.
Subject(s)
Chromosome Deletion , Chromosomes, Human, Pair 12 , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis , Li-Fraumeni Syndrome/diagnosis , Tumor Suppressor Protein p53/genetics , Diagnosis, Differential , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics , Li-Fraumeni Syndrome/genetics , Male , Middle Aged , Mutation , Myeloproliferative Disorders , SyndromeABSTRACT
The aim of this study is to assess the relationship between the carotid wall intima media thickness (IMT) and atheroma plaques due to atherosclerosis and platelet aggregation among elderly. The first stage of the study was performed by analyzing platelet aggregation in a total of 28 elderly patients divided into two groups. The first group consisted of 14 cases with carotid atheroma plaque (Patient group I) and the second group of patients were without carotid atheroma plaque (Control group I). At the second stage of the study, the cases were regrouped according to the carotid IMT. Patients with IMT above 1 mm (Patient group II, n=10) and under 1 mm (Control group II, n=14) were compared regarding platelet aggregation. Platelet aggregation was induced in the platelet-rich plasma using 5 micro M ADP, 0.2 mg/ml collagen and 1.2 mg/ml ristocetin. Between patients with and without atheroma, no difference was noted in terms of platelet aggregation. Between platelet aggregation results of patients with intimal thickness above and under 1 mm, no significant difference was also noted. Between elderly cases with or without atherosclerosis, there was no difference with respect to platelet aggregation. Platelet aggregation measurements cannot be used as a marker of atherosclerosis in elderly population.
Subject(s)
Carotid Artery Diseases/physiopathology , Platelet Aggregation , Aged , Aged, 80 and over , Carotid Artery Diseases/diagnostic imaging , Female , Humans , Male , UltrasonographyABSTRACT
OBJECTIVE: The aim of this study was to determine whether a relationship exists between gastric and oral Helicobacter pylori and oral hygiene in patients with vitamin B12 deficiency. STUDY DESIGN: One hundred eight patients with vitamin B12 deficiency who were H pylori -positive in their gastric mucosa were enrolled in the study. These patients were divided into 3 groups determined by Oral Hygiene Index (OHI) scores of good, fair, or poor. H pylori was detected in the dental plaque with camphylobacter-like organism test gels. All patients were treated with a combination regimen to eradicate H pylori. RESULTS: H pylori positivity in dental plaque was correlated with OHI scores; the positivity was 28.5%, 90.2%, or 100% in patients with good, fair, or poor OHI scores, respectively. The eradication of H pylori was associated with recovery from anemia and increased serum vitamin B12 level (P <.0001 and P <.0001). The patients with poor OHI scores had the most frequent gastric recurrence of H pylori (58.3%) compared with those with fair OHI scores (41.2%) and good OHI scores (4.8%). CONCLUSIONS: H pylori seems to be an etiologic factor in vitamin B12 deficiency, since anemia was cured and the level of vitamin B12 in the serum increased as a result of its eradication. However, eradication of H pylori from gastric mucosa alone is not enough to prevent gastric recurrence of the bacteria. Proper oral hygiene must be established to eliminate H pylori in dental plaque. Therefore, we suggest that control of H pylori in dental plaque is necessary to control recurrence of H pylori.
