Displaying all 15 publications

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  1. Lee KF
    Med J Malaysia, 1995 Mar;50(1):110-3.
    PMID: 7752964
    Spontaneous intracranial haemorrhage is one of the cerebrovascular complications in beta-thalassaemia major patients. This is a report of 2 cases of fatal intracranial haemorrhage. Their ages were 12 and 7 years respectively, and they had been receiving regular blood transfusion for the past 3 and 2 years respectively. They developed acute onset of headache, loss of consciousness and convulsions at 5 and 2 days respectively after their last blood transfusion. C-T scan of the brain showed massive intracranial haemorrhage with extension into the ventricles. The spontaneous intracranial haemorrhages in these two cases was probably multi-factorial in origin. The predisposing factors included recent blood transfusion, prolonged prothrombin time and partial thromboplastin time as well as reduced platelet count.
    Matched MeSH terms: beta-Thalassemia/complications*
  2. Ong ML, Hatle LK, Lai VM, Bosco J
    Int J Clin Pract, 2002 Jun;56(5):345-8.
    PMID: 12137442
    Iron deposition in the heart occurs in beta-thalassaemia major and contributes to cardiac dysfunction. Eighteen patients with beta-thalassaemia major were assessed clinically and had non-invasive investigations. They were young (15.5 +/- 3.6 years). Two patients had clinical heart failure. Doppler echocardiography demonstrated higher transmitral peak flow velocity in early and late diastole compared with controls (e: p<0.05, a: p<0.01). Transtricuspid peak late diastolic flow velocity was higher in patients (p<0.005). Isovolumic relaxation time was shortened (p<0.001). Pulmonary venous flow velocity was higher in diastole than systole (S: 0.51 +/- 0.11 m/s, D: 0.62 +/- 0.08 m/s). Reversal of pulmonary venous flow during atrial systole was seen in eight patients. These diastolic filling abnormalities did not significantly change with blood transfusion. Left ventricular ejection fraction was normal in patients. Two patients had cardiomegaly on chest X-ray. In beta-thalassaemia with iron overload, there is a restrictive pattern of diastolic dysfunction. This is not altered by recent blood transfusion. Left ventricular function remains relatively intact.
    Matched MeSH terms: beta-Thalassemia/complications*
  3. Jasmi AY, Thambidorai CR, Khairussalleh J
    Med J Malaysia, 2003 Aug;58(3):443-5.
    PMID: 14750388
    Gallstone disease is a common association in patients with haematological splenomegaly. When indicated, simultaneous splenectomy and cholecystectomy should be performed and traditionally this is accomplished by open surgery. We report a 17 year old thalassaemic girl with splenomegaly complicated by gallstone pancreatitis. We treated her with a combination of needlescopic cholecystectomy and laparoscopic splenectomy as well as delivering the huge spleen via a pfannenstiel incision to hide the scar. We believe this technique is an acceptable alternative mainly for rapid delivery of the spleen and to minimize visible scars hence improving cosmesis.
    Matched MeSH terms: beta-Thalassemia/complications*
  4. Nandakumal G, Ismail F, Mohamad NF, Lott PW, Chew KS, Ab Rahman S, et al.
    J Pediatr Hematol Oncol, 2021 04 01;43(3):101-103.
    PMID: 33560075 DOI: 10.1097/MPH.0000000000002077
    Hemolacria is a rare condition that causes a person to produce tears that are partially composed of blood. It can be a presenting feature of certain ocular and systemic conditions. Here, the authors describe an interesting case of a 12-year-old boy with an underlying beta-thalassemia trait, who presented with a 2-day history of bilateral blood-stained tears, and an episode of epistaxis. Ocular examination was normal, and syringing showed no nasolacrimal duct blockage. Systemic examination was unremarkable. Laboratory investigations confirmed type 2 von Willebrand disease. Management of hemolacria remains a clinical challenge given the rare occurrence of the disease. In this case report, the authors discuss the differential diagnosis and management approach to hemolacria.
    Matched MeSH terms: beta-Thalassemia/complications
  5. Jackson N, Zaki M, Rahman AR, Nazim M, Win MN, Osman S
    J Clin Pathol, 1997 May;50(5):436-7.
    PMID: 9215130
    A 35 year old man with a fatal Campylobacter jejuni infection is described. He had HbE/beta zero thalassaemia and had undergone splenectomy nine months previously for hypersplenism; he also had chronic hepatitis C infection. He presented with high grade fever but no gastrointestinal symptoms and rapidly progressed to septicaemic shock and hepatic encephalopathy despite treatment with penicillin, gentamicin, and, later, chloramphenicol and ceftazidime. Only one case of Campylobacter jejuni septicaemia occurring post-splenectomy has been reported previously, also in an iron overloaded thalassaemia patient. Unusual Gram negative bacilli must be covered by the chosen antibiotic regimen when splenectomised thalassaemic patients present with high grade fever.
    Matched MeSH terms: beta-Thalassemia/complications
  6. Ngim CF, Lai NM, Hong JY, Tan SL, Ramadas A, Muthukumarasamy P, et al.
    Cochrane Database Syst Rev, 2017 09 18;9:CD012284.
    PMID: 28921500 DOI: 10.1002/14651858.CD012284.pub2
    BACKGROUND: Thalassaemia is a recessively-inherited blood disorder that leads to anaemia of varying severity. In those affected by the more severe forms, regular blood transfusions are required which may lead to iron overload. Accumulated iron from blood transfusions may be deposited in vital organs including the heart, liver and endocrine organs such as the pituitary glands which can affect growth hormone production. Growth hormone deficiency is one of the factors that can lead to short stature, a common complication in people with thalassaemia. Growth hormone replacement therapy has been used in children with thalassaemia who have short stature and growth hormone deficiency.

    OBJECTIVES: To assess the benefits and safety of growth hormone therapy in people with thalassaemia.

    SEARCH METHODS: We searched the Cochrane Haemoglobinopathies Trials Register, compiled from electronic database searches and handsearching of journals and conference abstract books. We also searched the reference lists of relevant articles, reviews and clinical trial registries. Our database and trial registry searches are current to 10 August 2017 and 08 August 2017, respectively.

    SELECTION CRITERIA: Randomised and quasi-randomised controlled trials comparing the use of growth hormone therapy to placebo or standard care in people with thalassaemia of any type or severity.

    DATA COLLECTION AND ANALYSIS: Two authors independently selected trials for inclusion. Data extraction and assessment of risk of bias were also conducted independently by two authors. The quality of the evidence was assessed using GRADE criteria.

    MAIN RESULTS: One parallel trial conducted in Turkey was included. The trial recruited 20 children with homozygous beta thalassaemia who had short stature; 10 children received growth hormone therapy administered subcutaneously on a daily basis at a dose of 0.7 IU/kg per week and 10 children received standard care. The overall risk of bias in this trial was low except for the selection criteria and attrition bias which were unclear. The quality of the evidence for all major outcomes was moderate, the main concern was imprecision of the estimates due to the small sample size leading to wide confidence intervals. Final height (cm) (the review's pre-specified primary outcome) and change in height were not assessed in the included trial. The trial reported no clear difference between groups in height standard deviation (SD) score after one year, mean difference (MD) -0.09 (95% confidence interval (CI) -0.33 to 0.15 (moderate quality evidence). However, modest improvements appeared to be observed in the following key outcomes in children receiving growth hormone therapy compared to control (moderate quality evidence): change between baseline and final visit in height SD score, MD 0.26 (95% CI 0.13 to 0.39); height velocity, MD 2.28 cm/year (95% CI 1.76 to 2.80); height velocity SD score, MD 3.31 (95% CI 2.43 to 4.19); and change in height velocity SD score between baseline and final visit, MD 3.41 (95% CI 2.45 to 4.37). No adverse effects of treatment were reported in either group; however, while there was no clear difference between groups in the oral glucose tolerance test at one year, fasting blood glucose was significantly higher in the growth hormone therapy group compared to control, although both results were still within the normal range, MD 6.67 mg/dL (95% CI 2.66 to 10.68). There were no data beyond the one-year trial period.

    AUTHORS' CONCLUSIONS: A small single trial contributed evidence of moderate quality that the use of growth hormone for a year may improve height velocity of children with thalassaemia although height SD score in the treatment group was similar to the control group. There are no randomised controlled trials in adults or trials that address the use of growth hormone therapy over a longer period and assess its effect on final height and quality of life. The optimal dosage of growth hormone and the ideal time to start this therapy remain uncertain. Large well-designed randomised controlled trials over a longer period with sufficient duration of follow up are needed.

    Matched MeSH terms: beta-Thalassemia/complications*
  7. Fong SM, Wong KJ, Fukushima M, Yeo TW
    Clin Infect Dis, 2015 Jun 15;60(12):1802-7.
    PMID: 25767257 DOI: 10.1093/cid/civ189
    Melioidosis is an important cause of community-acquired infection in Southeast Asia and northern Australia. Studies from endemic countries have demonstrated differences in the epidemiology and clinical features among children diagnosed with melioidosis. This suggests that local data are needed to determine the risk factors and outcome in specific areas.
    Matched MeSH terms: beta-Thalassemia/complications*
  8. Hamidah A, Thambidorai CR, Jamal R
    Med J Malaysia, 2005 Oct;60(4):517-9.
    PMID: 16570722
    We describe a patient with HbE-beta thalassaemia and chronic hepatitis C virus infection (genotype 1a) who was treated successfully with peginterferon alfa-2b and ribavirin, following failure to respond to standard interferon and ribavirin therapy. She had sustained virological response for nearly 24 months after completing peginterferon alfa-2b and ribavirin therapy. Transfusion requirements were significantly increased during combination therapy due to ribavirin-induced haemolysis. The adverse effects of interferon were well tolerated. Combination therapy with peginterferon alfa-2b and ribavirin maybe a feasible treatment option for a subset of thalassaemia/HCV infected non-responders to standard interferon-based therapy.
    Matched MeSH terms: beta-Thalassemia/complications*
  9. Chong YM, Tan JA, Zubaidah Z, Rahimah A, Kuldip K, George E
    Med J Malaysia, 2006 Jun;61(2):217-20.
    PMID: 16898315
    Thalassaemia is an inherited blood disorder and is a significant public health problem in Malaysia, with many not knowing they carry the gene for thalassaemia. The two major forms are alpha and beta thalassaemia. An individual can co-inherit both the alpha and beta thalassaemia genes. This study determined the frequency of concurrent carriers of alpha thalassaemia in 231 beta thalassaemia carriers. Gap-PCR was done on extracted DNA of the beta thalassaemia samples to check for alpha thalassaemia 1 molecular defect. Eight (3.5%) samples were found to have concurrently inherited the alpha thalassaemia 1 (- -SEA) deletion. The significant carrier rate for alpha thalassaemia 1 indicates the need for the implementation of DNA analysis to complement thalassaemia screening in high risk populations.
    Matched MeSH terms: beta-Thalassemia/complications
  10. Ngim CF, Lai NM, Hong JY, Tan SL, Ramadas A, Muthukumarasamy P, et al.
    Cochrane Database Syst Rev, 2020 05 28;5:CD012284.
    PMID: 32463488 DOI: 10.1002/14651858.CD012284.pub3
    BACKGROUND: Thalassaemia is a recessively-inherited blood disorder that leads to anaemia of varying severity. In those affected by the more severe forms, regular blood transfusions are required which may lead to iron overload. Accumulated iron from blood transfusions may be deposited in vital organs including the heart, liver and endocrine organs such as the pituitary glands which can affect growth hormone production. Growth hormone deficiency is one of the factors that can lead to short stature, a common complication in people with thalassaemia. Growth hormone replacement therapy has been used in children with thalassaemia who have short stature and growth hormone deficiency. This review on the role of growth hormone was originally published in September 2017 and updated in April 2020.

    OBJECTIVES: To assess the benefits and safety of growth hormone therapy in people with thalassaemia.

    SEARCH METHODS: We searched the Cochrane Haemoglobinopathies Trials Register, compiled from electronic database searches and handsearching of journals and conference abstract books. Date of latest search: 14 November 2019. We also searched the reference lists of relevant articles, reviews and clinical trial registries. Date of latest search: 06 January 2020.

    SELECTION CRITERIA: Randomised and quasi-randomised controlled trials comparing the use of growth hormone therapy to placebo or standard care in people with thalassaemia of any type or severity.

    DATA COLLECTION AND ANALYSIS: Two authors independently selected trials for inclusion. Data extraction and assessment of risk of bias were also conducted independently by two authors. The certainty of the evidence was assessed using GRADE criteria.

    MAIN RESULTS: We included one parallel trial conducted in Turkey. The trial recruited 20 children with homozygous beta thalassaemia who had short stature; 10 children received growth hormone therapy administered subcutaneously on a daily basis at a dose of 0.7 IU/kg per week and 10 children received standard care. The overall risk of bias in this trial was low except for the selection criteria and attrition bias which were unclear. The certainty of the evidence for all major outcomes was moderate, the main concern was imprecision of the estimates due to the small sample size leading to wide confidence intervals. Final height (cm) (the review's pre-specified primary outcome) and change in height were not assessed in the included trial. The trial reported no clear difference between groups in height standard deviation (SD) score after one year, mean difference (MD) -0.09 (95% confidence interval (CI) -0.33 to 0.15 (moderate-certainty evidence). However, modest improvements appeared to be observed in the following key outcomes in children receiving growth hormone therapy compared to control (moderate-certainty evidence): change between baseline and final visit in height SD score, MD 0.26 (95% CI 0.13 to 0.39); height velocity, MD 2.28 cm/year (95% CI 1.76 to 2.80); height velocity SD score, MD 3.31 (95% CI 2.43 to 4.19); and change in height velocity SD score between baseline and final visit, MD 3.41 (95% CI 2.45 to 4.37). No adverse effects of treatment were reported in either group; however, while there was no clear difference between groups in the oral glucose tolerance test at one year, fasting blood glucose was significantly higher in the growth hormone therapy group compared to control, although both results were still within the normal range, MD 6.67 mg/dL (95% CI 2.66 to 10.68). There were no data beyond the one-year trial period.

    AUTHORS' CONCLUSIONS: A small single trial contributed evidence of moderate certainty that the use of growth hormone for a year may improve height velocity of children with thalassaemia although height SD score in the treatment group was similar to the control group. There are no randomised controlled trials in adults or trials that address the use of growth hormone therapy over a longer period and assess its effect on final height and quality of life. The optimal dosage of growth hormone and the ideal time to start this therapy remain uncertain. Large well-designed randomised controlled trials over a longer period with sufficient duration of follow up are needed.

    Matched MeSH terms: beta-Thalassemia/complications*
  11. Tan JA, Kok JL, Tan KL, Wee YC, George E
    Genes Genet Syst, 2009 Feb;84(1):67-71.
    PMID: 19420802
    Co-inheritance of alpha-thalassemia with homozygosity or compound heterozygosity for beta-thalassemia may ameliorate beta-thalassemia major. A wide range of clinical phenotypes is produced depending on the number of alpha-thalassemia alleles (-alpha/alphaalpha --/alphaalpha, --/-alpha). The co-inheritance of beta-thalassemia with alpha-thalassemia with a single gene deletion (-alpha/alphaalpha) is usually associated with thalassemia major. In contrast, the co-inheritance of beta-thalassemia with two alpha-genes deleted in cis or trans (--/alphaalpha or -alpha/-alpha) generally produces beta-thalassemia intermedia. In Southeast Asia, the most common defect responsible for alpha-thalassemia is the Southeast Asian (SEA) deletion of 20.5 kilobases. The presence of the SEA deletion with Hb Constant Spring (HbCS) produces HbH-CS disease. Co-inheritance of HbH-CS with compound heterozygosity for beta-thalassemia is very rare. This study presents a Malay patient with HbH-CS disorder and beta degrees/beta+-thalassemia. The SEA deletion was confirmed in the patient using a duplex-PCR. A Combine-Amplification Refractory Mutation System (C-ARMS) technique to simultaneously detect HbCS and Hb Quong Sze confirmed HbCS in the patient. Compound heterozygosity for CD41/42 and Poly A was confirmed using the ARMS. This is a unique case as the SEA alpha-gene deletion in cis (--SEA/alphaalpha) is generally not present in the Malays, who more commonly possess the two alpha-gene deletion in trans (-alpha/-alpha). In addition, the beta-globin gene mutation at CD41/42 is a common mutation in the Chinese and not in the Malays. The presence of both the SEA deletion and CD41/42 in the mother of the patient suggests the possible introduction of these two defects into the family by marriage with a Chinese.
    Matched MeSH terms: beta-Thalassemia/complications
  12. Hoe TS, Deng CT, Khuzaiah R
    PMID: 8160075
    Matched MeSH terms: beta-Thalassemia/complications*
  13. Tan JA, Tan KL, Omar KZ, Chan LL, Wee YC, George E
    Eur J Pediatr, 2009 Sep;168(9):1049-54.
    PMID: 19034506 DOI: 10.1007/s00431-008-0877-9
    INTRODUCTION: Interactions of different hemoglobin variants with thalassemia alleles can result in various clinical phenotypes. HbE-beta-thalassemia generally manifests with severe anemia where individuals exhibit beta-thalassemia major with regular blood transfusions or beta-thalassemia intermedia with periodic blood transfusions. This study presents a unique Malay family with three beta-globin gene defects-HbE, Hb South Florida, and IVS1-1 (G-->A).

    MATERIALS AND METHODS: HbE activates a cryptic splice site that produces non-functional mRNAs. Hb South Florida is a rare beta-hemoglobin variant, and its interactions with other beta-thalassemia alleles have not been reported. IVS1-1 is a Mediterranean mutation that affects mRNA processing giving rise to beta(o)-thalassemia.

    RESULTS AND DISCUSSION: Fifteen mutations along the beta-globin gene complex were analyzed using the amplification refractory mutation system. Hb South Florida was identified by direct sequencing using genomic DNA.

    CONCLUSION: The affected child with HbE/IVS1-1 produced a beta-thalassemia major phenotype. Compound heterozygosity for Hb South Florida/IVS1-1 produced a beta-thalassemia carrier phenotype in the mother.

    Matched MeSH terms: beta-Thalassemia/complications
  14. Zarina AL, Hamidah A, Zulkifli SZ, Jamal R
    PMID: 15916058
    Thalassemia is the commonest hemoglobinopathy in Malaysia. Patients with thalassemia major are transfusion dependent, and a large proportion of them will require splenectomy. As this particular group of patients is immunocompromized, overwhelming sepsis is a recognized complication. We report a series of three patients who all developed intra-abdominal abscesses following splenectomy.
    Matched MeSH terms: beta-Thalassemia/complications
  15. Furuumi H, Firdous N, Inoue T, Ohta H, Winichagoon P, Fucharoen S, et al.
    Hemoglobin, 1998 Mar;22(2):141-51.
    PMID: 9576331
    We have systematically analyzed beta-thalassemia genes using polymerase chain reaction-related techniques, dot-blot hybridization with oligonucleotide probes, allele specific-polymerase chain reaction, and sequencing of amplified DNA fragments from 41 unrelated patients, including 37 beta-thalassemia homozygotes, three with beta-thalassemia/Hb E, and one with beta-thalassemia/Hb S. Four different beta-thalassemia mutations were detected in 78 alleles. These are the IVS-I-5 (G-->C), codon 30 (AGG-->ACG) [also indicated as IVS-I (-1)], IVS-I-1 (G-->A), and codons 41/42 (-TTCT) mutations. The distribution of the beta-thalassemia mutations in the Maldives is 58 alleles (74.3%) with the IVS-I-5 (G-->C) mutation, 12 (15.4%) with the codon 30 (AGG-->ACG) mutation, seven (9%) with the IVS-I-1 (G-->A) mutation, and one with the codons 41/42 (-TTCT) mutation. The first three mutations account for 98.7% of the total number of beta-thalassemia chromosomes studied. These mutations are clustered in the region spanning 6 bp around the junction of exon 1 and the first intervening sequence of the beta-globin gene. These observations have significant implications for setting up a thalassemia prevention and control program in the Maldives. Analysis of haplotypes and frameworks of chromosomes bearing each beta-thalassemia mutation suggested that the origin and spread of these mutations were reflected by the historical record.
    Matched MeSH terms: beta-Thalassemia/complications
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