This document discusses neonatal G6PD deficiency, including its epidemiology, pathogenesis, clinical presentation, diagnosis, and management. It notes that G6PD deficiency is one of the most common enzymopathies worldwide and an important cause of neonatal jaundice. The deficiency results in impaired antioxidant defense in red blood cells and can lead to hemolysis when exposed to oxidative stress. Timely diagnosis and avoiding triggering factors are important to prevent severe complications like kernicterus. Newborn screening programs have helped identify at-risk infants.
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Discussion regarding Glucose 6 phosphate dehydrogenase deficiency and the genetics involved in inheritance of disease. The possible treatment options and mutations identified so far has also been discussed.
G6PDD is an inherited genetic disorder in the red blood cell enzyme known as G6PD. The effects of this disease are preventable by avoiding the triggers.
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
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Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
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3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Overview
Neonatal Hyperbilirubemia
Why are neonates prone to it
Pathological hyperbilirubemia
Approach to neonatal hyperbilirubemia
G6PD & its deficiency
What is it and its deficiency
Epidemiology, genetics and pathogenesis
Clinical presentation, diagnosis and
management
Neonatal screening program
3. A common, mostly benign
problem
60% terms, 80% preterms
Neonatal Hyperbilirubemia
4. Why neonates are prone to
hyperbilirubemia?
1. Increased bilirubin production
Decrease RBC survival, Increased mechanical fragility, More
prone to oxidant damage
2. Increased enterohepatic circulation
High beta- glucuronidase, Decreased intestinal bacteria and
motility
3. Defective uptake of bilirubin from plasma
Decreased ligandin
4. Immaturity of liver
Defective conjugation, Decreased hepatic excretion
5. When does this turn
pathological?
Onset in first 24 hours of life
Rate of rise of serum bilirubin
>0.2mg/dl/hr
Jaundice requiring phototherapy
Jaundice staining palms/soles
Persistence beyond 8 (term) and 14 days
(preterms)
6. How to approach a case of
NNJ?
Increased direct bilirubin
Increased indirect bilirubin
Sepsis
Intrauterine infections Coomb’s test +ve Coomb’s test -ve
Bile duct paucity Isoimmunisation
Biliary atresia Rh, ABO, Mi BG
Choledochal cyst
Tyrosenemia etc Hemoglobin
Jaundice in a neonate
Serum bilirubin
12. What is G6PD?
A house keeping enzyme critical in
redox metabolism of all aerobic cells
Role in RBCs very critical- The only
source of reduced NADP
NADPH directly or via reduced
glutathione defends RBCs against
oxidative stress
13. G6PD Deficiency
The most prevalent RBC enzymes
deficiency
400 million people are affected worldwide
(4.9%) [1]
Coincides with the geographic distribution of
endemic malaria
1.Frank JE. Diagnosis and management of G6PD deficiency. Am Fam Physician 2005;72:1277-82
15. The Indian scenario…
Incidence: 2-27%[2]
MC variant: G6PD Mediterranean
Mostly in:[3]
Vataliya prajapatis of north india
Parsis
Punjab, Kerala, Andhra Pradesh
[2]. Mohanti D, Mukherjee MB, Colah RB. G6PD deficiency in India. Indian J Pediar 2004;71:525-9.
[3]. Pao M, Kulkarni A, Gupta V, Kaul S, Balan S. Neonatal screening for G6PD deficiency. Indian J Pediatr 2005;72:835-7.
16. Genetics
Gene located on X-chromosome (sex
linked recessive)
Disease fully expressed in hemizygous
males and homozygous females
Variable intermediate expression by
heterozygous females
17. Clinical implications of molecular
basis of G6PD deficiency
A house keeping gene- Deletions of G6PD genes
incompatible with life (hydeletions); death in utero
Point mutations:
Sporadic:
No geographical specificity
No causal relationship with malaria selection
Manifests with CNSHA
Polymorphic:
Resulted from malaria selection
Correlate with specific geographical areas
18. WHO Classification of G6PD
variants
WHO Class Level of
deficiency
Enzyme activity Severity of
hemolysis
1 Severe <10% CNSHA
2 Severe <10% Intermittent
hemolysis
3 Moderate 10-60% Intermittent
hemolysis with
stressors
4 Mild to none 60-150% No hemolysis
5 None >150% No hemolysis
19. Pathogenesis
As red cells age, G6PD activity falls rapidly and
prematurely
So, diminished NADPH/NADP and GSH/GSSG
ratios
Impaired elimination of oxidants (H202)
Oxidation of hemoglobin and sulfhydrl groups in
membrane
20. Pathogenesis (cont.)
Red cell integrity impaired (on
exposure to oxidant drugs/ oxidant
response to infections and chemicals)
Oxidized hemoglobin precipitates to
form Heinz bodies, plucked out of the
cell leading to hemolysis and bite cell
blister cell morphology
22. When to suspect G6PD
deficiency in a neonate?
Development of hyperbilirubemia within
24 hours of life
History of neonatal jaundice in family
members of siblings
Have bilirubin level >95th
percentile
Have evidence of hemolysis with
negative DCT
23. Clinical Presentation
A. Neonatal hyperbilirubemia
B. Drug induced hemolysis
C. Favism
D. Chronic non-spherocytic hemolytic
anemia
24. Neonatal hyperbilirubemia in
G6PD deficient neonates
Severe manifestation of G6PD deficiency
and source of potential morbidity from
kernicterus
Probably starts in utero, but clinical problem
becomes apparent on day 2/3 of life
10-50% deficient neonates affected
Indian data: 13.3% of all jaundiced neonates
(and out of these 16% female neonates) [4]
[4]. Seema Kapoor et al. Newborn screening for G6PD deficiency; A 2-year data from north India. Indian J
Public Health.2015.
25. Neonatal hyperbilirubemia in
G6PD deficient neonates(cont.)
Mechanisms:
Reduced glucuronidation of bilirubin due to
defective G6PD activity in hepatocytes
Hemolysis triggered on exposure to oxidants like
naphthalene balls
Co-inheritance of UDP-glucuronyltransferase 1
deficiency of Gilbert syndrome
Pregnant women ingesting oxidant drugs,
transmitting it to her G6PD deficient fetus
26. Drugs carrying risk of
hemolysis in G6PD deficients
Drugs Definite risk Possible risk Doubtful risk
Antimalarials Primaquine
Dapsone
Chloroquine Quinine
Sulfonamides Sulphametoxazole Sulfasalizine
Sulfadimadine
Sulfisoxazole
Sulfadiazine
Antibiotics Nitrofurantoim
Nalidixic acid
Cotrimoxazole
Niridazole
Ciprofloxacin
Norfloxacin
Chloramphenicol
P-Aminosalicylic
acid
Antipyretics/
Analgesics
Acetanilide Aspirin(>3g/d) Aspirin(<3g/d)
Acetaminophen
Others NaphthaleneNaphthalene
Methylene blue
Vit K analogues
Ascorbic acid >1g
Rasburicase
Doxorubicin
Probenecid
Harrison’s Textbook of Internal Medicine-19th
edition
27. Laboratory diagnosis of G6PD
deficiency
Screening/ Qualitative tests:
Ultraviolet spot test
Methaemoglobin reduction test
Brilliant cresyl blue decolorisation test
Definitive/ Quantitative test:
Spectrophotometric analysis
Molecular diagnostic testing and DNA
analysis
28. Methord used in our case…
Dried blood spots collected by heel prick on blood
sample collection card (Whatman 903 s & s, GE
Healthcare)
Analysis done by fluroimmunoassey using Flurometer
Principal: DBS allowed to react with substrate (G6P
+NADP) for 30 mins at ambient temperature
Fluorescent measured using excitation wavelength of
355nm and emission wavelength of 460nm
Values <16U/dl considered deficient
29. Importance of quantitative
tests
Situation 1:
During a hemolytic attack, old RBCs destroyed, therefore
surviving young RBCs and reticulocytes have relatively
higher G6PD
Screening test can be false normal
Situation 2:
Heterozygous females diagnosis
Probability of clinically significant hemolysis in
heterozygote roughly correlates with proportion of G6PD
deficient cells
Hence, if a normal level of G6PD activity is found in a
heterozygotye, she is unlikely to be at risk of G6PD related
hemolysis
30. Prevention & Treatment
Phototherapy and exchange transfusion for
neonatal jaundice
Stop the offending drug
Blood transfusion if severe anemia
Folic acid supplementation
32. Wilson & Juegner criteria
for disease screening
1. The condition sought should be an important health
problem.
2. There should be an accepted treatment for patients with
recognized disease.
3. Facilities for diagnosis and treatment should be
available.
4. There should be a recognizable latent or early
symptomatic stage.
5. There should be a suitable test or examination.
6. The test should be acceptable to the population.
33. Wilson & Juegner criteria
for disease screening (cont.)
7. The natural history of the condition, including
development from latent to declared disease, should be
adequately understood.
8. There should be an agreed policy on whom to treat as
patients.
9. The cost of case-finding (including diagnosis and
treatment of patients diagnosed) should be economically
balanced in relation to possible expenditure on medical
care as a whole.
10. Case-finding should be a continuing process and not
a “once and for all” project
34. Diseases for which neonatal
screening is being done
Glucose 6 phosphate dehydrogenase
deficiency (G6PD levels)
Congenital hypothyroidism (TSH)
Congenital adrenal hyperplasia (17OHP)
Galactosemia
Biotinidase deficiency
35. Take home message
Answer to neonatal hyperbilirubemia is not just photo-
therapy and exchange transfusion, Do investigate for its
cause
G6PD deficiency is not very uncommon condition as
approximately 5% of world’s population is affected, so
should be kept in mind
In view of a high gene frequency for a disorder that is
manageable with just elimination of a few drugs and
foodstuffs, newborn screening is the need of the hour