Heinz-Body Anaemia in the Newborn

The association of Heinz-bodies within erythrocytes, extreme distortion of the size and shape of erythrocytes and hemolytic anemia in newborn infants, especially premature infants, has been sporadically reported in the medical literature since 1948. Heinz-bodies are thought to be either remnants of disintegrated membranes of erythocytes or abnormal products of hemoglobin metablism, and are demonstrable only by supravital staining techniques. The present study contributes two case reports and discusses the sequence of the clinical and hematologic manifestations. The first patient was a full-term infant who developed jaundice and symptoms attributable to anemia at 2 weeks of life. The second infant was prematurely born, did not develop jaundice but showed large numbers of Heinz-bodies (70%) as the anemia progressed. Both patients responded well to a single transfusion of packed blood cells, with complete reversal of the abnormal peripheral blood findings. None of the usual causes of hemolysis could be demonstrated by extensive laboratory tests. Agents such as phenylhydrazine, known to produce Heinz-bodies, could not be incriminated. The phenomenon of Heinz-body formation in infants may be more common than is apparent as the technique of demonstration is not commonly a part of the routine study of infants with evidence of hemolytic anemia. This technique is described and illustrations of erythrocytes containing Heinz-bodies are provided.

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Idiopathic Heinz Body Hemolytic Anemia in Newborn Infants

Journal of Pediatric Hematology/Oncology ◽

10.1097/00043426-198921000-00002 ◽

1989 ◽

Vol 11 (1) ◽

pp. 3-7 ◽

Cited By ~ 7

Author(s):

A. Ballin ◽

E. J. Brown ◽

A. Zipursky

Keyword(s):

Hemolytic Anemia ◽

Newborn Infants ◽

Heinz Body

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Letter: Heinz body hemolytic anemia

Archives of Internal Medicine ◽

10.1001/archinte.136.9.1067a ◽

1976 ◽

Vol 136 (9) ◽

pp. 1067a-1067

Author(s):

E. P. Gabor

Keyword(s):

Hemolytic Anemia ◽

Heinz Body

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Immunologic Studies of Antithrombin III Heparin Cofactor in the Newborn

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646736 ◽

1978 ◽

Vol 39 (03) ◽

pp. 624-630 ◽

Cited By ~ 21

Author(s):

W E Hathaway ◽

L L Neumann ◽

C A Borden ◽

L J Jacobson

Keyword(s):

Gestational Age ◽

Antithrombin Iii ◽

Newborn Infants ◽

Term Infant ◽

Sick Newborn ◽

At Iii ◽

Thrombotic Complications ◽

Low Levels ◽

Collection Methods ◽

Made In

SummarySerial quantitative immunoelectrophoretic (IE) measurements of antithrombin III heparin cofactor (AT III) were made in groups of well and sick newborn infants classified by gestational age. Collection methods (venous vs. capillary) did not influence the results; serum IE measurements were comparable to AT III activity by a clotting method. AT III is gestational age-dependent, increasing from 28.7% of normal adult values at 28-32 weeks to 50.9% at 37-40 weeks, and shows a gradual increase to term infant levels (57.4%) by 3-4 weeks of age. Infants with the respiratory distress syndrome (RDS) show lower levels of AT III in the 33-36 week group, 22% vs. 44% and in the 37-40 week group, 33.6% vs. 50.9%, than prematures without RDS. Infants of 28-32 week gestational age had only slight differences, RDS = 24%, non-RDS = 28.7%. The lowest levels of AT III were seen in patients with RDS complicated by disseminated intravascular coagulation and those with necrotizing enterocolitis. Crossed IE on representative infants displayed a consistent pattern which was identical to adult controls except for appropriate decreases in the amplitude of the peaks. The thrombotic complications seen in the sick preterm infant may be related to the low levels of AT III.

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Acute methemoglobinemia with hemolytic anemia following bio-organic plant nutrient compound exposure: Two case reports

Indian Journal of Critical Care Medicine ◽

10.4103/0972-5229.126089 ◽

2014 ◽

Vol 18 (2) ◽

pp. 115-117 ◽

Cited By ~ 1

Author(s):

Santoshi Balkrishna Malkarnekar ◽

Raveesha Anjanappa ◽

L. Naveen ◽

B. G. Kiran

Keyword(s):

Hemolytic Anemia ◽

Case Reports ◽

Plant Nutrient ◽

Compound Exposure

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Clinical spectrum and severity of hemolytic anemia in glucose 6-phosphate dehydrogenase–deficient children receiving dapsone

Blood ◽

10.1182/blood-2012-03-416032 ◽

2012 ◽

Vol 120 (20) ◽

pp. 4123-4133 ◽

Cited By ~ 60

Author(s):

Allan Pamba ◽

Naomi D. Richardson ◽

Nick Carter ◽

Stephan Duparc ◽

Zul Premji ◽

...

Keyword(s):

Blood Transfusion ◽

Hemolytic Anemia ◽

G6pd Deficiency ◽

Case Reports ◽

Drug Induced ◽

Once Daily ◽

Maximum Decrease ◽

Life Threatening ◽

The Mean ◽

Glucose 6 Phosphate Dehydrogenase

AbstractDrug-induced acute hemolytic anemia led to the discovery of G6PD deficiency. However, most clinical data are from isolated case reports. In 2 clinical trials of antimalarial preparations containing dapsone (4,4′-diaminodiphenylsulfone; 2.5 mg/kg once daily for 3 days), 95 G6PD-deficient hemizygous boys, 24 G6PD-deficient homozygous girls, and 200 girls heterozygous for G6PD deficiency received this agent. In the first 2 groups, there was a maximum decrease in hemoglobin averaging −2.64 g/dL (range −6.70 to +0.30 g/dL), which was significantly greater than for the comparator group receiving artemether-lumefantrine (adjusted difference −1.46 g/dL; 95% confidence interval −1.76, −1.15). Hemoglobin concentrations were decreased by ≥ 40% versus pretreatment in 24/119 (20.2%) of the G6PD-deficient children; 13/119 (10.9%) required blood transfusion. In the heterozygous girls, the mean maximum decrease in hemoglobin was −1.83 g/dL (range +0.90 to −5.20 g/dL); 1 in 200 (0.5%) required blood transfusion. All children eventually recovered. All the G6PD-deficient children had the G6PD A− variant, ie, mutations V68M and N126D. Drug-induced acute hemolytic anemia in G6PD A− subjects can be life-threatening, depending on the nature and dosage of the drug trigger. Therefore, contrary to current perception, in clinical terms the A− type of G6PD deficiency cannot be regarded as mild. This study is registered at http://www.clinicaltrials.gov as NCT00344006 and NCT00371735.

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Spurious, marked leukocytosis in 2 cats with Heinz body hemolytic anemia

Veterinary Clinical Pathology ◽

10.1111/vcp.12860 ◽

2020 ◽

Vol 49 (2) ◽

pp. 232-239

Author(s):

Courtney E. Johnson ◽

Davis M. Seelig ◽

Frances M. Moore ◽

Tammy J. Ruska ◽

Daniel A. Heinrich

Keyword(s):

Hemolytic Anemia ◽

Heinz Body

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Studies on Schmauch Bodies. I. The Incidence in Normal Cats (Felis Domestica) and the Morphologic Relationship to Heinz Bodies

Blood ◽

10.1182/blood.v25.6.999.999 ◽

1965 ◽

Vol 25 (6) ◽

pp. 999-1008 ◽

Cited By ~ 14

Author(s):

Anica Sirec ◽

Marija Sondić ◽

TIHOMIL BERITIĆ

Keyword(s):

Phase Contrast ◽

Phase Contrast Microscopy ◽

Heinz Bodies ◽

Morphologic Characteristics ◽

Wide Range ◽

Contrast Microscopy ◽

Supravital Staining

Abstract Inclusions in the erythrocytes of normal cats, called Schmauch bodies, have been demonstrated by means of phase contrast microscopy and supravital staining. A very wide range of their incidence, but no correlation with the age of animals has been noted. By their identical staining reactions and common morphologic characteristics Schmauch and Heinz bodies are quite similar, although they might be produced by quite different mechanisms.

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Chronic Lymphocytic Leukemia Presenting as a Subcortical Watershed Infarct

Case Reports in Hematology ◽

10.1155/2019/2089359 ◽

2019 ◽

Vol 2019 ◽

pp. 1-5

Author(s):

Mridul Gupta ◽

Divita Singh ◽

Patrick Lee ◽

Sandhya Kadiyam

Keyword(s):

Chronic Lymphocytic Leukemia ◽

Hemolytic Anemia ◽

Immune Thrombocytopenia ◽

Case Reports ◽

Pure Red Cell Aplasia ◽

Lymphocytic Leukemia ◽

Red Cell ◽

Cerebral Infarcts ◽

Autoimmune Cytopenia ◽

Watershed Infarcts

Internal watershed infarcts (WI) involve white matter between deep and superficial arterial systems of middle cerebral artery. These infarcts are considered to be either from low blood flow or microembolism. Anemia is an extremely rare cause of watershed infarcts. Very few cases of hemolytic anemia causing watershed cerebral infarcts have been reported. Chronic lymphocytic leukemia (CLL) is frequently complicated with secondary autoimmune cytopenia such as autoimmune hemolytic anemia (AIHA), immune thrombocytopenia (ITP), and pure red cell aplasia. AIHA is present in about 7–10% of patients with CLL. AIHA from CLL presenting as WI is an extremely rare phenomenon with no previously published case reports to the best of our knowledge.

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