Methemoglobinemia in Hemodialysis Patients due to Acute Chlorine Intoxication: A Case Series Calling Attention on an Old Problem.

INTRODUCTION: Hemodialysis uses municipal water that must be strictly purified and sterilized to be used for that procedure. Large amounts of decontaminants are often used, such as chlorine, and if these compounds are not subsequently removed they can be transferred to the blood of patients causing complications including methemoglobinemia. METHODS: In this case series study, dialysis patients in one unit were evaluated. We reviewed clinical characteristics and laboratory findings obtained on the day when the water supply was disinfected with chlorine, with the aim to quantify methemoglobin concentrations. Our objective was to characterize the clinical presentation and management of patients who presented with methemoglobinemia on a specific index day. We also reviewed reported cases in the literature regarding this underreported complication. RESULTS: Eight patients who presented with chlorine intoxication were evaluated. The methemoglobin concentrations were between 1.3% and 7.9% (reference value 0-1%). We believe this to be caused by water containing 0.78 mg/L of total chlorine. Seven patients presented with cyanosis, 4 with dizziness, 6 with dark brown blood, 4 with dyspnea, and 4 with headache and hemolytic anemia. Subjects were treated with supplemental oxygen, methylene blue, intravenous vitamin C, blood transfusions, and increased doses of erythropoietin. No patient died, and all continued with their usual hemodialysis sessions. CONCLUSION: Acute chlorine intoxication transferred by the water used during hemodialysis sessions can present with methemoglobinemia accompanied by cyanosis, oxygen desaturation, and hemolytic anemia. Chlorine levels should be carefully monitored in the water used for hemodialysis treatment.

Successful steroid tapering and partial treatment of suspected immune-mediated haemolytic anaemia in a dog with equine placenta extract supplementation: A case report.

Background: We report on the clinical management and outcome of an 11-year-old dog diagnosed with suspected refractory immune-mediated anemia (IMHA) and treated with equine placental extract supplementation. Case Description: The patient had received standard treatment with subcutaneous infusion of prednisone (2 mg/kg) and oral administration (1.3 mg/kg semel in die [sid]), with limited success as hematocrit (HCT) values continued to fall rapidly, and the patient continued to have severe symptoms of fatigue. The patient was then put on equine placental extract supplements, after which the patient's physical exhaustion was improved, and although the HCT level initially continued to fall, it eventually began to rise and remained near normal for approximately 2 years. A significant reduction in prednisone use was achieved with placental supplementation. Conclusion: Equine placental supplementation may be useful as a new complementary therapy for suspected refractory IMHA.

Severe Hemolytic Anemia and Metabolic Acidosis at Birth with Glutathione Synthetase Deficiency and Progressive Neurological Symptoms on Follow-Up.

BACKGROUND Glutathione synthetase deficiency (GSD) is a rare autosomal recessive disorder caused by glutathione synthetase (GSS) gene variants that occur in 1 in 1 million individuals. The severe form of GSD is characterized by hemolytic anemia, metabolic acidosis with 5-oxoprolinuria, progressive neurological symptoms, and recurrent bacterial infections. This case report presents a male Japanese infant with severe hemolytic anemia and metabolic acidosis at birth caused by GSD, who developed progressive neurological symptoms on follow-up. CASE REPORT A Japanese male term infant developed severe hemolytic anemia and metabolic acidosis in the early neonatal period. We suspected GSD based on his symptoms and a high 5-oxoproline urine concentration. We began correcting his metabolic acidosis and administering vitamins C and E supplements. The patient required blood transfusion twice during the acute phase for hemolytic anemia. After age 1 month, he maintained good control of metabolic acidosis and hemolytic anemia. A definitive diagnosis of GSD was made based on high concentrations of 5-oxoproline in urine, low concentrations of glutathione and GSS activity in erythrocytes, and genetic testing. Several episodes of febrile convulsions were started at age 11 months, but none occurred after 2 years. At the last follow-up at age 25 months, metabolic acidosis and hemolytic anemia were well controlled, but he had mild neurodevelopmental delay. CONCLUSIONS This case report shows that GSD can present with severe hemolytic anemia and metabolic acidosis at birth, and manifest with subsequent neurological impairment despite early diagnosis and treatment. Therefore, a careful long-term follow-up that includes neurological evaluation is essential for patients with GSD.

Transient neonatal hemolytic anemia due to the novel gamma globin gene mutation HBG2:C.290T>C, p.Leu97Pro (hemoglobin Wareham).

Unstable gamma globin variants can cause transient neonatal hemolytic anemia. We have identified a novel variant in a newborn who presented with jaundice and anemia requiring phototherapy and red blood cell transfusion. The patient was found to be heterozygous for the mutation HGB2:c.290T>C, p.Leu97Pro, which we have termed hemoglobin (Hb) Wareham. This substitution is expected to generate an unstable hemoglobin with increased oxygen affinity based on the homologous mutation previously described in the beta globin gene, which is termed as Hb Debrousse. The patient fully recovered by 9 months of age as expected with the transition from fetal to adult hemoglobin.

Ficus glumosa Del. reduces phenylhydrazine-induced hemolytic anaemia and hepatic damage in Wistar rats.

OBJECTIVES: Anemia is a direct or indirect consequence of oxidative stress via free radicals on erythrocytes and subsequently on other tissues like liver. Ficus glumosa constitute a rich pharmacologically compound that can prevent or repair oxidative damage. Therefore, this study seeks to evaluate the effect of F. glumosa on phenylhydrazine-induced hemolytic anemia and hepatic damage in rats. METHODS: Twenty-four (24) albino Wistar rats were assigned to four (4) experimental groups (n=6) as follows: Group I (non-anemic control) and Group 2 (anemic control) received normal saline, while Group III and IV (test groups) 200 and 400 mg/kg of aqueous leaf extract of F. glumosa (ALEFG), respectively. All the groups were treated orally (via a cannula) for seven consecutive days. Intraperitoneal (IP) injection of phenylhydrazine (PHZ) at 40 mg/kg for two consecutive days induced hemolytic anemia in group II to IV before treatment. Rats of all groups were anaesthetized and sacrificed 24 h after the last treatment. Blood and liver samples were collected for some hematological indices, liver function test, antioxidant parameter and histological analysis. RESULTS: The LD50 of ALEFG was assessed orally in rats and found to be above 5,000 mg/kg body weight. Significant (p<0.05) decreases in the level of red blood cell (RBC), hemoglobin (HGB) concentrations and packed cell volume (PCV) by 50% after 2 days of PHZ induction, were attenuated by more than 50% after 7 days administration of ALEFG at 200 and 400 mg/kg. The percentage change in body weight increased significantly (p<0.05) after 7 days post PHZ-induced anemia, but those that received oral administration of ALEFG (at 200 and 400 mg/kg) for 7 days increased significantly (p<0.05) by more than 2%, dose-dependently compared to anemic untreated group. Increased level of serum ALT, AST, ALP and GGT in PHZ-induced anemic animals, were significantly (p<0.05) attenuated in the groups that received oral administration of ALEFG (at 200 and 400 mg/kg) for 7 days. Decreased level of catalase (CAT) and superoxide dismutase (SOD) activities with concomitant increase in malondialdehyde (MDA) content from PHZ-induced untreated group, were significantly (p<0.05) mitigated in the rats that received oral administration of ALEFG (at 200 and 400 mg/kg) for 7 days. Histopathological analysis showed that ALEFG could remarkably though not completely mitigated PHZ-induced hepatic damage. CONCLUSIONS: Our data suggests that the leaves of F. glumosa contain important antioxidant(s) that could effectively reduce hemolytic anemia and hepatic damage, especially during phenylhydrazine-induced toxicity.

Low serum folate concentrations in dogs with non-associative immune-mediated haemolytic anaemia.

BACKGROUND: Folate deficiency in people can occur in conditions causing increased demand, including haemolytic anaemia. This has not been investigated in dogs with non-associative immune-mediated haemolytic anaemia (IMHA). METHODS: Cohort study of 15 dogs with non-associative IMHA. Haematocrit (HCT) and serum folate concentrations were measured at presentation and each subsequent venipuncture performed for monitoring. The relationship between serum folate concentrations and HCT was investigated using linear and logistic mixed-effects regression models and in paired samples using a one-tailed paired t-test. RESULTS: Low serum folate concentrations occurred in five of 15 dogs. In 126 samples, a significant positive relationship was found between HCT and corresponding serum folate concentrations. A significant relationship was found between dichotomised folate concentrations (below the reference interval or within/above the reference interval) and HCT and between serum folate concentrations and dichotomised HCT (less than or equal/above 0.30 L/L). For paired samples (available in eight dogs), the mean serum folate concentration of samples with the lowest HCT was significantly lower than that of samples in which the HCT first exceeded 0.30 L/L. CONCLUSIONS: Low serum folate concentrations were observed in some dogs with non-associative IMHA. Further studies are needed to determine the cause and investigate whether folate supplementation would be beneficial.

Acute Hemolytic Anemia Caused by G6PD Deficiency in Children in Mayotte: A Frequent and Severe Complication.

Severe hemolytic anemia is a rare complication of glucose-6-phosphate dehydrogenase (G6PD) deficiency. It occurs with the Mediterranean (Med) variant corresponding to a class 2 deficiency according to the World Health Organization (WHO) classification, and it correlates with a severe deficiency in G6PD activity. In Mayotte, the majority of patients have the African (A-) variant as a WHO class 3 deficiency. Yet we have observed numerous cases of severe hemolytic anemia defined by a hemoglobin level of <6 g/dL. In this study, we aimed to describe the epidemiological, clinical, and biological features as well as the treatment modalities of children presenting with a severe hemolytic crisis secondary to G6PD deficiency in Mayotte. The secondary objective was to study the disease genotype when this information was available. Between April 2013 and September 2020, 73 children presented with severe anemia because of G6PD deficiency in Mayotte. The median hemoglobin level during the hemolytic crises was 3.9 g/dL. All of the patients underwent a transfusion and hospitalization. Twenty patients had a disease genotype: 11 had the African mutation and 9 had the Med mutation. Although they are among the most common triggers of G6PD acute hemolytic anemia, drugs were found to not be present and fava bean ingestion was found in only 1 child. One of the specific triggers was traditional medicine, including Acalypha indica . Severe hemolytic crisis in children because of G6PD deficiency is a frequent occurrence in Mayotte. The patients had severe disease symptoms, but the severity did not correlate with the genotype: the African (A-) variant and the Med variant resulted in the same level of disease severity.

Therapeutic plasma exchange in non-immune hemolytic anemia associated with henna ingestion: A case report.

Henna is a herb that is used in traditional medicine for medical purposes as well as in the field of cosmetic. It is one of the agents that can trigger hemolytic crisis in G6PD deficient patients but it is considered safe in patients with normal G6PD enzyme. Here we present a case of non-immune hemolytic anemia occurred after ingestion of a homemade solution containing henna powder. Therapeutic plasma exchange was performed daily for 3 subsequent days and the hemoglobin levels and hemolytic markers were improved dramatically. Laboratory test revealed a normal G6PD enzyme level six weeks after recovery. We would like to emphasize the possibility of unexpected adverse effects and undefined ingredients of herbal products. Therapeutic plasma exchange can be a promising treatment option in such cases.

[A case of Hemolytic anemia caused by subacute lead poisoning].

Lead poisoning is characterized by nervous, digestive and blood system damage, such as neurasthenia, abdominal pain, abdominal distension, jaundice, small cell hypochromic anemia and so on. A case of severe hemolytic anemia caused by subacute lead poisoning was treated in Beijing Chaoyang Hospital Affiliated to Capital Medical University. The main symptoms of the patient were abdominal colic, constipation and hemolytic anemia.

Iron Therapy in Chronic Kidney Disease: Days of Future Past.

Anemia affects millions of patients with chronic kidney disease (CKD) and prompt iron supplementation can lead to reductions in the required dose of erythropoiesis-stimulating agents, thereby reducing medical costs. Oral and intravenous (IV) traditional iron preparations are considered far from ideal, primarily due to gastrointestinal intolerability and the potential risk of infusion reactions, respectively. Fortunately, the emergence of novel iron replacement therapies has engendered a paradigm shift in the treatment of iron deficiency anemia in patients with CKD. For example, oral ferric citrate is an efficacious and safe phosphate binder that increases iron stores to maintain hemoglobin levels. Additional benefits include reductions in fibroblast growth factor 23 levels and the activation of 1,25 dihydroxyvitamin D. The new-generation IV iron preparations ferumoxytol, iron isomaltoside 1000, and ferric carboxymaltose are characterized by a reduced risk of infusion reactions and are clinically well tolerated as a rapid high-dose infusion. In patients undergoing hemodialysis (HD), ferric pyrophosphate citrate (FPC) administered through dialysate enables the replacement of ongoing uremic and HD-related iron loss. FPC transports iron directly to transferrin, bypassing the reticuloendothelial system and avoiding iron sequestration. Moreover, this paper summarizes recent advancements of hypoxia-inducible factor prolyl hydroxylase inhibitors and future perspectives in renal anemia management.

Siblings with pediatric sodium chlorite toxicity causing methemoglobinemia, renal failure and hemolytic anemia.

INTRODUCTION: Over the past decade, Miracle Mineral Solution (sodium chlorite) has been promoted as a cure-all for many conditions. CASE REPORT: A 9-year-old boy presented with his brother after they accidentally ingested a small amount of undiluted 22.4% sodium chlorite. Symptoms included nausea, vomiting, diarrhea, and dyspnea. Oxygen saturation remained 71% despite supplemental oxygen (15L/min). The patient was noted to have dark chocolate-appearing blood, minimal urine output, diffuse pallor and cyanosis. He developed methemoglobinemia, renal failure requiring renal replacement therapy and hemolysis requiring blood transfusion. DISCUSSION: These are the 7th and 8th reported cases of sodium chlorite toxicity by ingestion and the second and third in children. Takeaway for Physicians: Miracle Mineral Solution is a commonly purchased potentially lethal compound that can cause methemoglobinemia with respiratory failure, hemolytic anemia requiring transfusion and renal failure requiring dialysis.

Interleukin-4 Administration or Zinc Supplementation Is Effective in Preventing Zinc Deficiency-Induced Hemolytic Anemia and Splenomegaly.

Nutritional zinc deficiency aggravates inflammation, subsequently causing anemia and splenomegaly in rats; however, the mechanism underlying such splenomegaly remains poorly understood. Therefore, in this study, we aimed to elucidate the mechanisms underlying the splenomegaly and anemia occurring in zinc-deficient rats and investigate whether these effects of zinc deficiency could be reversed by interleukin (IL)-4 administration or zinc supplementation. Five-week-old male Sprague-Dawley rats were fed a standard diet; fed a zinc-deficient diet (n = 7 each) and injected with saline or IL-4; or fed a zinc-deficient diet for 6 weeks followed by a standard diet for 4 weeks thereafter. White blood cells, segmented neutrophils, platelets, CD4+ T cells, CD11b/c+ granulocytes, CINC/GRO+ cells, and myeloperoxidase-positive cells in the blood and spleen of the zinc-deficient rats were significantly higher than those in all the other groups. Conversely, red blood cells, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, lymphocytes, and CD8+ T cells in the blood of the zinc-deficient rats were significantly lower than those in the other groups. Furthermore, serum aspartate aminotransferase, lactate dehydrogenase, indirect bilirubin concentrations, and erythrocyte osmotic fragility in the zinc-deficient rats were significantly higher than those in the other groups. Moreover, zinc deficiency significantly decreased the GATA1 protein levels in the spleen. Collectively, these results indicate that zinc deficiency aggravates the inflammatory response and causes hemolytic anemia and splenomegaly. Importantly, IL-4 administration and zinc supplementation can reverse the zinc deficiency-induced hemolytic anemia and splenomegaly.

High dose vitamin C induced methemoglobinemia and hemolytic anemia in glucose-6-phosphate dehydrogenase deficiency.

Investigational use of intravenous vitamin C has been on the rise, but its side effects may be underreported. A 75-year-old woman presented with acute onset of jaundice, dark urine and shortness of breath after receiving 30 g of vitamin C infusion as an unconventional therapy for her hemifacial spasm. Diagnosis of methemoglobinemia and hemolytic anemia was made clinically and confirmed on laboratory tests. She recovered with supportive treatment and packed cell transfusion. Her previously unrecognised underlying condition of glucose-6-phosphate dehydrogenase (G6PD) deficiency was confirmed months after the initial presentation. This is the first reported case of methemoglobinemia and hemolytic anemia induced by high dose vitamin C in a female patient with G6PD deficiency. The dosage of vitamin C administered was also relatively low compared with previous adult reports. When administered at physiological dose, vitamin C can be used as an alternative to methylene blue in treatment of methemoglobinemia in patients with G6PD deficiency. However at supraphysiological dose vitamin C can paradoxically lead to hemolytic anemia in the same group of patients. Physicians should be alert of these potential complications of high dose vitamin C.

Intractable mechanical hemolytic anemia complicating mitral valve surgery: a case series study.

BACKGROUND: Intractable, mechanical hemolytic anemia (IMHA) is a rare catastrophic complication following mitral valve surgery. We analyzed patient characteristics and IMHA management by reoperations after mitral valve surgery. METHODS: We collected medical records from mitral valve patients requiring reoperation due to IMHA. INCLUSION CRITERIA: hemoglobin < 100 g/L; positive hemolysis tests and echocardiography results; and exclusion of other hemolysis causes. RESULTS: Data from 25 IMHA cases included 10 (40%) early onset (1.3 (0.3,3.0) months) and 15 (60%) late onset (120 (24,204) months) cases. Early IMHA etiologies included surgical defects (6, 60%), uncontrolled infection (3, 30%) and Bechet's disease (1, 10%). Late IMHA etiologies included degeneration (13, 87%), new infection (1, 7%) and trauma (1, 7%). There were more mechanical valves (15, 88%) than bio-valves (2, 12%); the main valvular dysfunction was paravalvular leak (16, 64%). IMHA manifestations included jaundice (18, 72%), dark urine (21, 84%), heart failure (16, 64%), acute kidney injury (11, 44%), hepatomegaly (15, 60%), splenomegaly (15, 60%) and pancreatitis (1, 4%). Laboratory results showed decreased hemoglobin (70 ± 14 g/L) and increased bilirubin (72 ± 57 µmol/L), lactate dehydrogenase (2607 ± 2142 IU/L) and creatinine (136 ± 101 µmol/L) levels. Creatinine level negatively correlated with hemoglobin level (B = -3.33, S.E. B = 1.31, Exp(B) = 368.15, P = 0.018). Preoperative medications included iron supplements (20, 80%), erythropoietin (16, 64%) and beta-blocker (22, 88%). Two patients died of cardiac causes before reoperation. The other 23 underwent reoperation with long surgical times (aortic cross clamp 124 ± 50 min, cardiopulmonary bypass 182 ± 69 min) and blood transfusions (red blood cells 6 (6, 8) units, plasma 600 (400,800) ml, platelet 1(0,2) units). Postoperative complications included cardiac dysfunction (5, 22%), arrhythmia (10, 43%), sepsis (6, 26%), pulmonary infection (5, 22%), gastrointestinal bleeding (3, 13%), cerebral hemorrhage (2, 9%), chronic renal dysfunction (1, 4%) and surgical hemorrhage (1, 4%). Five (33%) patients died after reoperation from cardiac dysfunction (3, 60%), septic shock (1, 20%) and self-discharge (1, 20%). CONCLUSIONS: IMHA induces severe multi-organ dysfunction, contributing to high mortality. Perioperative management should focus on etiological treatment, organ protection, and blood management.

Successful management of Heinz body hemolytic anemia associated with leek (Allium ampeloprasum) ingestion in a South American coati (Nasua nasua).

OBJECTIVE: To describe the diagnosis, management, and outcome of Heinz body hemolytic anemia in a South American coati (Nasua nasua) secondary to suspected leek (Allium ampeloprasum) toxicosis. CASE SUMMARY: A South American coati presented with Heinz body hemolytic anemia following addition of leeks to its diet for 2-5 days prior to initial presentation. Administration of a whole blood transfusion from an animal of the same species (conspecific) and supportive care resulted in immediate improvement in clinical signs. Normal behavior fully returned within 6 days of transfusion. Hematological evidence of anemia resolved by 4 weeks and there were no significant features of oxidative injury present by 8 weeks following initial presentation. NEW INFORMATION PROVIDED: This is the first reported case of Heinz body hemolytic anemia, suspected leek toxicosis, and administration of a blood transfusion in this species.

Infantile Pyknocytosis: An Uncommon Cause of Newborn Hemolytic Anemia.

Infantile pyknocytosis is a rare cause of neonatal hemolytic anemia, which presents in the first few weeks of life. We report a classic case of infantile pyknocytosis that presented to our institution with rebound hyperbilirubinemia after receiving phototherapy. The infant was found to have a hemoglobin of 5.8 g/dL, requiring a total of 15 mL/kg of red blood cells (in 2 separate transfusions) before discharge. The diagnosis was ultimately made by a review of the peripheral blood smear. We review the literature and suggest pediatricians consider infantile pyknocytosis on their differential when hemolytic anemia presents in the newborn period.

Serum Folate Levels in Patients with Chronic Hemolytic Anemia on Regular Folic Acid Supplementation Before and After Dose Modification.

OBJECTIVE: In light of the recommendation of folic acid supplementation in chronic hemolytic anemia, with possible supratherapeutic dosing and associated side effects, we performed this study to investigate serum folate levels in children with chronic hemolytic anemia. METHODS: Phase 1 was a cross-sectional study of 134 patients in the Pediatric Hematology service, documenting daily dosage and performing serum folate levels. In phase 2, we reduced the dose to 1 mg for 148 patients and repeated the testing after six months. RESULTS: We found very high serum folate levels with Phase 1, with 93.2% above the upper level of normal. In Phase 2, values remained high with 42.5% above the acceptable upper limit. CONCLUSION: Doses of folic acid given to sickle cell and thalassemia patients exceed their actual needs. This should be re-evaluated to strike a balance between benefit and harm, with close monitoring of serum folate levels.

Hemolytic anemia caused by non-D minor blood incompatibilities in a newborn.

Hyperbilirubinemia is one of the most widely seen cause of neonatal morbidity. Besides ABO and Rh isoimmunization, minor blood incompatibilities have been also been identified as the other causes of severe newborn jaundice. We report a newborn with indirect hyperbilirubinemia caused by minor blood group incompatibilities (P1, M, N, s and Duffy) whose hemolysis was successfully managed with intravenous immunoglobulin therapy. A thirty-two gestational weeks of preterm male baby became severely icteric on postnatal day 11, with a total bilirubin level of 14.66 mg/dl. Antibody screening tests revealed incompatibility on different minor groups (P1, M, N, s and Duffy (Fya ve Fyb)). On postnatal day thirteen, the level of bilirubin increased to 20.66 mg/dl although baby was under intensive phototherapy. After the administration of intravenous immunoglobulin and red blood cell transfusion, hemoglobin and total bilirubin levels became stabilised. Minor blood incompatibilities should be kept in mind during differential diagnosis of hemolytic anemia of the newborn. They share the same treatment algorithm with the other types hemolytic anemia. New studies revealed that intravenous immunoglobulin treatment in hemolytic anemia have some attractive and glamorous results. It should be seriously taken into consideration for treatment of minor blood incompatibilities.

Severe Hyperkalemia Immediately After Birth.

BACKGROUND Hyperkalemia is an important cause of arrhythmias and a medical emergency that requires urgent treatment. The etiology is usually multifactorial. It is most frequently caused by impaired potassium secretion, followed by transcellular potassium shifts and an increased potassium load. CASE REPORT A male newborn developed monomorphic ventricular tachycardia 2 hours after birth. He was born in the 35th week of gestation by urgent C-section following placental abruption. Laboratory results showed hemolytic anemia (Hb 99 g/L, Hct 0.31) with increased bilirubin levels and reticulocytosis, thrombocytopenia (39×109/L), hypoglycemia (0.8 mmol/L), and severe hyperkalemia (9.8 mmol/L). Umbilical artery blood gas analysis showed hypoxemia with acidosis (pO2 3.8 kPa, pH 7.21, pCO2 7.84 kPa, HCO3 23.3 mmol/L, BE -5 mmol/L). Creatinine (102 µmol/L) and urea (9.8 mmol/L) were mildly elevated. Inflammatory markers were also increased (CRP 26 mg/L, blood leukocyte count 24×109/L). Early-onset sepsis, caused by Candida albicans, was confirmed approximately 24 hours after birth. Non-invasive ventilation with 35-40% O2 was necessary due to transient tachypnea. The neonate received a transfusion of packed red blood cells, a 10% glucose infusion, and empirical antibiotic therapy. Hyperkalemia accompanied by arrhythmias was treated with calcium gluconate, insulin, Sorbisterit enema, and, finally, by exchange transfusion. CONCLUSIONS We report a case of severe hyperkalemia in a newborn immediately after birth. Making a decision as early as possible regarding exchange transfusion is essential in patients with hyperkalemia with electrocardiogram changes and hemodynamic instability.

[Study on blood enrichment mechanism of steamed notoginseng based on metabolomics method].

In this paper,ultra performance liquid chromatography coupled with time-of-flight mass spectrometry( UPLC-Q-TOFMS) technique was used to study the effects of steamed notoginseng on endogenous markers in plasma of rats with hemolytic anemia induced by N-acetyl phenyl hydrazine( APH). The aim was to find out the potential biomarkers and possible blood enriching mechanism of steamed notoginseng on hemolytic anemia rats. In the experiment,steamed notoginseng medicine pair( steamed notoginseng-ginseng)and compound medicines( Sanqi Yangxue Capsules) were used respectively to intervene in APH-induced hemolytic anemia model rats.Then blood routine indexes such as red blood cells( RBC),hemoglobin( Hb) and related organ indexes were determined. As compared with the blank group,the RBC and Hb levels in the model group were substantially decreased( P< 0. 01),while the liver and spleen organ indexes were increased( P< 0. 05). The results of blood routine and organ index demonstrated that the blood deficiency model was successfully established. Steamed notoginseng can significantly increase the RBC level of rats( P<0. 01),and the related indicators of each drug group had a trend of returning to normal levels,verifying the blood enriching effect of steamed notoginseng. The UPLC-Q-TOF-MS technique,principal component analysis( PCA) and partial least squares-discrimination analysis( PLS-DA) were used to analyze the metabolic profiles between the normal group and the model group. Twenty-six potential biomarkers for hemolytic anemia were screened in plasma. Nine metabolites such as retinol,L-valine,and arachidonic acid were down-regulated in the blood deficiency rats,and 17 metabolites such as protoporphyrin Ⅸ and niacinamide were up-regulated. The metabolic level of biomarkers could be changed to a normal state after rats were given with steamed notoginseng,drug pairs,and compound prescriptions. It can be speculated that steamed notoginseng may play a role of blood tonifying by improving biosynthesis of valine,leucine and isoleucine,as well as metabolic pathways such as retinol metabolism and arachidonic acid metabolism.