Acquired copper deficiency following prolonged jejunostomy feeds

2005 ◽  
Vol 42 (3) ◽  
pp. 227-231 ◽  
Author(s):  
S Jayakumar ◽  
P D Micallef-Eynaud ◽  
T D B Lyon ◽  
R Cramb ◽  
A N Jilaihawi ◽  
...  
Keyword(s):  
Copper Concentration ◽  
Copper Deficiency ◽  
Serum Vitamin ◽  
Liver Function Tests ◽  
Bone Marrow Examination ◽  
Serum Copper ◽  
Normal Serum ◽  
Jejunostomy Tube ◽  
Erythroid Hyperplasia ◽  
Copper Therapy

A 19-year-old man who developed extensive oesophageal lye (Alkali) stricture and received long-term enteral nutrition (eight months) with a jejunostomy tube developed macrocytic anaemia (Hb: 41 g/L) with leucopenia (white blood cell [WBC]: 3.0 x 109/L). The patient's serum vitamin B12, folate, iron and liver function tests were normal. Bone marrow examination revealed gross erythroid hyperplasia and cytoplasmic vacuolization of erythroid and myeloid elements. Further investigations revealed low serum copper (0.3 μmol/L) and ceruloplasmin concentrations (<30 mg/L) with marginally low normal serum concentration of red cell peroxidase (13 U/gHb), establishing the diagnosis of copper deficiency anaemia. The anaemia and leucopenia responded intermittently to intravenous copper therapy, but the serum copper concentration dropped when intravenous copper therapy was withdrawn. Enteral jejunostomy copper supplementation failed to maintain adequate serum copper concentrations. After stabilizing the general condition of the patient, a pharyngo-gastric anastamosis was performed and normal oral diet commenced, which restored normal serum copper concentration. This case report suggests that copper supplements in the form of copper sulphate are not adequately absorbed when administered through a jejunostomy tube.

scholarly journals Progressive myeloneuropathy with symptomatic anaemia

2019 ◽  
Vol 12 (12) ◽  
pp. e230025 ◽  
Author(s):  
Charlene L Rohm ◽  
Sara Acree ◽  
Louis Lovett
Keyword(s):  
Bone Marrow ◽  
Delayed Diagnosis ◽  
Serum Vitamin ◽  
Neurological Impairment ◽  
Serum Copper ◽  
Normal Serum ◽  
Neurological Deficits ◽  
Caucasian Woman ◽  
Symptomatic Anaemia ◽  
Unnecessary Procedures

Hypocupremia is a rare and under-recognised cause of bone marrow dysplasia and myeloneuropathy. A 47-year-old Caucasian woman had progressive ascending peripheral neuropathy and gait ataxia over 3 months and fatigue, dyspnoea and unintentional weight loss over 8 months. She had profound macrocytic anaemia and neutropenia. Initial workup included normal serum vitamin B12. Bone marrow biopsy was suggestive of copper deficiency. Serum copper levels were later confirmed to be undetectable. The patient received oral copper repletion which resulted in complete normalisation of haematological abnormalities 16 weeks later. However, neurological deficits persisted. This case describes a delayed diagnosis of hypocupremia as initially suggested through invasive testing. Associating myeloneuropathy with cytopenia is imperative for accurate and prompt diagnosis of hypocupremia, which can be confirmed by serum analysis alone. Developing an accurate differential diagnosis can help prevent unnecessary procedures. Furthermore, initiating prompt copper repletion prevents further neurological impairment. Neurological deficits are often irreversible.

Hematopathological Findings in Patients with Copper Deficiency and Hematologic Manifestations.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1680-1680
Author(s):  
Thorvardur R. Halfdanarson ◽  
Chin-Yang Li ◽  
Robert L. Phyliky ◽  
Neeraj Kumar ◽  
William J. Hogan
Keyword(s):  
Bariatric Surgery ◽  
Bone Marrow ◽  
Toxic Effect ◽  
Copper Deficiency ◽  
Plasma Cells ◽  
Bone Marrow Examination ◽  
Refractory Anemia ◽  
White Blood Count ◽  
Ringed Sideroblasts ◽  
Erythroid Hyperplasia

Abstract Background: Copper deficiency is increasingly being diagnosed in adults with malabsorption syndromes, especially following GI surgery such as gastric and bowel resections and bariatric surgery. The most common hematologic manifestations are refractory anemia and neutropenia and patients have been misdiagnosed as having myelodysplasia. Certain findings on bone marrow examination are felt to be characteristic for copper deficiency such as maturation arrest in the myeloid lineage, vacuolization of the erythroid and myeloid precursors and ringed sideroblasts. Methods: We reviewed all cases of copper deficiency diagnosed at the Mayo Clinic from 1974 – 2005. We also reviewed all cases of low serum copper (&lt; 0.75 μg/ml) identified in our heavy metals laboratory. Results: 123 patients with hypocupremia were identified. 77 patients were excluded as the hypocupremia was either transient or due to other factors such as Wilson’s disease. Twenty-five patients had hematologic manifestations, including anemia and leukopenia (13), isolated anemia (6), pancytopenia (5), and isolated neutropenia (1). Eighteen patients had a bone marrow biopsy. We were able to retrieve and review bone marrow slides in 11 cases. The bone marrow examination findings are shown in the table. The marrow cellularity was decreased in four cases. All cases had granulocytic hypoplasia but preserved megakaryopoiesis. Nine cases had relative erythroid hyperplasia. All but one bone marrow had cytoplasmic vacuoles in pronormoblasts and myelocytes. Increased iron within macrophages was seen in 9 cases and increased iron in plasma cells was noted in 8 cases. This was especially prominent in the cases with low peripheral white blood count. Ringed sideroblasts were seen in 4 cases and were more commonly seen in anemic patients. The initial bone marrow examination commonly suggested toxic effect (drugs or alcohol), myelodysplasia or were non-diagnostic. Conclusion: We have described the bone marrow findings in 11 copper deficient patients with abnormal blood counts. None of these patients was suspected of copper deficiency based on the initial marrow examination. The initial impression was commonly toxic effect due to the presence of cytoplasmic vacuolization. Patients with ringed sideroblasts were suspected of having MDS. Copper deficiency should be considered in patients with cytopenias and the described bone marrow findings, especially if there is evidence of malabsorption or a history of GI surgery such as gastric resection or bariatric surgery. Bone marrow findings Patient Cellularity Ery/gran/meg Vacuoles Iron (mø/PC) RS Hgb/Plt WBC/ANC nl: normal, 0: absent, Ery/gran/meg: erythro-/granulo-/megakaryopoiesis, Iron (mø/PC): Iron in macrophages and plasma cells, RS: Ringed sideroblasts 1 ↓ ↑/↓/nl Yes ↑/↑ No 11.3/203 3.2/1.1 2 Nl ↑/↓/nl Yes 0/0 No 11.4/192 5.6/4.0 3 Nl ↑/↓/nl No ↑/0 No 10.6/95 3.0/2.2 4 ↓ ↑/↓/nl Yes ↑/↑ No 13.6/128 4.2/0.92 5 Nl ↑/↓/nl Yes ↑/↑ 10% 9.8/215 1.4/0.6 6 ↓ ↑/↓/nl Yes ↑/↑ No 7.9/292 1.8/0.18 7 Nl ↑/↓/nl Yes ↑/↑ No 10.6/280 2.7/1.4 8 Nl nl/↓/nl Yes ↑/↑ 20% 8.1/330 1.5/0.24 9 Nl ↑/↓/nl Yes ↑/↑ &lt;1% 9.4/252 1.3/0.25 10 ↓ Nl/↓/nl Yes 0/0 No 10.5/167 2.4/1.67 11 Nl ↑/↓/nl Yes ↑/↑ yes 12.5/224 4.2/3.9

P10. Copper deficiency myelopathy despite of normal serum copper levels?

2012 ◽  
Vol 123 (10) ◽  
pp. e105-e106
Author(s):  
K. Haaf ◽  
U.W. Buettner ◽  
S. Biethahn
Keyword(s):  
Copper Deficiency ◽  
Serum Copper ◽  
Normal Serum

scholarly journals Reversal of Jaundice in Two Patients with Inoperable Cholangiocarcinoma Treated with Cisplatin and Gemcitabine Combination

2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
Maarten Criel ◽  
Filip Geurs ◽  
Siegfried Ponette ◽  
Katrien Bulte ◽  
Johan Ponette
Keyword(s):  
Liver Function ◽  
Combination Chemotherapy ◽  
Serum Bilirubin ◽  
Liver Function Tests ◽  
Normal Serum ◽  
Tumor Type ◽  
Chemotherapeutic Approach ◽  
Function Tests ◽  
Severe Jaundice

Two patients are presented with severe jaundice, due to inoperable cholangiocarcinoma. The chemotherapeutic approach in patients with severe jaundice is discussed. Many schedules of chemotherapy were developed in this tumor type with normal serum bilirubin. We report here the first successful use of cisplatin and gemcitabine combination chemotherapy in these patients. Tolerability was good and liver function tests gradually improved.

Copper Deficiency with Cow's Milk Diet

PEDIATRICS ◽  
1981 ◽  
Vol 68 (3) ◽  
pp. 397-400
Author(s):  
Yehezkel Naveh ◽  
Anna Hazani ◽  
Moshe Berant
Keyword(s):  
Serum Iron ◽  
Copper Deficiency ◽  
Iron Concentration ◽  
Bone Age ◽  
Serum Copper ◽  
Term Infant ◽  
Deficiency Anemia ◽  
Cow’S Milk ◽  
Cow's Milk ◽  
Iron Folic Acid

A 6-month-old full-term infant had severe anemia and neutropenia. The patient was being fed cow's milk and a diet of corn flour. Thorough investigation revealed low serum iron concentration, severe hypocupremia, low ceruloplasmin, retardation of bone age, and metaphysial irregularities and spurring. Bone marrow aspirate revealed cytoplasmic vacuolization in precursors of the erythroid and myeloid series and ringed sideroblasts. Therapy with oral iron, folic acid, and vitamin C was futile. Administration of copper sulfate resulted in brisk increase in neutrophils and reticulocytes. The child maintained normal levels of hemoglobin, neutrophils, serum copper and ceruloplasmin, and serum iron one year after copper therapy was discontinued. The probable role of unrecognized copper deficiency in causing anemia in infants more than 6 months of age is discussed, and the importance of serum copper examination in refractory iron deficiency anemia and neutropenia is stressed. To the best of our knowledge, no such case has previously been described in the literature.

scholarly journals Clinical Factors Associated With Serum Copper Concentration In Patients On Hemodialysis

2012 ◽  
Vol 31 (2) ◽  
pp. A38
Author(s):  
Ryota Ikee ◽  
Masataka Tsunoda ◽  
Naomi Sasaki ◽  
Megumi Sato ◽  
Nobuo Hashimoto
Keyword(s):  
Copper Concentration ◽  
Serum Copper ◽  
Clinical Factors ◽  
Factors Associated

scholarly journals Role of LDH levels in differentiating anemias

2021 ◽  
Vol 12 (9) ◽  
pp. 79-83
Author(s):  
Noorin Zaidi ◽  
Rasha Zia Usmani ◽  
Kshama Tiwari ◽  
Sumaiya Irfan ◽  
Syed Riaz Mehdi
Keyword(s):  
Megaloblastic Anemia ◽  
Serum Vitamin ◽  
Bone Marrow Examination ◽  
Serum Lactate ◽  
Deficiency Anemia ◽  
Serum Lactate Dehydrogenase ◽  
Biochemical Tests ◽  
Schilling Test ◽  
Blood Smears ◽  
Complete Blood Counts

Background: There is a need to differentiate megaloblastic anemia from mixed deficiency anemia as both require different management protocols. With the acquisition of more information about them, tests such as serum vitamin estimation and Schilling test, were found to have their limitations. Hence there is a need to search newer diagnostic candidates to differentiate between megaloblastic anemia and mixed deficiency anemia. Aims and Objective: The current study was undertaken to find usefulness of serum Lactate Dehydrogenase (LDH) in differentiating megaloblastic anemia from mixed deficiency anemia. Materials and Methods: 100 patients were included in the study. Blood smears were stained and analysed. Complete blood counts were performed. Bone marrow examination was done, where needed. Biochemical tests were performed for estimation of vitamin B12, Folate and for LDH. Results: Out of the 100 cases 51 were diagnosed as megaloblastic anemia and 49 were diagnosed as mixed deficiency anemia. The LDH levels were significantly higher in cases of megaloblastic anemia as compared to mixed deficiency anemia. Conclusion: Serum LDH levels can be used in differentiating megaloblastic anemia from mixed deficiency anemia.

scholarly journals Copper metabolism in mottled mouse mutants: copper therapy of brindled (Mobr) mice

1979 ◽  
Vol 180 (3) ◽  
pp. 605-612 ◽  
Author(s):  
J R Mann ◽  
J Camakaris ◽  
D M Danks ◽  
E G Walliczek
Keyword(s):  
Growth Response ◽  
Copper Deficiency ◽  
Lysyl Oxidase ◽  
Sebacic Acid ◽  
Copper Metabolism ◽  
Single Subcutaneous Injection ◽  
Mouse Mutants ◽  
Brindled Mouse ◽  
Copper Therapy ◽  
Early Effects

Copper therapy was applied to brindled mouse mutants, which suffer from lethal hypocupraemia, by using cuprous and cupric solutions. The method of treatment was a single subcutaneous injection of 50 microgram of copper at 7 days of age. Early effects of the dose were: prevention of the tremors and spasms seen in untreated mutants, raising to normal and near-normal of caeruloplasmin oxidase and lysyl oxidase activities and pigmentation of skin and fur. Growth of mutants was retarded up to 23 days of age, but thereafter they rapidly gained weight to be nearly normal by 60 days of age. At 3 days after injection, copper concentrations in previously deficient mutant organs apart from liver were at least as much as those of treated normals, which had remained unchanged. Copper in mutant livers had increased only slightly in comparison with the normal control. A state of copper deficiency recurred in mutant tissues by 25 days after injection. A solution of Cu+, retained as such by an alkyl polyether, and sebacic acid resulted in greater growth rates after 23 days than did three other copper treatments. Cu+ may have resulted in an improved growth response owing to it being more readily metabolized than C12+. Delayed release of copper from the site of injection may have played an important role.

Sign in / Sign up

Export Citation Format

Share Document