Profound Iron Deficiency Research Articles

Chronic Iron‐deficiency Anemia Caused by a Jejunojejunal Intussusception on a Solitary Hamartomatous Polyp

Chronic Iron‐deficiency Anemia Caused by a Jejunojejunal Intussusception on a Solitary Hamartomatous Polyp

Endoscopically Diagnosed Blue Rubber Bleb Nevus Syndrome in an Elderly Patient with Anemia and Heme Positive Stool

Purpose: Blue Rubber Bleb Nevus syndrome (BRBNS) is a rare disorder that is characterized by multiple recurrent vascular malformations such as hemangiomas, and these primarily involve the skin and the gastrointestinal tract. Typically, it results in profound iron deficiency anemia or overt gastrointestinal blood loss due to involvement of the internal organs. A 79 year-old Caucasian man with no prior history of anemia or gastrointestinal bleeding was admitted to our hospital for elective Coronary Artery Bypass Graft surgery. After surgery, he was started on Aspirin and Plavix. A few days later he developed anemia and heme positive stools. He underwent a colonoscopy which showed numerous large bluish vascular malformations throughout the colon and multiple flat polyps (tubulovillous adenomas). On further inspection, he had bluish nevi on his forearm. These were biopsied and they were consistent with BRBNS.Figure

Profound iron deficiency anemia caused by a small-intestinal cavernous hemangioma

Profound iron deficiency anemia caused by a small-intestinal cavernous hemangioma

Profound and chronic iron deficiency anemia in a male Jehovah's Witness

Profound and chronic iron deficiency anemia in a male Jehovah's Witness

Ibuprofen codeine combination precipitating severe hypokalaemia in a patient with pre-existing type 1 renal tubular acidosis.

Sir, A 36-year-old lady presented to the A&E with a 2-day history of generalized, severe progressive weakness of her limbs. Two days prior to her presentation, she had been exercising vigorously at the gym and subsequently developed muscle pain. In the hours following, she developed progressive weakness in her upper and lower limbs. She became unable to walk or stand. She described several previous episodes of leg weakness and numbness, especially at night, over a few months. On further questioning, she stated that she had been taking up to eight tablets of an ibuprofen codeine combination (200 mg + 12.8 mg respectively) everyday for 3 months for backache. She had been admitted previously with profound iron deficiency anaemia and weakness but mild hypokalaemia 19 months before, which had resolved completely with oral supplementation. There was no other relevant family or drug history. On examination, the patient was dehydrated, afebrile (37.4°C), with a regular pulse rate of 90 bpm and blood pressure 123/83 mmHg. She had decreased power in all four limbs (MRC score of 3/5 in the lower limbs and 4/5 in the upper limbs). Blood tests on admission showed a serum potassium of 1.7 mmol/L and a high serum creatinine level of 282 mmol/L and urea 12.8 mmol/L (sodium 130 mmol/L, chloride 95 mmol/L, creatinine kinase 289 i.u./mL). Arterial blood gas sampling revealed a metabolic acidosis (pH 7.20, pCO2 3.04 kPa (23 mmHg), pO2 15.7 kPa (118 mmHg), HCO3 11.0 mmol/L, base deficit 18) with an anion gap of 25 mmol/L. Serum lactate was normal (0.9 mmol/L) and salicylate was undetected. An E. coli UTI was discovered and treated. ECG changes were consistent with severe hypokalaemia. Her urine sodium at presentation was 42 mmol/L, potassium 12.4 mmol/L, urea 27 mmol/L and osmolality of 134 mOsm/kg. The urine osmolal gap was −1.8, making recent toluene abuse unlikely. Immunological tests were negative (inter alia, Hep 2 cells, ANA, and autoimmune profile negative). Subsequent investigations showed transient polyuria (urine volume up to 4.3 L/day), high 24-h urinary K+ wasting (175 mmol/day). CT scan of the abdomen showed marked bilateral nephrocalcinosis, but no other abnormalities. The patient re-presented to the emergency department with similar symptoms a month later. On this occasion, she was also found to be hypokalaemic (2.1 mmol/L) with hyperchloraemic metabolic acidosis (pH 7.23, HCO3 14.7 mmol/L, base deficit 12.6). Her serum anion gap was normal (13 mmol/L). Whilst acidotic, her urine anion gap was + 7 mmol/L and urine pH 6.52. She was again treated with fluid resuscitation and potassium repletion. She denied further NSAID or diuretic use. In view of the recurrent hypokalaemia, advanced nephrocalcinosis, urine pH, positive urine anion gap and normal anion gap metabolic acidosis, a diagnosis of longstanding type 1 RTA was made. She made a full recovery and was discharged 5 days later on potassium citrate supplementation, and remained potassium replete on follow-up. There have been reports of ibuprofen codeine combination, particularly in excess doses, causing acute and transient RTA [1–4]; when characterized it has been reported to be type 2. Our patient now meets criteria for a diagnosis of type 1 RTA. This pre-existing condition was not diagnosed until her admission with life-threatening hypokalaemia, after taking an ibuprofen codeine combination for 3 months. This presentation with far graver hypokalaemia than before was accompanied by no alternative explanation for the development of 0.76 mol potassium deficit, and was associated with transient hypophosphataemia. We speculate that at the time of presentation she had developed a proximal tubulopathy, attributable to the ibuprofen codeine combination, resulting in a combined renal tubular acidosis with dramatic consequences. Vigilance in eliciting a detailed analgesic history remains important in patients with acute acidoses, especially in patients with pre-existing renal conditions. Conflict of interest statement. None declared.

Normal Pulmonary Artery Pressure in Sickle Cell Patient with Severe Iron Deficiency Anemia.

One-third of adults with sickle cell disease (SCD) have echocardiographic (ECHO) evidence of pulmonary hypertension (PHTN), a complication associated with early mortality. Because the pulmonary artery pressures in most SCD patients with PHTN are only mildly elevated, the question arises whether such increases are primarily a reflection of the high cardiac output state that accompanies the anemia.Recently we treated a 45 year-old woman with homozygous sickle-cell disease and profound iron deficiency due to heavy menstrual flow. Two ECHOs were done while she was severely iron deficient (Hb 5 g/dl, MCV 57 fl, reticulocytes 72,407/mm3, serum bilirubin 0.5 mg/dl, iron 29 mcg/dl, transferrin 376 mg/dl, and ferritin 3.6 ng/ml). Her pulmonary artery systolic pressure (PAs) was calculated from the tricuspid regurgitant jet velocity (TRV) using the Bernoullie equation: 4(TRV3) + central venous pressure (assumed at 10 mm Hg). The PAs was normal, 24 mm Hg, even though the patient also had M-mode evidence of left ventricular diastolic dysfunction and a small pericardial effusion. Treatment with intravenous iron and red cell transfusion partially improved her iron deficiency and anemia (Hb 7 g/dl, MCV 67 fl, serum bilirubin 0.7 mg/dl, iron 54 mcg/dl, transferrin 322 mg/dl, and ferritin 33.9 ng/ml) but also increased her hemolytic rate: though LDH data are unavailable, the reticulocyte count rose to 117,900/mm3. Repeat ECHO exams at this time showed that her pulmonary artery systolic pressures increased to 35–36 mm Hg. These values are at or near the lower range of pulmonary artery systolic pressures (36–70 mm Hg) measured in SCD patients in whom PHTN was diagnosed at cardiac catheterization. The figure compares hematologic values, and pulmonary artery systolic pressure in our iron deficient SS patient at baseline and during treatment.This experience, though anecdotal, suggests that the PHTN in SCD is unrelated to the anemia per se and, by implication, also unrelated to the high cardiac output. The patient's mild pulmonary systolic hypertension actually developed with improvement of her anemia. Our hypothesis is that when the patient's iron deficiency was most severe, the low MCHC decreased Hb S polymerization and decreased hemolysis, as in other iron deficient SCD patients. Her relatively low hemolytic rate may have prevented the mild PHTN, which developed once treatment improved her iron deficiency but increased hemolysis. Our hypothesis is consistent also with an emerging new paradigm in sickle cell disease pathophysiology: a strong link between hemolysis-related nitric oxide system (NO) dysfunction and risks for pulmonary hypertension, leg ulcers, priapism, and death. In this context it is interesting that iron deficiency anemia up-regulates vascular nitric oxide synthase in animals. In humans iron deficiency increases NO production even in the absence of anemia. Hence, this patient's iron depletion may have contributed to the maintenance of her low pulmonary pressures also by a direct NO-mediated vascular effect. [Display omitted]

Familial Adenomatous Polyposis and Factor VII Deficiency in a Young Man

To report a case of Familial adenomatous polyposis in a young man with concomitant Factor VII deficiency. A 29 y/o African American male presented with complaints of weakness and recent shortness of breath. He attributed the symptoms to several nosebleeds in the past six months. He denied any trauma or other medical history. Patient reported frequent nose bleeds for last six months though denied any vomiting, malena, hematochezia or other sources of bleeding. His father died at age of 42 with colon cancer and uncle also had colon cancer but denied any bleeding disorders in family. He was a smoker, occasional alcohol user but denied illicit drug abuse. On examination, he was tachycardic with blood pressure of 110/50. Rest of the exam was remarkable only for heme positive brown stool on rectal exam. Lab data showed hematocrit 11 with MCV 67, Platelet 473K, TIBC 431, Serum Iron 9 and Ferritin 3 ng/mL. His coagulation profile showed PTT elevated to 20.7 seconds and INR elevated to 1.8. He was admitted and received 3 units of packed red blood cells. With profound iron deficiency anemia and strong familial history of colon cancer, gastrointestinal consultation was sought. Panendoscopy was remarkable for innumerable polyps in colon. FAP was most plausible diagnosis. Biopsies revealed adenomatous polyps without high-grade dysplasia or malignancy. Coagulation parameters did not correct after transfusions. Mixing study showed correction of prothrombin time. Coagulation factor deficiency seemed possible cause. Factor VIII and IX were normal. Factor VII levels was drawn later, after hematology consultation, it was 12 (reference 70–130). A diagnosis of factor VII deficiency was made. He underwent colectomy and received recombinant factor VII perioperatively. Patient was counseled and genetic counseling was advised along with surveillance in other family members. This is an interesting presentation of two rare familial disorders in same patient. Familial adenomatous polyposis is autosomal dominant diseases caused by mutations in the adenomatous polyposis coli on chromosome 5q21. FAP occurs in approximately 1/10000–30000 live births, and accounts for less than 1 percent of the total colon cancer risk in the USA. With estimated prevalence of 1: 500 000, inherited FVII deficiency is also a rare, autosomal recessive coagulation disorders. The FVII gene (F7) is located on chromosome 13. There has been no reported link between these two relatively rare disorders and this might be just a coincidence or not!

The assessment of frequency of iron deficiency in athletes from the transferrin receptor-ferritin index.

The transferrin receptor-ferritin index (sTfR/logFerr) was determined in 131 male and 121 female athletes in order to assess the frequency of iron deficiency (threshold value of that index taken as 1.8). Blood was drawn for determining morphological indices as well as sTfR, ferritin, iron, total iron binding capacity (TIBC), and haptoglobin. A significantly (p <.01) higher incidence of iron deficiency was observed in women (26%) than in men (11%). The iron deficiency was latent, since no subject was found to be anemic. The plasma iron was significantly lower and TIBC higher (p <.001) in both iron-deficient subgroups than in the non-deficient ones. This confirmed the latent character of iron deficiency. Some hematological indices (Hb, MCH, MCHC, MCV) were significantly lower in iron-deficient female athletes than in male athletes, which suggested a more profound iron deficiency in the former. The sTfR/logFerr index might thus be useful in detecting iron deficiency in athletes, especially in those with erythropoiesis disorders, since physical loads may affect the widely used ferritin levels.

A case of profound iron deficiency anemia owing to corrosive esophagitis in a 20-year-old developmentally delayed male

The level of severe compensated iron deficiency anemia incompatible with life is not defined in the pediatric or adolescent literature. A hemoglobin of 1.5 gm/dl in an older adolescent with few physical symptoms is distinctly unusual. A case of profound iron deficiency anemia in a 20-year-old developmentally delayed male is the subject of this brief report. There were only subtle physical findings in spite of this severe anemia. The anemia was the result of corrosive esophagitis associated with a hiatal hernia and reflux. Physicians dealing with developmentally delayed adolescents should be aware of the fact that a severe anemia may develop, and such individuals should be periodically screened for anemia, melena, hematochezia, and hematemesis.

High haematocrit in haemodialysis patients can be controlled by theophylline administration

Three patients on chronic maintenance haemodialysis have progressively increased their haematocrit to reach values between 40 and 45%, a situation associated with an increased risk of thrombosis of their arteriovenous fistulae. Two of them had been submitted to repeated phlebotomies, which remained unsuccessful despite the induction of a profound iron deficiency in one of them. Hence, a trial with oral theophylline was performed in the three patients, resulting in a sustained decrease of the haematocrit (from 43.6 to 33%) and endogenous erythropoietin (from 46 to 15 mU/ml) levels. In two patients, theophylline therapy was stopped transiently due to gastrointestinal side-effects, which resulted in a rapid return to previous haematocrit levels; rechallenge with a better tolerated preparation, however, was efficient again. We conclude that oral theophylline appears to be an efficient treatment to control too high haematocrit levels in dialysis patients.

Long-term consequence of early iron-deficiency on dopaminergic neurotransmission in rats

Nutritional iron-deficiency (ID) induced in rats caused a reduction in peripheral as well as central iron metabolism. This effect was markedly greater in the liver than the brain. Although the decrease in the rate of brain non-haem iron was slower than that of serum and liver, significant diminutions of behavioral response to apomorphine (2 mg/kg) and maximum [3H]spiperone binding (Bmax) in caudate nucleus were noted in these animals. These effects of ID can be reserved byron supplementation in young (21-day-old) and adult (48-day-old) rats. In contrast, if ID is induced in new born (10-day-old) animals, the diminished brain non-haem iron, behavioral response to apomorphine and [3H]-spiperone binding in caudate nucleus will not recover even after 6 weeks of iron supplementation. However, these animals have normal serum iron, haemoglobin and liver iron. These data point to the profound effect early ID can have on the development of dopaminergic neurotransmission, since brain iron concentration increases its maximum in the 4–5 weeks after birth. The implications of the present finding is that the prevalence of ID in children occurs in the first decade of life, when brain iron accumulation reaches values observed in adults. The profound cognitive changes associated with ID in children is thought to be dopamine-dependent and is not always reversible with iron therapy.

8 - Iron Deficiency in the Tropics

Iron in food is classified as belonging to the haem pool, the nonhaem pool, and extraneous sources. Haem iron is derived from vegetable and animal sources with varying bioavailability. Hookworm infestation of the intestinal tract affects 450 million people in the tropics. Schistosoma mansoni caused blood loss in 7 Egyptian patients of 7.5- 25.9 ml/day which is equivalent to a daily loss of iron of .6-7.3 mg daily urinary loss of iron in 9 Egyptian patients. Trichuris trichiura infestation by whipworm is widespread in children with blood loss of 5 ml/day/worm. The etiology of anemia in children besides iron deficiency includes malaria, bacterial or viral infections, folate deficiency and sickle-cell disease. Severe infections cause profound iron-deficiency anemia in children in central American and Malaysia. Plasmodium falciparum malaria-induced anaemia in tropical Africa lowers the mean haemoglobin concentration in the population by 2 g/dI, causing profound anaemia in some. The increased risk of premature delivery, low birthweight, fetal abnormalities, and fetal death is directly related to the degree of maternal anemia. Perinatal mortality was reduced from 38 to 4% in treated anemic mothers. Mental performance was significantly lower in anemic school children and improved after they received iron. Supplements of iron, soy-protein, calcium, and vitamins given to villagers with widespread malnutrition, iron deficiency, and hookworm infestation in Colombia reduced enteric infections in children. Severe iron-deficiency anemia was treated in adults in northern Nigeria by daily in Ferastral 10 ml, which is equivalent to 500 mg of iron per day. Choloroquine, folic acid, rephenium hydroxynaphthoate, and tetrachlorethylene treat adults with severe iron deficiency from hookworm infestation in rural tropical Africa. Blood transfusion is indicated if the patient is dying of anaemia or is pregnant with a haemoglobin concentration 6 gm/dl. In South East Asia, mg per day prevented iron-deficiency anaemia in pregnancy. Field-trials on nutritional iron deficiency include an acidified milk formula plus ferrous sulphate for infants; biscuits with added bovine hemoglobin for children in Chile; sugar plus sodium ferric EDTA in Guatemala; salt with ferric orthophosphate and sodium acid sulphate in India; and Salt with ferrous sulphate plus sodium hexametaphosphate.

Intracolonic formation of struvite crystals in a patient with congenital megacolon

Intracolonic formation of large crystals and their subsequent rectal passage with hematochezia has not been previously described. We report the case of a patient with Hirschsprung's disease with a long history of anemia and passing crystals in his stool. These crystals were shown, by x-ray diffraction analysis, to be pure struvite (magnesium ammonium phosphate). It is likely that their sharp edges caused rectal bleeding and profound iron-deficiency anemia in this patient.

Iron‐deficiency in the Tropics

Different populations in the tropics show wide variation in their iron status, even when living in the same area. These differences range from the most profound iron-deficiency anaemia to nutritional haemosiderosis. The extremes of dietary iron content so far reported are 5 mg per day in Mauritius to 180 mg per day in Ethiopia. Contamination with inorganic iron is an important source in some communities. Generally, the iron in food is in excess of requirement, but lumenal factors are all important in deciding how much is available for absorption. The iron of some diets is readily absorbed, but in other only a small percentage is utilizable. Hookworm infection is the commonest cause of severe iron-deficiency in many parts of the world. Its prevalence and its density depends on social habits, and may vary considerably even within tribes. The development of iron-deficiency anaemia depends on the hookworm load being sufficient to cause iron loss in excess of available intake. Anaemia impairs work capacity, reproductive ability of women and the development of children, and has wide social and economic repercussions. An intramuscular preparation by which 500 mg of iron may be administered in one injection has most useful application in areas where medical care is minimal.

Lactic Acidosis Associated With Iron Deficiency Anemia

Severe lactic acidosis occurred in a patient with profound iron deficiency anemia. Rapid improvement was observed following the administration of blood, and the patient made a complete recovery.