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Adult female Wistar rats were injected with 125 mg/kg b.w. of human methemoglobin (M-Hb) in order to induce a first episode of hemodynamically-mediated acute renal failure (HMARF). Eleven days after the injection of M-Hb, other groups of rats received another equal dose of the drug in order to induce a second episode of HMARF. Evaluation of renal function, histopathology studies, and determinations of plasma and kidney erythropoietin (Epo) titers by radioimmunoassay in normoxic and hypoxic conditions were performed 1, 2, 3, 5 and 10 days after M-Hb administration. Treatment induced transient increases in plasma urea concentration, fractional sodium excretion, and urine volume, and significant depression in urine osmolality. In every case, the maximal effect of the first injection of M-Hb on the individual parameters was always greater than that of the second injection, and observed on the 5th post-injection day. Histologic sections showed interstitial cellular infiltration, desquamation of the proximal tubular epithelium and collapse or dilation of the tubular lumen. Treatment with M-Hb depressed Epo titers in both kidney homogenates and plasma in normoxic as well as hypoxic rats. Here again, the effect of the first injection of the drug was higher than that of the second one. These observations indicate that there is a negative correlation between kidney tubule injury and Epo production in normoxic and hypoxic conditions. The findings give support to the concept that Epo production is related to proximal tubular function.
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PMID:Depressed plasma erythropoietin levels in rats with hemodynamically-mediated acute renal failure. 209 64

Sickle cell anemia (SCA) is a disease caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within the red blood cell to cause rigid deformation of the cell. This deformation impairs the ability of the cell to pass through small vascular channels; sludging and congestion of vascular beds may result, followed by tissue ischemia and infarction. Infarction is common throughout the body in the patient with SCA, and it is responsible for the earliest clinical manifestation, the acute pain crisis, which is thought to result from marrow infarction. Over time, such insults result in medullary bone infarcts and epiphyseal osteonecrosis. In the brain, white matter and gray matter infarcts are seen, causing cognitive impairment and functional neurologic deficits. The lungs are also commonly affected, with infarcts, emboli (from marrow infarcts and fat necrosis), and a markedly increased propensity for pneumonia. The liver, spleen, and kidney may experience infarction as well. An unusual but life-threatening complication of SCA is sequestration syndrome, wherein a considerable amount of the intravascular volume is sequestered in an organ (usually the spleen), causing vascular collapse; its pathogenesis is unknown. Finally, because the red blood cells are abnormal, they are removed from the circulation, resulting in a hemolytic anemia. For the patient with SCA, however, the ischemic complications of the disease far outweigh the anemia in clinical importance.
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PMID:Sickle cell anemia. 1145 73

The effects of acute renal failure on the impeded (IER) and unimpeded (UER) eruption dental rate and attrition rate (AR) were investigated. Adult female Wistar rats were injected with 125 mg/kg b.w of human methemoglobin (M-Hb) in order to induce a first episode of hemodynamically-mediated acute renal failure (H-ARF). Ten days after the injection of M-Hb, other groups of rats received another equal dose of the drug in order to induce a second episode of H-ARF. A group of six animals was pair-fed daily and individually with rats of M-Hb groups. Evaluation of renal function, histopathology studies, IER, UER, food intake (FI), AR and body weight gains was performed at different times after the first and second injections, of M-Hb. Treatment induced transient increases in plasma urea concentration and urine volume, and significant depression in urine osmolality, body weight gains, IER, UER and AR. In every case, the maximal effect of the first injection of M-Hb on the individual parameters was always greater than that of the second injection. Histologic sections showed interstitial cellular infiltration, desquamation of the proximal tubular epithelium and collapse or dilation of the tubular lumen. The functional values of kidney, histologic findings, IER, UER and AR of the pair-fed rats were not significantly different from control values. The results of the present study indicate that dental eruption rate (IER and UER) is relatively low in uremic rats with kidney tubule lesions and that both parameters are related.
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PMID:Depressed eruption dental rate in rats with hemodynamically-mediated acute renal failure. 1188 31

Cyanide poisoning may result from different exposures: residential fires, industrial accidents, drug and plant intoxication. Clinical features include coma, respiratory arrest and cardiovascular collapse. The biological hallmark is lactic acidosis. A plasma lactate concentration > or = 10 mmol/L in fire victims without severe burns and > or = 8 mmol/L in pure cyanide poisoned patients is a sensitive and specific indicator of cyanide intoxication. Many antidotes are available and efficient. However, therapeutic strategies are still debated. Our objective was to compare conventional treatments to hydroxocobalamin. This article reviews the literature on cyanide poisoning treatment. Conventional treatment of cyanide poisoning includes decontamination, supportive and specific treatment. Decontamination should be adapted to the route of poisoning and never postpone supportive treatment. Basic life support includes immediate administration of high flow of oxygen, airway protection and cardiopulmonary resuscitation. Advanced life support includes mechanical ventilation, catecholamine and sodium bicarbonate infusion. Supportive treatment is efficient but does not modify the time course or the body burden of cyanide. Numerous antidotes are available. Oxygen counteracts efficiently cyanide action at the mitochondrial level. Sodium thiosulfate, methemoglobin forming agents and cobalt compounds act efficiently by complexing or transforming cyanide into non-toxic stable derivatives. However, regarding the main clinical condition of cyanide poisoning, i.e. smoke inhalation, we should take into account not only the efficiency of antidotes but also their safety. Sodium thiosulfate is both efficient and safe, but acts with delay. Methemoglobin-forming agents are potent, but due to the transformation of hemoglobin into methemoglobin, they impair tissue delivery of oxygen. Experimental data showed increased mortality in carbon monoxide- and cyanide-poisoned rats treated with these agents. Cobalt EDTA and hydroxocobalamin are efficient and act immediately. Cobalt EDTA is more potent on a molar basis; however, numerous side effects limit its use to evidenced cyanide poisoning. In a prospective study, hydroxocobalamin appeared safe in fire victims with or without cyanide poisoning. The only reported side effect was a red coloration of skin and urine. In conclusion, antidotes are beneficial in cyanide poisoning. In suspected cyanide-poisoned patients, we recommend the use of hydroxocobalamin as first-line antidote, owing to its safety. In massive cyanide poisoning, due to the limited potency of hydroxocobalamin, continuous infusion of sodium thiosulfate should be associated.
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PMID:Antidotal treatment of cyanide poisoning. 1285 70

PEG-bHb was developed by Kaizheng Biotech (Beijing, China), and pre-clinical research was completed. The objective of this study was to investigate the safe concentration of MetHb in PEG-bHb. The study was accomplished by examining the effects of PEG-bHb containing 5%, 8%, 15%, and 25% methemoglobin (MetHb), respectively, on cardiovascular system, blood chemistry, pathology of liver and kidney in rabbits following a 50% exchange transfusion. The results showed that PEG-bHb containing 5%, 8%, 15%, and 25% MetHb could keep four groups of experimental rabbits (5/5) alive until the 8th day after 50% exchange infusion as autologous whole blood did, and were superior to dextran 40 (2/5). MetHb concentration in PEG-bHb, no more than 25%, did not affect the PEG-bHb function on resuscitation of hemorrhaged rabbits by physiological measurements and blood chemistry assays. Histology study using optic and electron microscopy showed that there were slight pathological changes in hepatocytes and renal tubule epithelia in rabbits, which were infused by PEG-bHb containing 5%, 8%, and 15% MetHb. Partial organelles collapse was observed in rabbits resuscitated by PEG-bHb containing 25% MetHb. In conclusion, PEG-bHb is safe and effective when the MetHb concentration is at or below 15%.
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PMID:Polyethylene glycol conjugated bovine hemoglobin containing 15% MetHb plays approving effect in exchange transfusion rabbit model. 1792 14

Sickle cell anemia (SCA) is an inherited disorder of hemoglobin due to the presence of abnormal hemoglobin in a homozygous state. Manifestation is usually in infancy or early childhood due to gradual decrease in hemoglobin F level as age advances. Diagnosis in middle age is unusual. We present a woman who was diagnosed of SCA for the first time at middle age. The aim was to bring to the knowledge of physicians that patients with SCA can also present late so high index of suspicion is required to make diagnosis. A 52-year-old woman presented to orthopedic clinic with complaints of generalized bone pain and low back pain. There was no history of trauma prior to the onset of the pain. There was no associated fever, weight loss, loss of appetite, nor weakness of the lower limbs. X-ray of the spine done showed wedge collapse of the 12th thoracic and first lumbar vertebrae with posterior angulation of the thoracolumbar junction giving dorsal kyphosis. Her mode of presentation raised a suspicion of tuberculosis of the spine to rule out multiple myeloma. However, investigations for tuberculosis and multiple myeloma were all negative. This necessitated the investigation for SCA and the diagnosis was confirmed. The diagnosis of SCA is usually made in infancy or early childhood. High index of suspicion is required to make the diagnosis at middle age.
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PMID:Hemoglobin SS Nigerian Woman First Diagnosed at the Age of 52 years with Manifestation Mimicking Tuberculosis of the Spine. 3267 4

Sickle cell disease (SCD) is a genetic trouble of the hemoglobin synthesis inherited as an autosomal recessive trait, whose prevalence can vary from 5 to 25% in the different parts of the world. It is characterized by the presence of abnormal hemoglobin HbS instead of hemoglobin A. Patients suffering from major forms of SCD present the risk of developing epiphyseal necrosis. Aseptic osteonecrosis of the femoral head (AOFH) caused by ischemia, or bone infarction can affect between 20 and 50% of SCD patients. The femoral head is the most frequent epiphyseal location with a range of 74.6%. AOFH can affect patients at any age, but is mainly detected in men under 50 years. Indeed, a large majority of cases, in a range of 60%, have been diagnosed at an early radiological stage in young adults whose average age varies, in the literature, between 27 and 36 years. A surgical procedure becomes sometimes necessary due to the severity of pain and the functional consequences, frequently following the mechanical collapse of the osteonecrosis area. It is estimated that approximately 25-30% of SCD patients will undergo a total hip arthroplasty before 50y. Although the mortality rate, between 0.2-2.6%, tends to be similar to the general population rate undergoing a prosthetic surgery, the perioperative complications vary from 11.5 to 67%. Here, we clarify the epidemiological data and present an exhaustive update on the different preventive and therapeutic strategies, as well as the perioperative management in patients with an AOFH caused by SCD and risking multiple complications.
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PMID:Aseptic osteonecrosis of the femoral head in patients with sickle cell anemia. 3289 11