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At least 19 recordsLinked to original sources
PubMed1992

Hematin as a peroxidase substitute in hydrogen peroxide determinations.

Hematin can substitute for horseradish peroxidase (HRP) as the catalyst in the determination of hydrogen peroxide using phenolic substrates such as p-hydroxyphenylacetate or p-cresol. Although the peroxidatic activity of hematin from bovine blood is not as great as HRP in terms of unit iron content, the activity per unit weight is substantially greater. Hematin is 500 times less expensive than HRP per unit peroxidatic activity. In hematin-catalyzed systems, reaction development and fluorescence measurement can both be conducted optimally in the same ammoniacal buffer. Hydroxyalkyl hydroperoxides are rapidly hydrolyzed to H2O2 at this pH and are also determined. On the other hand, for methyl hydroperoxide, hematin exhibits only approximately 10% of the sensitivity exhibited by HRP. Hematin is significantly more stable in solution than HRP. The use of hematin as catalyst and p-cresol as the substrate leads to a particularly inexpensive and sensitive system, permitting a limit of detection (LOD) of 7 nM H2O2 in a flow-injection configuration.

Buffers↗
PubMed1978

Transitory renal failure following rapid administration of a relatively large amount of hematin in a patient with acute intermittent porphyria in clinical remission.

Transitory renal failure occurred in a patient with acute intermittent porphyria in clinical remission following i.v. administration of 1 000 mg hematin. The clinical and biochemical picture suggested "acute tubular necrosis", which was followed by a prompt and complete return of renal function without any late sequelae. The renal failure is thought to have resulted from the presence of circulating free hematin, formed as a result of rapid administration of such a relatively large amount. Such a complication has not occurred in patients given hematin for acute porphyric relapse, in whom much smaller amounts have been infused.

Acute Kidney Injury↗
PubMed1979

Hematin and propranolol in acute intermittent porphyria. Full recovery from quadriplegic coma and respiratory failure.

The authors present a case of acute intermittent porphyria (AIP) in an almost fatal relapse with quadriplegia, bulbar paralysis and coma. Intravenous hematin produced an immediate arousal from coma and allowed a gradual resumption of bulbar and autonomic functions. Persistent tachycardia and hypertension necessitated huge doses of intravenous propranolol. Both hematin and propranolol administrations were followed by a remarkable decrease in urinary amino-levulinic acid and porphobilinogen excretion. Nevertheless, after the acute stage, the patient was left with a severe generalized muscle wasting. After 7 months of intensive physical therapy, complete recovery of all neuromuscular functions was achieved. The modern aspects of the management of AIP are presented; the efficacy and the limits of hematin and propranolol therapy are discussed.

Acute Disease↗
PubMed1977

Effect of hematin in porphyric neuropathy.

Early, intravenous administration of hematin in a patient with acute intermittent porphyria and severe quadriparesis may have produced partial but remarkable improvement of neuropathy, and resulted in simultaneous decline of porphyrin precursors in the blood. Intermittent, biweekly hematin infusions given 1 month after the onset of the porphyric relapse had no effect on recovery of the residual neuropathy. We believe hematin may be effective in the treatment of porphyric neuropathy, if administered before irreversible neuronal damage has occured.

Adult↗
PubMed1979

Hematin administration to an adult with lead intoxication.

Lead poisoning and acute intermittent porphyria (AIP) may exhibit similar neurologic manifestations, and they have in common elevated excretion of urinary aminolevulinic acid (ALA). Despite their similarities, the possible pathophysiologic connection between AIP and lead poisoning in not known. Because intravenous hematin administration has produced biochemical improvement in AIP, a hematin trial in lead intoxication was of interest with respect to some of the heme metabolism abnormalities observed in the condition. Significant diminution of urinary ALA and coproporphyrin excretion occurred in association with intravenous hematin administration.

Heme↗
PubMed1976

Hematin treatment of acute porphyria. Early remission of an almost fatal relapse.

Intravenous infusions of hematin in a young woman with acute porphyria in profound relapse was followed within 48 hours by remission of symptoms and rapid recovery. From a state of severe central and peripheral nervous-system involvement, the patient recovered so completely that she was able to leave the hospital in less than a month, with only a residual weakness of her arms. Serial studies of serum and urinary levles of porphyrin precursors and serum level of hematin provided highly important information about the effect of hematin on acute porphyria.

Acute Disease↗
PubMed1977

Postulated deficiency of hepatic heme and repair by hematin infusions in the "inducible" hepatic porphyrias.

There is compelling, indirect evidence of hepatic heme deficiency due primarily to the respective genetic errors of the three inducible hepatic porphyrias, acute intermittent porphyria, porphyria variegata, and hereditary coproporphyria. The induction is enhanced by exogenous inducers such as barbiturate, estrogens and other "porphyrogenic" chemicals and factors, including glucose deprivation. The newer knowledge of the induction of delta-aminolevulinic acid synthetase [delta-aminolevulinate synthase; succinyl--CoA:glycine C-succinyltransferase (decarboxylating), EC 2.3.1.37] in relation to inadequate heme, and repression by heme, stimulated early trials of hematin infusions to overcome the acute relapse in the foregoing inducible porphyrias. Recently this experience has been considerably expanded, 143 infusions of hematin having been given in 22 cases. Studies of the effect on the serum concentrations of delta-aminolevulinic acid and porphobilinogen have shown a highly significant decline, often to 0, especially of delta-aminolevulinic acid. A distinct relationship to the clinical severity of the attack has been evident in the frequency and magnitude of decline of serum delta-aminolevulinic acid and porphobilinogen. This was regularly associated with objective clinical improvement.

5-Aminolevulinate Synthetase↗
PubMed1979

Hematin therapy for acute porphyria.

1. A therapeutic trial of intravenous hematin is presented. Eleven cases of AIP and one of VP who did not improve with conventional treatment (high carbohydrate intake) received this new agent. 2. Urinary ALA, PBG and, when possible, uroporphyrin and coproporphyrin were used to monitor the chemical response to the treatment. Objective clinical parameters of hypertension and tachycardia were followed when present in addition to subjective estimates of acute porphyric symptomatology (abdominal pain, backache, extremity pain and paresthesias, weakness, depression, etc.). 3. At a dosage of approximately 3 mg/kg, diminution of urinary ALA and PBG excretion was achieved in every patients. Hypertension and tachycardia improved in those instances where they were observed in association with the attack. Also, subjective improvements in the clinical status of the patients were observed frequently. 4. Hematin appears to be a promising therapeutic agent for the treatment of acute attack forms of porphyria.

Acute Disease↗
PubMed1975

Effect of hemoglobin and hematin on plasma clearance of hemopexin, photo-inactivated hemopexin and albumin (38575).

The plasma half clearance time (T1/2) of isotope-labeled rabbit hemopexin was 35.5 plus or minus 1.9 hr in rabbits. After intra-and extra-vascular equilibration of 125I-hemopexin and 131I-albumin, injection of either hematin, hemoglobin or methemoglobin (12.5 mg of heme/kg body wt) resulted in the rapid removal of 60-80% of circulating hemopexin (T1/2 = 7.2 plus or minus 0.6 hr) but did not affect albumin catabolism. After selective photo-inactivation of hemopexin, the T1/2 of this hemopexin was comparable to that of the native molecule. However, its plasma disappearance curve was not appreciably affected by administration of hematin. These findings demonstrate that hemopexin is cleared and catabolized at an enhanced rate during states of plasma heme load, and that modification of critical histidine residues of hemopexin eliminates its biological function in plasma heme disposal.

Animals↗
PubMed1975

Effects of hematin in hepatic porphyria. Further studies.

The present study was carried out in five cases of hepatic porphyria, including three of acute intermittent porphyria, one of variegate porphyria, and one of porphyria cutanea tarda in clinical remission. In two cases of acute intermittent porphyria (in relapse), a marked lowering effect on serum and urine porphobilinogen and delta-aminolevulinic acic was observed, together with prompt and gratifying clinical improvement. In a third case, in chemical remission but with longstanding psychoneurosis, no significant effects were noted, nor were any observed in the case of porphyria cutanea tarda. Although clinical improvements occurred in the case of variegate porphyria, the results were inconclusive for reasons given. Hematin was generally well tolerated. Preliminary reference is made to a transitory renal injury, without sequelae, where an excess of hematin was given in relation to time. Limits of tolerance are proposed. In the light of these observations the basic mechanism of the acute attack is diccussed.

Adult↗
PubMedDate not supplied

[Hematin treatment of porphyric neuropathy].

The authors report a case of acute intermittent porphiria with peripheral motor neuropathy and a syndrome of inadequate ADH excretion in a male patient aged 36 years. Treatment with hypertonic glucose and prostigmine did not yield any beneficial results, while a subsequent treatment with hematine (4 mg/kg/day for a period of four days) produced a dramatic improvement in the clinical picture and in ALA and PGB levels. A back-to-normal shift of plasma and urinary electrolytes was also observed. It appears that there was a close relation between the administration of hematine and the clinical-biochemical remission.

Adult↗
PubMed1992

[Acute intermittent porphyria in pregnancy: glucose or hematin therapy?].

The symptoms and management of acute intermittent porphyria (AIP) during pregnancy and delivery are presented on the basis of three case reports. Two patients became asymptomatic after infusion of a concentrated glucose solution (600 ml 50% glucose = 300 g glucose per day), while the third patient needed treatment with hematin (1 mg/kg body weight, 6 infusions at intervals of 12 hours) because of deterioration of psychic state in spite of glucose infusion. Whenever an attack of AIP occurs, concentrated glucose solution should be administrated as a first measure accompanied by an analgesic and possibly a neuroleptic agent after elimination of precipitating factors. However, if symptoms persist for 48-96 hours or the psychic and/or neurological state of the patient further deteriorates, administration of 1-3 mg hematin per kg body weight can be recommended.

Acute Disease↗
PubMed1992

Recurrent aphthous stomatitis: the efficacy of replacement therapy in patients with underlying hematinic deficiencies.

A group of thirty-four patients with recurrent aphthous stomatitis (RAS) and single hematinic deficiencies were given replacement therapy after any reason for the deficiency had been sought and excluded. The response of the RAS was assessed in an open trial. The aphthae in 70% of patients subjectively improved with hematinic replacement therapy, a benefit exceeding the defined placebo response in recurrent aphthous stomatitis.

Adolescent↗
PubMed1979

[Hematin treatment of acute intermittent porphyria. A case report (author's transl)].

A young woman with acute intermittent porphyria in profound relapse and severe nervous and respiratory involvement was treated by intravenous infusions of hematin, followed by improvement of symptoms. The diet with high carbohydrate and protein content and a B-adrenergic blocking agent, not showed any beneficial effect on acute attack. The infusion of hematin was followed by a lowering effect on urine porphybilinogen and delta-aminolevulinic acid and clinical improvement. The return to normal of porphyrin precursors in the urine was accompanied by almost complete clinical remission. The relationship of remission and repression of delta-aminolevulinic acid, decrease of urinary levels of porphyrin precursors, pulmonaries tests and electromyograms, were discussed.

Adolescent↗
PubMed1976

Formalin pigment (acid hematin) and related pigments.

Black to brown amorphous to microcrystalline granules are encountered in histologic sections prepared from tissues fixed in formalin having a low pH. This pigment is produced by acid acting upon hemoglobin and is known as formalin pigment or acid hematin. A similar pigment is also observed in sites of bleeding ulcers in areas of acid production such as the stomach. These pigments exhibit many physical and histochemical properties similiar to pigments produced by some animal parasites as in malaria, schistosoma and pulmonary mites. These parasites disintegrate erythrocytes in an unknown manner, and liberate an acid hematin-like pigment which is phagocytized by the reticuloendothelial system. Since formalin pigment can be considered as an artifact, confusion with other pigments can be avoided by the use of neutral buffered formalin for the fixation of tissues.

Animals↗
PubMed1979

Identification of 15-keto-9, 11-peroxidoprosta-5, 13- dienoic acid as a hematin-catalyzed decomposition product of 15-hydroperoxy-9, 11-peroxidoprosta-5, 13-dienoic acid.

A labile prostaglandin was isolated as one of the products generated from [1-14C] eicosatetraenoic acid incubated with sheep vesicular gland microsomes. The eicosatetraenoic acid metabolite amounted to ca. 16% of the total radiolabeled products. Formation of this new prostaglandin was prevented when heat-denatured microsomes were employed or when incubation mixtures were supplemented with indomethacin or phenol. However, incubation of prostaglandin G2 (PGG2) with hematin in the presence or absence of catalytically active or heat-inactivated microsomes led to production of approximately the same quantity of the new prostaglandin. These results indicated that the new prostaglandin can be formed nonenzymically. The new prostaglandin was conclusively identified by gas liquid chromatography-mass spectrometry analysis as 15-keto-9,11-peroxidoprosta-5,13-dienoic acid (15-keto-PGG2) after chemical conversion to known prostaglandins. The effects of 15-keto-PGG2 and PGG2 were similar on canine lateral saphenous vein; both promoted contraction followed by prolonged relaxation, but 15-keto-PGG2 appeared to be 1/50 as potent as PGG2.

Animals↗