Aplastic anemia associated with submassive hepatic necrosis. Report of four cases

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.

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Early Development of Drug-Induced Hepatic Necrosis

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100066942 ◽

1971 ◽

Vol 29 ◽

pp. 576-577

Author(s):

F. G. Zaki ◽

E. Detzi ◽

C. H. Keysser

Keyword(s):

Early Development ◽

Hepatic Necrosis ◽

Screening Tests ◽

Dense Matrix ◽

Sprague Dawley ◽

Electron Microscopic ◽

Drug Induced ◽

Hepatocellular Damage ◽

Sprague Dawley Rats ◽

Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

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A Comparison of the Ultrastructural Morphology of Hepatic Necrosis in BDF1 Mice

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100099350 ◽

1981 ◽

Vol 39 ◽

pp. 586-587

Author(s):

Becky Jackson

Keyword(s):

Endoplasmic Reticulum ◽

Smooth Endoplasmic Reticulum ◽

Preliminary Investigation ◽

Hepatic Necrosis ◽

Hepatic Tissue ◽

Pronounced Increase ◽

Glycogen Store ◽

Ultrastructural Morphology ◽

Mitochondrial Integrity ◽

Glycogen Stores

Preliminary investigation has indicated similarity in hepatic ultrastructural morphology in nutritional deprivation, and cyanide induced hepatic necrosis. Analysis of hepatic tissue has indicated disruption of intracellular membranes, specifically, reduction in rough endoplasmic reticulum (RER) mitochondrial integrity, and glycogen stores. An increase in smooth endoplasmic reticulum (SER) portion was observed.To further investigate the apparent equivalence of necrotic morphology, ultrastructura1ly, BDF1 mice were subjected to senescence, nutritional deprevation, potassium cyanide (KCN) induced toxemia, and acetaminophen induced toxemia. Controls were utilized to ellucidate non-necrotic hepatocellular normals. U1trastructura1 investigation of controls (Fig. 1) shows densely granular RER, abundant glycogen stores, and morphologically normal mitochondria. Subjects with acetaminophen induced necrosis exhibit reduced normal RER with increased levels of dialated, vesicular RER in apparent conversion to SER (Fig. 2), loss of mitochondrial integrity, and glycogen store reduction. Senescent subjects exhibit a pronounced increase in SER and loss of glycogen store. (Fig. 3). Investigation of the senescent SER at high magnification (Fig. 5) indicates that the SER is arising from degranulating and vesiculating RER.

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Homeopathy in a child with “very severe aplastic anemia”

Allgemeine Homöopathische Zeitung ◽

10.1055/s-0037-1601204 ◽

2017 ◽

Vol 262 (02) ◽

pp. 2-76

Author(s):

C Schuldt

Keyword(s):

Aplastic Anemia ◽

Severe Aplastic Anemia

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TO STUDY THE ETIOPATHOLOGICAL SPECTRUM OF ADULT PATIENTS WITH PANCYTOPENIA

International Journal of Medical and Biomedical Studies ◽

10.32553/ijmbs.v4i10.1461 ◽

2020 ◽

Vol 4 (10) ◽

Author(s):

Harimohan Garg ◽

Haritej Anand Khirawari ◽

Sona Priyadarshi

Keyword(s):

Acute Leukemia ◽

Aplastic Anemia ◽

Indian Subcontinent ◽

Megaloblastic Anemia ◽

Anaplastic Carcinoma ◽

Adult Patients ◽

Research Centre ◽

New Delhi ◽

Nutritional Anemia ◽

Male Preponderance

Background: Pancytopenia is diagnosed when there is a reduction in all three hematopoietic cell lines. Till date there is limited number of studies on the frequency of various causes of pancytopenia. Of these some have been reported from the Indian subcontinent. There appears to be a changing spectrum of pancytopenia over the past two decades. The objective was to study the etiopathological spectrum of adult patients with pancytopenia over a period of one and half year. Methods: The Prospective and retrospective observational study was conducted in the Department of Family Medicine, Batra Hospital and Medical Research Centre, New Delhi. A total of 120 Patients were included in the study. All patients gave their consent to take part in the study and were subjected to a questionnaire regarding symptoms, past relevant history, lifestyle and detailed clinical examination and investigations as mentioned in materials and methods. Results: Six broad diagnostic groups could be identified in adults with pancytopenia. Megaloblastic anemia (D1) was the largest group comprising 57.5% of all patients. 11.7% of patients with pancytopenia were diagnosed as Aplastic anemia (D2).11.7% of patients with pancytopenia were diagnosed as leukemia/lymphoma (D3) such as lymphoma (1), metastatic anaplastic carcinoma (1), acute leukemia (11), and metastatic gastric carcinoma (1). 15% of patients with pancytopenia were diagnosed with infections (D4) such as complicated malaria cases (7), HIV (5), disseminated tuberculosis (4), viral (2). We also encountered (D5) 0.8% was Myelophthisis/Storage disorder as myelodysplastic syndrome (1) and 3.3% were other (D6) as reactive marrow (4). Conclusion: Pancytopenia is not a disease itself. It is a hematological feature of varying etiology with slight male preponderance. Megaloblastic anemia along with mixed nutritional anemia is leading cause of pancytopenia in India followed by infections being second and aplastic anemia and acute leukemia being third common causes. Keyword: Pancytopenia, Megaloblastic anemia, Nutritional anemia.

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