scholarly journals Brucella terminal ileitis: a rare cause of intestinal obstruction about a case

2021 ◽  
Vol 9 (9) ◽  
pp. 2831
Author(s):  
Alejandro Antonio Ayala Correa ◽  
Irving Yair Grande Zamora ◽  
Santos Enrique Platas Galván ◽  
Oswaldo Natanael González Rivera
Keyword(s):  
Intestinal Obstruction ◽  
Acute Abdomen ◽  
Antithrombin Iii ◽  
Clinical Manifestations ◽  
Systemic Infection ◽  
Terminal Ileitis ◽  
Unusual Manifestation ◽  
Unpasteurized Milk ◽  
History Of ◽  
Antithrombin Iii Deficiency

Brucellosis is a bacterial zoonosis transmitted by contact with fluids from infected domestic animals, by consumption of unpasteurized milk products, or by inhalation of infected aerosols. Systemic infection has clinical manifestations from asymptomatic cases to those that are fatal. Focal infections occur in 30% of cases and affect any organ. Gastrointestinal manifestations are rare and unspecific. We reported the case of a patient with antithrombin III deficiency who presented with a clinical picture of abdominal pain at the emergency department, with failure of conservative treatment and with progression to acute abdomen, for which surgical treatment was offered, resolving the condition of intestinal obstruction and taking a biopsy that confirmed terminal brucella ileitis, antibiotic treatment and intestinal rest were indicated with successful results. Brucella terminal ileitis is an unusual manifestation of brucellosis. History of consumption of unpasteurized milk and derivatives and contact with livestock should be carefully examined in patients with acute abdomen in Brucella endemic countries. This will lead to a full and uncomplicated recovery from this disease.

The Prevalence of Hereditary Antithrombin-III Deficiency in Patients with a History of Venous Thromboembolism

1985 ◽  
Vol 54 (04) ◽  
pp. 744-745 ◽  
Author(s):  
R Vikydal ◽  
C Korninger ◽  
P A Kyrle ◽  
H Niessner ◽  
I Pabinger ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Antithrombin Iii ◽  
Positive Family History ◽  
Normal Range ◽  
The Family ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Recurrent Venous Thrombosis ◽  
Antithrombin Iii Activity ◽  
Slight Deficiency

SummaryAntithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

Antithrombin III Deficiency in a Japanese Family

1979 ◽  
Author(s):  
M. Nakagawa ◽  
T. Kawamura ◽  
H. Tsuji ◽  
Y. Okajima ◽  
S. Urano ◽  
...  
Keyword(s):  
Antithrombin Iii ◽  
Sinus Thrombosis ◽  
Elevated Serum ◽  
Peptic Ulcers ◽  
Autosomal Dominant Disorder ◽  
Japanese Family ◽  
Vein Thrombosis ◽  
Chromogenic Assay ◽  
History Of ◽  
Antithrombin Iii Deficiency

Antithrombin III has been reported to be decreased in the cases of several thrombotic disorders and the decreased Antithrombin III is known to induce the hypercoagulable state. This study was started from the 28 year-old male patient who developed the superior sagital sinus thrombosis after appendectomy and it was followed by deep vein thrombosis of extremities. Antithrombin III level was 19 mg/dl and activity was 68% by the progressive antithrombin assay and other laboratory examinations were within normal range excepts for the elevated serum lipids. Antithrombin III was assayed for his family members in three consecutive generations by single radial immunodifusion method, coagulation assay, and chromogenic assay. Four out of eight members were confirmed to have low Antithrombin III level and activity ranging from 59%-68% of normal values, although the two of this four members had no history of thrombosis. Mother of this propositus is deceased, but it was suspected of having the defect of Antithrombin III. History of peptic ulcers were found in all members of this family. The inheritance pattern of Antithrombin III deficiency was characteristic of an autosomal dominant disorder.

scholarly journals Platelet Antithrombin Deficiency: A New Clinical Entity

1977 ◽  
Author(s):  
J.L. Tullis ◽  
K. Watanabe
Keyword(s):  
Antithrombin Iii ◽  
Family Members ◽  
Clinical Entity ◽  
Clear Relationship ◽  
Secondary Effect ◽  
Antithrombin Deficiency ◽  
Consistent Effect ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Immunologic Assay

A kindred with a history of multiple thromboses was studied for coagulant abnormalities. A deficiency of plasma antithrombin III was found in approximately half of the 13 family members by either coagulant or immunologic assay. No clear relationship between plasma antithrombin III deficiency and a history of thrombosis was present. Platelet antithrombin assays were studied in the same family. Ten of the 13 members were deficient. None of the three who was normal had a history of thrombosis. The plasma antithrombin III assays could be influenced by heparin or coumarin treatment. The same medications were without consistent effect on platelet antithrombin. On the basis of these findings, it is proposed that familial hypercoagulability in some cases may be due to a platelet antithrombin deficiency and that the plasma antithrombin III deficiency is a secondary effect.

The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism

1986 ◽  
Vol 41 ◽  
pp. 129
Author(s):  
C. Korninger ◽  
R. Vikydal ◽  
P.A. Kyrle ◽  
H. Niessner ◽  
I. Pabinger ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Antithrombin Iii ◽  
History Of ◽  
Antithrombin Iii Deficiency

Inherited Antithrombin III Deficiency and Cerebral Thrombosis in a Child

PEDIATRICS ◽  
1980 ◽  
Vol 65 (1) ◽  
pp. 125-131
Author(s):  
Daniel R. Ambruso ◽  
Linda J. Jacobson ◽  
William E. Hathaway
Keyword(s):  
Antithrombin Iii ◽  
Index Case ◽  
Cerebral Thrombosis ◽  
Recurrent Thrombosis ◽  
Normal Pattern ◽  
Crossed Immunoelectrophoresis ◽  
Warfarin Sodium ◽  
At Iii ◽  
History Of ◽  
Antithrombin Iii Deficiency

Identification of a family affected by antithrombin III-heparin cofactor (AT-III) deficiency was made after diagnosis of the index case, a 15-year-old boy who suffered cerebral thrombosis. The proband had a two-year history of recurrent thrombosis involving the lower extremities. His mother and sister were also affected. Studies showed a decreased biological activity (AT-IIIc) and antigen (AT-IIIag) by the Laurell technique in the proband (AT-IIIc = 0.32, AT-IIIag = 46%), his sister (AT-IIIc = 0.29, AT-IIIag = 47%), and his mother (AT- IIIc = 0.41, AT-IIIag 56%). Crossed immunoelectrophoresis (CIE) of the affected individuals' plasma in agarosecontaining heparin demonstrated a normal pattern of migration. Treatment with warfarin sodium (Coumadin) resulted in an increase in activity in two of three affected family members, and in antigen in all three. Anticoagulant therapy did not affect the pattern of AT-III on CIE. This family represents a quantitative deficiency in antithrombin III. A review of the reported cases of antithrombin III deficiency indicates that individuals with this disorder may have thromboembolic disease in childhood.

scholarly journals Familial Thrombosis Due to Antithrombin III Deficiency

Blood ◽  
1974 ◽  
Vol 43 (2) ◽  
pp. 219-231 ◽  
Author(s):  
Ewa Marciniak ◽  
Claude H. Farley ◽  
Philip A. DeSimone
Keyword(s):  
Antithrombin Iii ◽  
Clinical Symptoms ◽  
Oral Anticoagulants ◽  
Laboratory Diagnosis ◽  
Blood Component ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Recurrent Venous Thrombosis

Abstract A large kindred from eastern Kentucky, with extensive history of recurrent venous thrombosis and pulmonary embolism, was studied. Low antithrombin III titers, ranging from 26% to 49% of normal values, were found in plasma of nine members in three consecutive generations; another five members, four of whom were not available for study, are suspected of having the biochemical defect. There was a good correlation between clinical symptoms and antithrombin III deficiency, although three of the younger members with the defect still remained free of thrombosis. In serum of the affected subjects antithrombin III was almost completely utilized, which indicates that stoichiometric binding to coagulation enzymes dominates under biological conditions. Antithrombin and antifactor Xa activities residing in the macroglobulin region of plasma and serum remained unchanged. The responsiveness to heparin in vitro and in vivo confirmed the evidence that antithrombin III is the sole blood component through which heparin exerts its anticoagulant effect. In five affected members therapy with oral anticoagulants increased very significantly the level of antithrombin III in plasma and contributed to a remarkable increase of residual antithrombin III in serum. This objective improvement after warfarin therapy may create significant difficulties in the laboratory diagnosis of antithrombin III deficiency.

scholarly journals Prevalence of Hematological Disorders among Children with Brucellosis

2017 ◽  
Vol 5 (2) ◽  
Author(s):  
Saber A. M. El-Sayed ◽  
Yasser F. Ali ◽  
Mostafa M. Ahmady ◽  
Salah F. Alsayed ◽  
Ahmed M. Baraka
Keyword(s):  
Blood Culture ◽  
Positive Family History ◽  
Clinical Manifestations ◽  
Systemic Infection ◽  
Positive Serology ◽  
Excessive Sweating ◽  
Hematological Disorders ◽  
Presenting Symptoms ◽  
History Of

Background: Brucellosis is a zoonotic systemic infection due to infection by Brucella organisms with a various clinical manifestations and complications. Hematological disorders is the most common and serious complications among children. Objectives: Our study aimed to evaluate frequency of hematological complications among brucellosis infected children. Patients and Methods: All 75 patients enrolled in the study with fever more than 5 days, arthralgia , myalgia, low back pain , hematological disorders and positive serology test ( positive results when the tires > 1:80 ) were referred to the infectious diseases unit in King Khalid hospital ,Al-kharj city ,K.S.A. during  April 2013 to August 2015, and  C.B.C., blood culture and bone marrow study were made for all patients .Results:  out of 75children with brucellosis with age 5-18 y, 63 (84%) gave a history of raw animal milk ingestion and 33 patients 44% had a positive family history of brucellosis. The commonly presenting symptoms and signs included; excessive sweating 43 patients (57.3%) bone aches 65 patients (62%) chills 40 patients (53.3%), arthritis 27 patients (36%). Hepatomegaly 10 patients (13.3%) and splenomegaly     11 patients (14.6%). The most commonly detected hematological manifestations included; anemia in 34 patients (45%). leukopenia in 30 patients (40%) and leukocytosis in 18 patients (24%). Meanwhile, pancytopenia was detected in 24 patients (32%). Positive blood culture for brucella was seen in 30 patients (40%). B. melitensis from 26 patients (34.6%) was cultured in vitro. Out of 15 BM aspiration cultures, 5 were positive for B. melitensis while 10 cultures were negative. Out of 24 patients (32%) with pancytopenia, 17 patients 71% presented with bone aches and weakness, 12  patients 50% presented with sweating and chills,12  patients 50%  had petechiae and purpura , 12 patients50% had splenomegaly and also 9 patients 37.5% had hepatomegaly.Conclusions: Our study showed that the clinical manifestations and hematological disorders in children with brucellosis are 45% of patients were anemic, 40% were leukopenia, pancytopenia were in 32% while leukocytosis were in 24% similar to that in the adults; specially in endemic areas like K.S.A. 

scholarly journals Management of antithrombin III deficiency in pregnancy: a representative case and a literature review

2021 ◽  
Vol 15 (4) ◽  
pp. 441-450
Author(s):  
S. V. Akinshina ◽  
P. K. Genina ◽  
V. O. Bitsadze ◽  
J. Kh. Khizroeva ◽  
V. I. Tsibizova ◽  
...  
Keyword(s):  
Antithrombin Iii ◽  
Blood Clot ◽  
Low Molecular Weight ◽  
Monitoring Therapy ◽  
At Iii ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Therapeutic Doses ◽  
Generation Test ◽  
Indications For Use

The work is aimed at discussing pregnancy management for the most thrombogenic genetic thrombophilia - antithrombin III (AT-III) deficiency. A detailed analysis of the literature and clinical case of pregnancy management in a patient with AT-III deficiency, pulmonary embolism and habitual history of miscarriage has been performed and presented. Patients with AT-III deficiency are at high risk for developing thrombotic and obstetric complications even despite using therapeutic doses of anticoagulants. Indications for use and modes of administration of AT-III concentrate have not been currently defined clearly. Monitoring therapy with low molecular weight heparin is largely complicated because a test for determining anti-Xa activity is AT-III-dependent. In addition to standard methods for controlling antithrombotic therapy, we used tests characterizing the dynamic blood clot parameters: thromboelastography and thrombin generation test. The peak risk resulting in both thrombotic and hemorrhagic complications in such patients occurs during period of labor and the postpartum period, when a change in the regimen of anticoagulant therapy is required with its temporary withdrawal and additional administration of AT-III concentrate.

Antithrombin III Deficiency in A Japanese Family

1979 ◽  
Author(s):  
M. Nakagawa ◽  
T. Kawamura ◽  
H. Tsuji ◽  
Y. Okajima ◽  
S. Urano ◽  
...  
Keyword(s):  
Antithrombin Iii ◽  
Sinus Thrombosis ◽  
Elevated Serum ◽  
Peptic Ulcers ◽  
Autosomal Dominant Disorder ◽  
Japanese Family ◽  
Vein Thrombosis ◽  
Chromogenic Assay ◽  
History Of ◽  
Antithrombin Iii Deficiency

Antithrombin IEC has been reported to be decreased in the cases of several thrombotic disorders and the decreased Antithrombin III is known to induce the hypercoagulable state. This study was started from the 28 year-old male patient who developed the superior sagital sinus thrombosis after appendectomy and it was followed by deep vein thrombosis of extremities. Antithrombin III level was 19 mg/dl and activity was 68% by the progressive antithrombin assay and other laboratory examinations were within normal range excepts for the elevated serum lipids. Antithrombin III was assayed for his family members in three consecutive generations by single radial immunodifusion method, coagulation assay, and chromogenic assay. Four out of eight members were comfirmed to have low Antithrombin III level and activity ranging from 59%-68% of normal values, although the two of these four members bad no history of thrombosis. Mother of this propositus is deceased, but it was suspected^of having the defect of Antithrombin III. History of peptic ulcers were found in all members of this family. The inheritance pattern of Antithrombin III deficiency was characteristic of an autosomal dominant disorder.

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