scholarly journals BLOOD CORTISOL CONCENTRATION, HEMODYNAMICS AND METABOLISM OF PATIENTS WITH SECONDARY HYPERPARATHYROIDISM, POSSIBILITIES OF PERIOPERATIVE CORRECTION

Author(s):  
R.YU. SOBKO ◽  
M. KOVALOV ◽  
O.I. DOROSH ◽  
U.A. FESENKO

A clinical case of severe bleeding from the wells of extracted teeth in a 9-year-old girl with Glanzman’s thrombasthenia is reported. Literature data on diagnosis and management of such patients are given. The authors emphasize that in the treatment of such patients sometimes it is necessary to make extraordinary decisions that can save the patient’s life. In this case, a direct blood transfusion was performed.

2021 ◽  
Vol 19 (4) ◽  
Author(s):  
І.Т. Rusnak ◽  
V.K. Tashchuk ◽  
N.O. Slyvka ◽  
V.T. Kulachek ◽  
Y.V. Kulachek

This article presents a clinical case of peripartum cardiomyopathy in a 21-year-oldpatient with a gestational age of 32 weeks, accompanied by clinical manifestationsof heart failure and Lown-Ganong-Levine (LGL) syndrome. The patient underwentlaboratory and instrumental examinations, including echocardiography and Holtermonitoring. Thyrotoxic cardiomyopathy was ruled out in the process of differentialdiagnosis. The final diagnosis and management of the patient were determinedafter consultation with the State Institution "Institute of Pediatrics, Obstetrics andGynecology, named after Academician O.M. Lukyanova, of the National Academy ofMedical Sciences of Ukraine". Medical treatment significantly improved the patient'scondition and vaginal delivery went without complications. Manifestations of theperipartum cardiomyopathy gradually regressed and completely disappeared 6 monthsafter delivery.This case indicates the importance of timely diagnosis of peripartum cardiomyopathyfor a positive prognosis of patients.


2021 ◽  
Vol 38 (1) ◽  
pp. 161-167
Author(s):  
S. G. Shulkina ◽  
D. O. Sirin ◽  
E. N. Smirnova ◽  
V. G. Zhelobov ◽  
N. Yu. Kolomeets ◽  
...  

Hyperparathyroidism is an endocrine disease characterized by excessive production of parathyroid hormone in the main cells of the parathyroid glands. Depending on the cause of this disease, there are primary, secondary (SHPT) and tertiary hyperparathyroidism. The most common causes of SHPT are vitamin D deficiency and chronic kidney disease (CKD). Vitamin D is converted to its active form by hydroxylation in the renal tubules. Developmental abnormalities and chronic kidney diseases lead to atrophy of the tubular epithelial cells that causes a violation of vitamin D metabolism and the development of SHPT, which in turn are accompanied by a violation of calcium-phosphorus metabolism and a syndrome of musculoskeletal disorders. This article presents an analysis of a clinical case of a patient diagnosed secondary hyperparathyroidism against the background of vitamin D deficiency combined with polycystic kidney disease. This clinical case reflects the complexity of the differential diagnosis of the disease and the tactics of patient's management.


Gut ◽  
1998 ◽  
Vol 42 (5) ◽  
pp. 750-752 ◽  
Author(s):  
P A McCormick ◽  
H Ooi ◽  
O Crosbie

Background—It is believed that severe portal hypertensive gastropathy probably accounts for most non-variceal bleeding episodes in patients with cirrhosis. Gastric antral vascular ectasia (GAVE) also occurs in these patients. It is not clear whether it is a variant of portal hypertensive gastropathy or a distinct condition.Patient—A patient, a 66 year od woman, with cirrhosis initially diagnosed as having portal hypertensive gastropathy and subsequently classified as GAVE is described. She required transfusion with a total of 130 units of packed red cells for gastrointestinal blood loss.Results—The bleeding did not respond to portal decompression with TIPS or beta blockers. Following treatment with oral tranexamic acid she has not required further blood transfusion over a period of 30 months.Conclusion—Tranexamic acid may be a useful treatment for refractory bleeding due to gastric antral vascular ectasia in patients with cirrhosis.


2019 ◽  
Vol 13 (2) ◽  
pp. 190-199
Author(s):  
E.Z. Golukhova ◽  
M.M. Alshibaya ◽  
D.V. Mrikaev ◽  
T.V. Mashina ◽  
L.S. Lifanova

2011 ◽  
Vol 17 (1) ◽  
pp. 69-79 ◽  
Author(s):  
G. Stanek ◽  
V. Fingerle ◽  
K.-P. Hunfeld ◽  
B. Jaulhac ◽  
R. Kaiser ◽  
...  

2020 ◽  
Vol 5 (4) ◽  
pp. 84-89
Author(s):  
E. A. Ilyicheva ◽  
D. A. Bulgatov ◽  
A. V. Zharkaya ◽  
V. N. Makhutov ◽  
E. G. Grigoryev

Parathyroidectomy is the leading treatment for drug-refractory secondary and tertiary hyperparathyroidism in patients with chronic kidney disease. Difficulties in performing this surgery are mainly associated with the anatomical features of the parathyroid glands, in particular with the variability of their number and topographic anatomy. Ectopic parathyroid glands are one of the most common causes of persistence or recurrence of secondary hyperparathyroidism after surgery. One of the common variants of ectopia is the localization of the parathyroid gland in the anterior-superior mediastinum. The article discusses the features of surgical treatment of secondary hyperparathyroidism in patients with end-stage chronic kidney disease with this ectopia. A new method of treating hyperparathyroidism in patients with an atypical location of the parathyroid gland in the anterior-superior mediastinum is presented. This method is characterized by low invasiveness of access, ease of implementation without using special equipment and instruments. The proposed method was used in the treatment of a patient with secondary hyperparathyroidism due to chronic renal failure as a result of chronic glomerulonephritis. The duration of hemodialysis at the time of the surgery was more than 17 years. In the presented clinical case, ectopia of one of the pathologically altered parathyroid glands in the anterior-superior mediastinum was found at the preoperative stage. As a method of surgical treatment, we carried out total parathyroidectomy with autotransplantation of a fragment of parathyroid tissue into the brachioradialis muscle. Thanks to this method, it was possible to remove the atypically located parathyroid gland from the cervicotomy access and to discharge the patient within the standard terms for a given volume of surgery.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4834-4834 ◽  
Author(s):  
Fabiana Mendes Conti ◽  
Ana Paula Hitomi Yokoyama ◽  
Marcia R Dezan ◽  
Thiago H Costa ◽  
Maria Giselda Aravechia ◽  
...  

Abstract Background Post-transfusion purpura (PTP) is a rare yet serious disease characterized by severe thrombocytopenia occurring after a blood transfusion. It is caused by alloimmunization against platelet antigens, anti-HPA-1a being the most frequent antibody. We report two cases of PTP and discuss the clinical presentation, diagnosis and management of this serious condition. Case Report Case 1) Female patient, 90 years old, Caucasian, had a fracture in the umerus and head trauma in 2012, followed by upper GI bleeding. Four days after receiving two units of packed RBCs, she presented with a low platelet count (14.000/mm3), petechiae, gum bleeding and oozing from venipuncture sites. The platelet count further dropped to 2.000/mm3the following day. HPA genotyping and HPA antibody identification by MAIPA were performed to investigate post-transfusion purpura, which showed: HPA1bb, 3aa, 5aa and 15ab and presence of antibodies anti-HPA-1a. IVig 400 mg/kG was infused in two consecutive days, with normal platelet counts observed after a week. Two of her three children had the same HPA1bb genotype and performed a matched platelet and RBC donation by apheresis. One matched RBC unit was transfused to correct symptomatic anemia caused by bystander hemolysis seven days after the first transfusion. No platelet transfusions were needed. Case 2) Female patient, 29 years old, afrodescendant, had a hemorrhagic shock after an emergency hysterectomy due to placenta percreta in 2012. She received 14 RBC units, 10 fresh frozen plasmas and 10 units of cryoprecipitate. Two days later, another surgery was necessary to remove a retained coagulum, and she received 10 units of random platelets. Five days later, the platelet count dropped to 5.000/mm3, followed by sudden anemia (Hb=9--> 4,5 g/dL), without clinical or laboratory signs of hemolysis or evidence of bleeding, with normal coagulation times. HPA genotyping and antibody identification by MAIPA were performed and showed an HPA1bb genotype and presence of an anti-HPA-1a antibody. No platelet transfusions were administered and IVig 500mg/Kg was prescribed for 2 days. Only washed RBC units were transfused thereafter. The platelet count rose four days after starting IVig to 134.000/mm3, yet a second course of IVig was necessary a week later to reach normal platelet counts. Discussion Both reports illustrate severe thrombocytopenia in patients who presented with sudden thrombocytopenia up to a week after blood transfusion. Platelet alloimmunization happens after exposure to HPA antigens by transfusion or pregnancy, and severe thrombocytopenia occurs as an anamnestic response after reexposure to platelet antigens in any blood product that contains contaminating platelet membranes. The thrombocytopenia may evolve as an autoimmune process, which may also cause hemolytic anemia due toa bystander phenomenom. Diagnosis is based on the identification of the antibody in the serum of a patient who lacks the corresponding antigen, anti-HPA-1a being the most common. IVig 0,5-1g/Kg for 2 days is the treatment of choice. The RBC units must be washed to avoid exposure to platelet membranes and recurrence of thrombocytopenia. In future transfusions, washed RBCs or HPA1bb blood products should be used. Disclosures: No relevant conflicts of interest to declare.


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