scholarly journals Treatment of severe thrombocytopenia with platelet biotherapic and Phosphorus

Author(s):  
Bruna Scardoeli ◽  
Natália José Aith ◽  
Adalberto Von Ancken ◽  
Cidéli Paula Coelho

Background Thrombocytopenia is a decrease in the number of platelets in the blood resulting from disorders of production, distribution or destruction, leading to bleeding. The respective treatment of thrombocytopenia is usually based on corticotherapy and platelet transfusion. Aims Report the evolution of homeopathic treatment in a 12 years old Maltese canine cardiopathic patient with thrombocytopenia associated with the diagnosis of Ehrlichia canis. Methods Replacement of corticoid and transfusion by Platelet Biotherapic, to stimulate platelet production and high diluted Phosphorus to contain the bleeding. Results On 01/28/19, the patient presented thrombocytopenia of 5.000/mm³ with large platelets, petechials and suffusion hemorrhages in dorsal and ventral regions, extensive acute cervical hematoma due to blood collection; anisocytosis, polychromasia and Howell Jolly corpuscle in red series; and also reactive lymphocytes, monocytes active and toxic neutrophils in white series. On 01/30/19, initiated the administration of 3 globules of Platelet Biotherapic 12CH every 12 hours; 3 globules of Phosphorus 6CH every 24 hours, both oral; and topical phytotherapeutic use of Arnica montana once daily. Three days later, it was observed the complete absence of petechials and suffusion hemorrhages, with elevation of platelets count to 74.000/mm³ and mild leukocytosis with improvement in overall patient well-being. On 02/06/19, there was regression of hematoma and leukocytosis, in addition to the platelet count in 95.000/mm³. On 02/14/19, due to slight decrease in platelets to 92.000/mm³, the frequency of Phosphorus 6CH was changed every 12 hours. On 02/20/19, the new platelet count reached 126.000/mm³ with standardized morphology and no Howell Jolly record. Conclusion The homeopathies (High dilution medicine) have proven to be successful in the treatment of thrombocytopenia without causing side effects.

2019 ◽  
Vol 26 (09) ◽  
pp. 1398-1403
Author(s):  
Yasmeen Batool ◽  
Sabeen Fatima ◽  
Gulzaib Pervaiz ◽  
Naseem Akhtar ◽  
Maliha Asif ◽  
...  

Pakistan is an endemic area for malaria. Malaria is considered to be associated with thrombocytopenia. The frequency of thrombocytopenia varies in different studies. This study was done to determine the frequency of thrombocytopenia among patients with malaria. Objectives: To determine the frequency and severity of thrombocytopenia in patients of malaria. Study Design: Cross-sectional survey. Setting: Pathology Department, Nishtar Medical University, Multan. Period: Eight months; (04-03-2018 to 03-11-2018). Materials & Methods: One hundred and fifty patients with malaria were included in the study. Platelet count of all the patients was done on Sysmex-K167. The patients were categorized according to the presence of thrombocytopenia (yes or no) and the severity of thrombocytopenia (mild, moderate or severe). The data was described as frequency distribution table. Results: The mean age of the patients was 31.81 + 15.31 years. There were 46 (30.7%) female patients and 104 (69.3%) male patients. Thrombocytopenia was present among 103 (68.7%) patients. Mild, moderate and severe thrombocytopenia was found in 60 (58.3%), 24 (23.3%) and 19 (18.4%) patients, respectively. Conclusion: This study concludes that frequency of thrombocytopenia is very high among patients with malaria. Severity of thrombocytopenia is mild to moderate, with few patients presenting with severe thrombocytopenia. This finding signifies that malaria is an important cause of thrombocytopenia. So the platelet count should be monitored closely in patients of malaria to avoid possible complications of thrombocytopenia. Moreover, it is suggested that malaria is an important differential diagnosis of thrombocytopenia with fever but needs confirmation by thick and thin smears for malarial parasite. In case of viral infections like dengue fever, smears will be negative for malarial parasite and patients will present with leucopenia and thrombocytopenia and majority of peripheral blood leucocytes will be reactive lymphocytes.


1987 ◽  
Vol 21 (11) ◽  
pp. 882-884 ◽  
Author(s):  
Alice K. Pau ◽  
Melanie A. Fisher ◽  
Wanda Maldonado ◽  
Marc Lebel

Rifampin-induced thrombocytopenia has been recognized as an immunological reaction associated with intermittent high-dose therapy, and rarely seen with daily low-dose regimens. Our patient was a 33-year-old male with Marfan's syndrome who was given rifampin 600 mg/d po along with intravenous vancomycin for the treatment of Staphylococcus epidermidis endocarditis. His platelet count dropped from a baseline of 519000/mm3 to 4000/mm3 after four doses of rifampin. Petechiae were present on the lower extremities without the presence of other bleeding sites. Rifampin, low-dose aspirin, and dipyridamole were discontinued. His platelet count returned to normal nine days after discontinuation of therapy. With the increasing use of rifampin for the treatment of nontuberculosis infections, clinicians should recognize the possibility of this drug causing such serious immunological reactions as thrombocytopenia, hemolytic anemia, acute renal failure, and shock with daily or intermittent therapy. Extracto Rifampin es un agente antibacteriano el cual es utilizado ampliamente en el tratamiento de tuberculosis y de otras infecciones bacterianas. El fármaco puede causar reacciones inmunológicas severas que pueden resultar en trombocitopenia púrpura, anemia hemolítica, insuficiencia renal, y shock. Estas están usualmente asociadas a dosis altas administradas en una manera intermitente, y la descontinuación del fármaco usualmente resulta en resolución de la reacción. Los autores describen el caso de un hombre de 33 años de edad con el Síndrome de Marfan que desarrolla una trombocitopenia severa luego de la administración de 600 mg diarios de rifampin para el tratamiento de endocarditis causado por Staphylococcus epidermidis. El paciente recibió también conjuntamente con rifampin, vancomicina 1 gm iv q 12h, aspirina 600 mg po qd, dipyridamole 25 mg po tid, y propranolol 80 mg po q12h. Cuatro horas luego de la cuarta dosis de rifampin (Día numero 4) el paciente desarrolló petequias en las extremidades inferiores, y el contaje de plaquetas obtenido inmediatamente reveló una concentración de 4000/mm3, el cual refleja una disminución significativa en comparación con el contaje obtenido ocho días antes de 519000/mm3. Tanto rifampin como aspirina y dipyridamole fueron descontinuados. Una marcada trombocitopenia y petequias perduraron por una semana, otras fuentes de sangramiento fueron descartadas y no hubo ningún cambio significativo en el estado de coagulación o en el recuento sanguíneo. Las plaquetas regresaron a un nivel normal nueve días después de descontinuado el rifampin. Aunque las plaquetas aumentaron de 11000/mm3 a 36000/mm3 el día en que propranolol fue descontinuado, los autores expresan que esta respuesta es muy rápida para considerar a éste como el agente causante. Aunque no se puede establecer con certeza que la trombocitopenia fuera causada por rifampin o aspirina solamente, o por un efecto sinergístico de ambos, rifampin parece ser el agente causante más probable. Es importante reconocer el potencial que posee rifampin para causar reacciones adversas serias como trombocitopenia, anemia hemolítica, insuficiencia renal aguda, y shock. La terapia con rifampin debe de descontinuarse si alguna de estas ocurren y otras causas no se pueden identificar. Resume Les thrombocytopénies associées avec la rifampicine sont reconnues comme des réactions immunologiques rencontrées particulièrement avec des thérapies à hautes doses. Le cas décrit par les auteurs est celui d'un patient mâle agé de 33 ans présentant un syndrome de Marfan à qui on a administré 600 mg de rifampicine en dose unique quotidienne en combinaison avec vancomycine iv pour le traitement d'une endocardite à Staphylococcus epidermidis. Le décompte plaquettaire a chuté d'une valeur de 519000/ml à 4000/ml seulement quatre heures après la dose de rifampicine. Des pétéchies étaient apparentes au niveau des jambes en absence de saignements à d'autres sites. Rifampicine, acide acétylsalicylique à faible dose, et dipyridamole furent suspendus. Les plaquettes sont revenus a leur niveau normal neuf jours apres l'arrêt de la thérapie. Devant l'augmentation de l'utilisation de la rifampicine pour le traitement des infections non-tuberculeuses, les cliniciens devront reconnaître le potentiel de ce medicament à causer des réactions immunologiques sévères telles que thrombocytopénie, anémie hémolytique, insuffisance rénale et choc.


1990 ◽  
Vol 64 (01) ◽  
pp. 117-120 ◽  
Author(s):  
Alessandra Casonato ◽  
M Teresa Sartori ◽  
Luigi de Marco ◽  
Antonio Girolami

SummaryWe have investigated the effects of 1-desamino-8-D-arginine vasopressin (DDAVP) infusion on platelet count and bleeding time in 4 patients with type IIB von Willebrand’s disease (vWd). Three of four patients showed a normalization of the bleeding time within 1 h after the infusion, while bleeding time was not modified in the fourth. In accordance with the literature, thrombocytopenia was observed after DDAVP infusion, but this thrombocytopenia was due to the anticoagulants used for blood collection. In two patients (F. I., G. F.) no thrombocytopenia was observed when platelets were counted by fingerstick method but there was a 20% platelet decrease in blood samples collected in sodium citrate and a 50% decrease in samples collected in EDTA. Dramatic falls in platelet counts (70–95%) were observed in the additional two patients (C. A., D.Z.) after DDAVP infusion, when both sodium citrate or EDTA were used as anticoagulants. In the latter two patients there was also a 50% decrease in platelet count when the fingerstick method was used. The decrease in the patient’s platelet count in EDTA samples after DDAVP infusion could be prevented, in part, by the previous additions of an anti GPIb monoclonal antibody and an anti GPIIb-IIIa monoclonal antibody.Thus, the thrombocytopenia observed in the four IIB vWd patients studied after DDAVP infusion seems to be, at least partially, a pseudothrombocytopenia depending on the calcium concentration in the blood samples and the availability of GPIb and GPIIb-IIIa receptors. These findings and the normalization of the bleeding time observed in three of the four patients has led us to reconsider the possible use of DDAVP in the treatment of our IIB vWd patients.


Author(s):  
Alessandro Squizzato ◽  
Silvia Galliazzo ◽  
Elena Rancan ◽  
Marina Di Pilla ◽  
Giorgia Micucci ◽  
...  

AbstractOptimal management of venous thromboembolism (VTE) in cancer patients with thrombocytopenia is uncertain. We described current management and clinical outcomes of these patients. We retrospectively included a cohort of cancer patients with acute VTE and concomitant mild (platelet count 100,000–150,000/mm3), moderate (50,000–99,000/mm3), or severe thrombocytopenia (< 50,000/mm3). Univariate and multivariate logistic regression analyses explored the association between different therapeutic strategies and thrombocytopenia. The incidence of VTE and bleeding complications was collected at a 3-month follow-up. A total of 194 patients of whom 122 (62.89%) had mild, 51 (26.29%) moderate, and 22 (11.34%) severe thrombocytopenia were involved. At VTE diagnosis, a full therapeutic dose of LMWH was administered in 79.3, 62.8 and 4.6% of patients, respectively. Moderate (OR 0.30; 95% CI 0.12–0.75), severe thrombocytopenia (OR 0.01; 95% CI 0.00–0.08), and the presence of cerebral metastasis (OR 0.06; 95% CI 0.01–0.30) were independently associated with the prescription of subtherapeutic LMWH doses. Symptomatic VTE (OR 4.46; 95% CI 1.85–10.80) and pulmonary embolism (OR 2.76; 95% CI 1.09–6.94) were associated with the prescription of full therapeutic LMWH doses. Three-month incidence of VTE was 3.9% (95% CI 1.3–10.1), 8.5% (95% CI 2.8–21.3), 0% (95% CI 0.0–20.0) in patients with mild, moderate, and severe thrombocytopenia, respectively. The corresponding values for major bleeding and mortality were 1.9% (95% CI 0.3–7.4), 6.4% (95% CI 1.7–18.6), 0% (95% CI 0.0–20.0) and 9.6% (95% CI 5.0–17.4), 48.2% (95% CI 16.1–42.9), 20% (95% CI 6.6–44.3). In the absence of sound evidence, anticoagulation strategy of VTE in cancer patients with thrombocytopenia was tailored on an individual basis, taking into account not only the platelet count but also VTE presentation and the presence of cerebral metastasis.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michinori Mayama ◽  
Mamoru Morikawa ◽  
Takashi Yamada ◽  
Takeshi Umazume ◽  
Kiwamu Noshiro ◽  
...  

Abstract Background Currently, there is a disagreement between guidelines regarding platelet count cut-off values as a sign of maternal organ damage in pre-eclampsia; the American College of Obstetricians and Gynecologists guidelines state a cut-off value of < 100 × 109/L; however, the International Society for the Study of Hypertension in Pregnancy guidelines specify a cut-off of < 150 × 109/L. We evaluated the effect of mild thrombocytopenia: platelet count < 150 × 109/L and ≥ 100 × 109/L on clinical features of pre-eclampsia to examine whether mild thrombocytopenia reflects maternal organ damage in pre-eclampsia. Methods A total of 264 women were enrolled in this study. Participants were divided into three groups based on platelet count levels at delivery: normal, ≥ 150 × 109/L; mild thrombocytopenia, < 150 × 109/L and ≥ 100 × 109/L; and severe thrombocytopenia, < 100 × 109/L. Risk of severe hypertension, utero-placental dysfunction, maternal organ damage, preterm delivery, and neonatal intensive care unit admission were analyzed based on platelet count levels. Estimated relative risk was calculated with a Poisson regression analysis with a robust error. Results Platelet counts indicated normal levels in 189 patients, mild thrombocytopenia in 51 patients, and severe thrombocytopenia in 24 patients. The estimated relative risks of severe thrombocytopenia were 4.46 [95 % confidence interval, 2.59–7.68] for maternal organ damage except for thrombocytopenia, 1.61 [1.06–2.45] for preterm delivery < 34 gestational weeks, and 1.35 [1.06–1.73] for neonatal intensive care unit admission. On the other hand, the estimated relative risks of mild thrombocytopenia were 0.97 [0.41–2.26] for maternal organ damage except for thrombocytopenia, 0.91 [0.62–1.35] for preterm delivery < 34 gestational weeks, and 0.97 [0.76–1.24] for neonatal intensive care unit admission. Conclusions Mild thrombocytopenia was not associated with severe features of pre-eclampsia and would not be suitable as a sign of maternal organ damage.


2015 ◽  
Vol 8 (2) ◽  
pp. 256-263 ◽  
Author(s):  
Jiaxin Niu ◽  
Teresa Goldin ◽  
Maurie Markman ◽  
Madappa N. Kundranda

Background: Immune thrombocytopenic purpura (ITP) is a rare acquired bleeding disorder with an estimated incidence of 1 in 10,000 people in the general population. The association of ITP with breast cancer is an even rarer entity with very limited reports in the English literature. Case Presentation: We report a case of a 51-year-old female with no significant past medical history who presented with sudden onset of malaise, syncope, gingival bleed and epistaxis. She was found to have severe thrombocytopenia (platelet count 6,000/μl) and anemia (hemoglobin 7.2 g/dl). Her workup led to the diagnosis of metastatic ductal breast cancer with extensive bone metastasis. Bone marrow biopsy demonstrated myelophthisis which was initially thought to be consistent with her presentation of thrombocytopenia and anemia. Therefore, the patient was started on hormonal therapy for the treatment of her metastatic breast cancer. After 3 months of therapy, she did not improve and developed severe mucosal bleeding. Her clinical presentation was suspicious for ITP and immune-mediated anemia, and hence she was started on steroids and intravenous immunoglobulin. The patient had a dramatic response to therapy with normalization of her platelet count and hemoglobin within 2 weeks. Conclusion: To our knowledge, this is the first reported case of metastatic breast cancer presenting with symptomatic ITP and anemia, and both symptoms are postulated to be immune-mediated.


2021 ◽  
pp. 089719002110647
Author(s):  
Widyati ◽  
Nurul Latifah ◽  
Maya Ramadhani

Introduction Pantoprazole is a proton pump inhibitor (PPI) class drug that is widely used in the treatment of SRMD (stress-related mucosal disease in critical ill patients. PPI are one class of drugs used commonly both for treatment and prophylactic therapy for stress ulcers in intensive care unit (ICU). Case We report a case of a 51-year old male who was referred to PKU Hospital. He was admitted to ICU with diagnosis of Hyperosmolar Hyperglymic State and bronchopneumonia. Thrombocytopenia was noted in admission. There was more than 70% decrease in platelet count after initiation of pantoprazole. Patient received Thrombocyte Concentrate (TC) transfusion and corticosteroid iv for several days, but only had minor increase in platelet count. The platelets recovered after stopping pantoprazole. Discussion In the present case report, another exposures to parenteral pantoprazole in a dose of 40 mg once daily reproduced the same adverse drug reaction. In comparison to lansoprazole, thrombocytopenia from pantoprazole is more severe that necessitate TC transfusion and corticosteroid trial. However, in the present case, TC transfusion and corticosteroid fail to escalate platelet count. This finding suggests probability of non-immune mechanism of pantoprazole-induced thrombocytopenia. Conclusion Pantoprazole may induce thrombocytopenia with new features that were immediately developed, resulting a decrease in platelet count >70%. The mechanism found in this case may be non-immune. Drug-induced thrombocytopenia is one of the rare complications that has to be kept in mind with the use of pantoprazole.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tia C Kohs ◽  
Vikram Raghunathan ◽  
Patricia Liu ◽  
Ramin Amirsoltani ◽  
Michael Oakes ◽  
...  

Introduction: Extracorporeal membrane oxygenation (ECMO) is used to provide circulatory support and facilitate gas exchange via cardiopulmonary bypass. The relationship between ECMO and the incidence of severe thrombocytopenia (platelet count <50 x 10 9 /L) and subsequent clinical consequences are ill defined. We aimed to identify the risk factors for the development of thrombocytopenia and its clinical implications. Methods: This is a single-center retrospective cohort study of adults who received venoarterial (VA) ECMO. We examined consecutive platelet counts while on ECMO. Univariate logistic regression was used to determine if mean platelet count, platelet count range, or severe thrombocytopenia were predictors of overall survival, hemorrhage and thrombosis. A multivariate logistic regression model was used to identify factors that contribute to the development of the aforementioned patient outcomes. Results: In our cohort, 33 patients were included with a mean age of 55 years and duration of ECMO of 5.9 days. All patients received heparin, 33.3% received antiplatelet therapy and 45.5% developed severe thrombocytopenia. In univariate, analysis the development of severe thrombocytopenia increased the odds of major bleeding by 450% (OR 5.500, 95% CI 1.219 - 24.813, P -value 0.027), and the odds of surviving hospitalization decreased 84.1% (OR 0.159, 95% CI 0.033 - 0.773, P -value 0.023). Multivariate logistic regression controlling for additional clinical variables found no significant association between the development of severe thrombocytopenia and rates of thrombosis, hemorrhage, or overall survival. Platelet count decreased over time while on ECMO. Conclusions: Nearly half of the patients requiring VA-ECMO developed severe thrombocytopenia, which was associated with an increased risk of hemorrhage and in-hospital mortality. Additional studies are required to clarify the clinical implications of severe thrombocytopenia in ECMO patients.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.


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