scholarly journals A rare case of Acute Motor and Sensory Axonal Neuropathy (AMSAN) and Immune Thrombocytopenic Purpura (ITP) related to Hemophilus influenzae

2021 ◽  
Vol 2 (5) ◽  
Author(s):  
Vivek Satyasi ◽  
Aiesha Ahmed ◽  
Amtul Farheen
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Rare Case ◽  
Molecular Mimicry ◽  
Case Reports ◽  
Axonal Neuropathy ◽  
Autoimmune Disorder ◽  
Severe Thrombocytopenia ◽  
Thrombocytopenic Purpura ◽  
Upper Respiratory Infection ◽  
Hemophilus Influenzae

We describe a rare case presenting with both signs of acute motor and sensory axonal neuropathy (AMSAN) and immune thrombocytopenic purpura (ITP) possibly triggered by Hemophilus influenzae. Guillain-Barre is an autoimmune disorder purported to be due to molecular mimicry, often with a preceding infection, leading to myelin sheath or even axonal damage, AMSAN, in the peripheral nervous system (PNS). Rarely, there have been case reports of concurrent acute autoimmune disorders leading to a more complex presentation and additional comorbidities. A 42-year-old man presented with 2 days of progressive lower and upper extremity paresthesia’s, ataxia preceded by an upper respiratory infection. Examination showed areflexia and purpura, recent oral mucosal hemorrhage. Lab results showed severe thrombocytopenia suspicious for ITP. Over the ensuing weeks while inpatient, his condition quickly deteriorated to requiring an intubation for respiratory failure and not immediately responsive to IVIG. Recovery, both for AMSAN confirmed by EMG and ITP, was eventually achieved with time and five treatments of plasmapheresis and eventually was discharged to a rehabilitation facility. A thorough infectious workup revealed a possible trigger being Haemophilus influenzae. There have been rare occasions of concurrent GBS and ITP, but even more rare is the presence of both AMSAN and ITP which requires quick recognition and evaluation. This case highlights the need for a thorough initial history taking and a general physical exam, in addition to unique management decisions and strategies in patients with suspected GBS as there may be signs of other associated disorders that require immediate attention.

scholarly journals Immune Thrombocytopenic Purpura (ITP) as an Uncommon Extraintestinal Complication of Crohn’s Disease: Case Vignette and Systematic Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Raisa Epistola ◽  
Tiffanie Do ◽  
Ritika Vankina ◽  
Daniel Wu ◽  
James Yeh ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Immune Thrombocytopenic Purpura ◽  
Case Reports ◽  
Case Vignette ◽  
Mucosal Permeability ◽  
Extraintestinal Manifestation ◽  
Thrombocytopenic Purpura ◽  
Disease Case ◽  
Inflammatory Bowel

While the association of immune thrombocytopenic purpura (ITP) and inflammatory bowel disease (IBD) has been described in a few case reports, management of ITP as an extraintestinal manifestation of Crohn’s disease (CD) is less studied. There are approximately a dozen cases describing the management of patients dually diagnosed with CD/ITP. Previous reports postulated that the mechanism of ITP in CD was through the presence of circulating immune complexes in the serum and antigenic mimicry due to increased mucosal permeability in active colitis, versus increased mucosal production of TH1-type proinflammatory cytokines during CD flares, which may account for remission of ITP with surgery for CD. We present a case of a 27-year-old man who presented with medically refractory CD and ITP who responded to surgical management with colectomy and splenectomy, along with a systematic review of the literature. These cases suggest that colectomy should be considered in the treatment of medically refractory ITP among patients with concomitant CD.

scholarly journals Metastatic Breast Cancer with Extensive Osseous Metastasis Presenting with Symptomatic Immune Thrombocytopenic Purpura and Anemia: A Case Report and Review of the Literature

2015 ◽  
Vol 8 (2) ◽  
pp. 256-263 ◽  
Author(s):  
Jiaxin Niu ◽  
Teresa Goldin ◽  
Maurie Markman ◽  
Madappa N. Kundranda
Keyword(s):  
Breast Cancer ◽  
Platelet Count ◽  
Metastatic Breast Cancer ◽  
Immune Thrombocytopenic Purpura ◽  
English Literature ◽  
Metastatic Breast ◽  
Response To Therapy ◽  
Severe Thrombocytopenia ◽  
Thrombocytopenic Purpura ◽  
Immune Mediated

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.

scholarly journals Campylobacter Species and Guillain-Barré Syndrome

1998 ◽  
Vol 11 (3) ◽  
pp. 555-567 ◽  
Author(s):  
Irving Nachamkin ◽  
Ban Mishu Allos ◽  
Tony Ho
Keyword(s):  
Molecular Mimicry ◽  
Current Knowledge ◽  
Axonal Neuropathy ◽  
Autoimmune Disorder ◽  
Acute Motor Axonal Neuropathy ◽  
Acute Inflammatory Demyelinating Polyneuropathy ◽  
Campylobacter Species ◽  
Antecedent Infection ◽  
Different Strains ◽  
Campylobacter Infection

SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.

scholarly journals Clinical and Morphological Profile of Immune Thrombocytopenic Purpura in Children - A Five Year Study in a Paediatric Tertiary Health Care Centre of South India

2020 ◽  
Vol 7 (46) ◽  
pp. 2724-2729
Author(s):  
Ashida M. Krishnan ◽  
Deepthi Raj M.L ◽  
Priya V.S ◽  
Arya R.S
Keyword(s):  
Health Care ◽  
Bone Marrow ◽  
Immune Thrombocytopenic Purpura ◽  
Peripheral Blood ◽  
South India ◽  
P Value ◽  
Severe Thrombocytopenia ◽  
Care Centre ◽  
Health Care Centre ◽  
Thrombocytopenic Purpura

BACKGROUND Immune Thrombocytopenic Purpura (ITP) is one of the most commonly encountered disease in paediatric practice. Thorough clinical and morphological study of peripheral blood and bone marrow is required for confirming ITP. Clinicomorphological aspects of paediatric ITP is a less studied topic especially in developing countries like India. The objective was to study the clinical and morphological profile of paediatric cases of ITP. METHODS This is a 5-year record based retrospective study conducted in a paediatric tertiary health care centre in Kerala, South India. Data of all paediatric cases diagnosed as ITP including clinical presentation, clinical findings, blood counts, peripheral blood morphology, bone marrow morphology, and treatment response was collected and entered in SPSS software version 16.0 and analysed. For assessing correlation, chi-square test was used. RESULTS The age of children ranged from 3 months to 15 years. H/o viral fever was noted in 53 % cases. Cases which had moderate and severe thrombocytopenia were 74 % and 21 % respectively. Isolated thrombocytopenia was the most common peripheral blood picture observed with few cases showing coexisting eosinophilia and anaemia. All cases showed megakaryocyte proliferation in marrow with 9 % cases showing coexisting iron deficiency anaemia. Majority of cases showed rapid response to steroid / IVIG therapy and the response had no correlation with grade of thrombocytopenia (p value < 0.05). CONCLUSIONS Paediatric cases of ITP usually present following viral infections or vaccination, with worrisome bleeding episodes, petechiae, ecchymosis or purpura. KEYWORDS ITP, Paediatrics, Platelet Count, Thrombocytopenia, Vaccination

scholarly journals Thrombotic Thrombocytopenic Purpura Following Honeybee Envenomation: A Case Report

2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Zahra Khalighi ◽  
Golnaz Azami ◽  
Elham Shafiei ◽  
Ali Sahebi ◽  
Aliashraf Mozafari
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
Case Reports ◽  
Major Complication ◽  
The Body ◽  
Severe Thrombocytopenia ◽  
Thrombocytopenic Purpura ◽  
Toxic Reaction ◽  
Bee Sting ◽  
Life Threatening ◽  
Underlying Diseases

Background: Thrombotic Thrombocytopenic Purpura (TTP) is a rare and life-threatening disorder characterized by severe thrombocytopenia, microangiopathic hemolytic anemia, fever, renal dysfunction, and neurological deficient. TTP leads to the formation of blood clots in small blood vessels throughout the body. TTP is associated with many risk factors such as pregnancy, HIV, cancer, lupus, and infections. Recently there have been few published case reports of bee sting associated TTP.Methods: A 67-year-old man from a rural area of the Southwest Province of Iran, Ilam, was referred to the academic general hospital because of fever, chills, sweating, vomiting and dizziness following the honeybee sting on his body. Results: this study showed that,multiple co-morbidities including CVD and diabetes, along with coagulation abnormalities after honeybee stings, seriously exacerbated patient hemodynamic status.Conclusion: TTP, as a major complication due to the toxic reaction of a large number of bee stings with underlying diseases in patients, should be given more attention.

scholarly journals Immune Thrombocytopenic Purpura With Unusual Presentations – Reports of Two Cases

2020 ◽  
Vol 38 (4) ◽  
pp. 218-222
Author(s):  
Tasmina Chowdhury ◽  
Abdul Basit Ibne Momen ◽  
Hironmoy Barman ◽  
Mohammad Tariqul Ahsan Khan ◽  
Kohinoor Begum ◽  
...  
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Ovarian Hyperstimulation Syndrome ◽  
Intracranial Haemorrhage ◽  
Hemorrhagic Stroke ◽  
Clinical Course ◽  
Case Reports ◽  
Alveolar Haemorrhage ◽  
Thrombocytopenic Purpura ◽  
Immune Mediated ◽  
Uncommon Disease

Immune thrombocytopenic purpura (ITP) is an immune mediated bleeding disorder, usually has a relatively benign clinical course. Deep seated bleeding like intracranial haemorrhage or haemoperitonium or massive haemorrhage requiring transfusion or other intervention are rare in ITP, unless platelet count are extremely low or other complicating conditions coexist. Here are two case reports of ITP presenting in uncommon and devastating manners. The 1st  one is of a 21- yearold married nulliparaous lady with ITP complicating her undiagnosed ovarian hyperstimulation syndrome leading to haemoperitonium (ruptured ovarian cyst), post operative alveolar haemorrhage resulting in ARDS and later on DVT of right leg on her 9th  POD. She was managed by multi discipline team. A new consequence of her disease one after another was striking and made her management more challenging. Ultimately the lady recovered and was discharged with advice which was not less than a miracle. The 2nd  case is of a 50- year- old elderly lady who had a hemorrhagic stroke as a presenting feature of ITP. Though ITP is not an uncommon disease but in these cases its presentation, consequences and severity was unusual and making its management very much challenging. J Bangladesh Coll Phys Surg 2020; 38(4): 218-222  

Alteration of Circulating Regulatory T Cells in Japanese Adult Patients with Immune Thrombocytopenic Purpura after Eradication of Helicobacter Pylori.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3410-3410
Author(s):  
Koji Miyazaki ◽  
Mikio Danbara ◽  
Manabu Ohsaka ◽  
Yuhko Suzuki ◽  
Ryouichi Horie ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Regulatory T Cells ◽  
Immune Thrombocytopenic Purpura ◽  
Mononuclear Cells ◽  
Eradication Therapy ◽  
Autoimmune Disorder ◽  
Japanese Adult ◽  
Thrombocytopenic Purpura ◽  
Platelet Counts

Abstract Immune thrombocytopenic purpura (ITP) is an autoimmune disorder, and eradication of Helicobacter pylori (HP) has been demonstrated to be an effective and tolerable firstline treatment for the patients infected with HP in Japan. However the mechanism has still remained to be uncovered. Recently CD4+CD25high+Foxp3+ regulatory T cells (Tregs), which regulate autoreactive T cells, have been identified, and suggested to play an important role in pathogenesis of ITP, as well as other autoimmune disorders. It has been shown that Tregs are reduced and suppressed in the ITP patients. And a recent report has demonstrated that the defective Tregs are restored upon the rituximab treatment. However, the effects of HP eradication therapy on Tregs have not been determined. The aim of this study is to investigate the circulating Tregs in ITP patients treated with HP eradication. And we also attempted to elucidate the mechanisms of the treatment. The peripheral blood CD4+CD25high+ Tregs were measured by flow cytometry before and after the treatment in 21 Japanese adults with HP-positive chronic ITP. We also confirmed the expression of Foxp3 in this cellular population with the permeabilized mononuclear cells. Among 21 patients, the platelet counts increased in 13 cases (responders), but not in 9 cases (non-responders). In responders the numbers of Tregs have been restored, but not in non-responders after the treatment. It is interesting here that the amounts of Tregs were still transiently elevated in an early phase (2–3weeks) after the treatment in some non-responders without recovery of the platelet counts. Furthermore, in three cases, who failed in pylorus elimination, Tregs were also transiently increased in number associated with brief recovery of the platelet counts, and reduced to the initial level in about two months. After the successful re-eradication, the numbers of Tregs and platelets have been restored. From these results it is shown that HP eradication can modulate Tregs to increase the platelet counts for ITP patients. We also demonstrate that the increase of Tregs by HP eradication was more rapid than that by rituximab, which required about three months. Further, it might be suggested that there are two phases of the therapy with HP eradication for ITP. In an initial stage, the therapy itself could have an effect modulating the immune systems to potentiate Tregs. Some drugs, such as macrolide antibiotics including clarithromycin have been demonstrated to be a potent immunomodulator. However, this phase is not sufficient for the successful treatment, as shown in the cases of failure in HP elimination. In a retentive stage, extermination of HP is also necessary for sustainment of restored Tregs.

Mycoplasma Pneumonia Infection - a Possible unrecognized Cause for Immune Thrombocytopenic Purpura

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4555-4555
Author(s):  
Shraga Aviner ◽  
Daniel London ◽  
Shulamith Horowitz ◽  
Menachem Schlesinger ◽  
Gilles Lugassy
Keyword(s):  
Platelet Count ◽  
Clinical Diagnosis ◽  
Intracranial Hemorrhage ◽  
Immune Thrombocytopenic Purpura ◽  
Complete Blood Count ◽  
Case Reports ◽  
English Literature ◽  
Severe Bleeding ◽  
Thrombocytopenic Purpura ◽  
Mycoplasma Pneumonia

Abstract Mycoplasma pneumonia (M. pneumonia) is usually not considered among the several pathogens that induce immune thrombocytopenic purpura (ITP). We report a case of a child with a clinical diagnosis of severe ITP (as defined by the American Society of Hematology panel guidelines of 1994), that was associated with M. pneumonia pneumonia, and reviewed the few cases described in the English literature. A 7-year-old girl was admitted to the pediatric department with 1 day history of fever, purpura and petechiae on her legs, buttocks, arms, face, hard palate, oral mucous membranes and lips. Crepitations were heard over both lungs’ lower fields. Complete blood count revealed WBC of 22.3×103/ μL, Hemoglobin of 11.1 gr/dL, and platelet count of 2×103/μL. Red cells appeared normal on blood film with no features of microangiopathy. A chest X-ray demonstrated right middle lobe infiltrate. Presumptive diagnoses of ITP and RML pneumonia were made and treatment was initiated with one dose of IVIG 0.8 g/kg and daily IV Ceftriaxon at 50 mg/kg. Twelve hours after the IVIG administration, platelet count was 1.2×103/μL. Bone marrow examination revealed normal cellularity with young megakaryocytes, compatible with the diagnosis of ITP. Since there was no response to IVIG, Methylprednisolone 4 mg/ kg for 4 days was started. An extensive search of the literature for ITP or thrombocytopenia and pneumonia retrieved only 7 case reports. In all cases M. pneumonia was the only identified pathogen. Therefore, clarithromycin 15 mg/kg/d was added to the treatment regimen, prior to obtaining the serology results. Thereafter severe hemoptysis developed; the patient was admitted to the PICU and received 4 units of platelets and a second dose of IVIG. Hemoptysis resolved after another day, when the platelet count started to increase gradually, only to drop after the cessation of steroids. A second course of steroids at the same dose was begun and tapered off gradually over 21 days, while the platelet count steadily increased, exceeding 150×103/μL at 4 weeks from presentation. A positive Mycoplasma IgM titer at diagnosis and a 1:160 titer at 2 months confirmed the clinical diagnosis. The child is by now 20 months after the event with normal CBC. Several features of the 8 cases described (including our case) distinguish them from “classic” ITP: Thrombocytopenia occurred concomitantly with the infection as opposed to a few days to a few weeks interval between infection and ITP. Severe bleeding in 4 out of 8 patients including 2 with fatal intracranial hemorrhage in contrast to around 3% severe bleeding and around 1‰ fatal intracranial hemorrhage in “classic” ITP. Three of the authors who looked for specific anti-platelet antibodies were unable to demonstrate it, whereas such antibodies are found in many patients with ITP. Several mechanisms are suggested to explain these differences; though it remains unclear whether Mycoplasma associated thrombocytopenia represents a subset of ITP or constitutes a separate entity. We conclude that M. pneumonia should be looked for in any case of pneumonia and thrombocytopenia or ITP, and early specific anti-Mycoplasma therapy should be initiated to rapidly eliminate the causative agent. This may enhance recovery of the platelet count and decrease the rate of complications.

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