Thrombocytopenic purpura as a manifestation of pulmonary tuberculosis is very rare. We report a case of 25-year-old female who presented with thrombocytopenia-induced purpuric spots and an abnormal chest X-ray. There was no hepatosplenomegaly while the bone marrow examination revealed normal maturation of myeloid and erythroid series with increased megakaryocytes. Acid fast bacilli were seen in the sputum microscopy. A diagnosis of sputum smear positive pulmonary tuberculosis along with immune thrombocytopenia was made. High dose intravenous immunoglobulin therapy along with antituberculous drugs corrected the thrombocytopenia and also cured pulmonary tuberculosis. This case report illustrates the causal association between immune thrombocytopenia and tuberculosis.
Immune thrombocytopenia; Pulmonary tuberculosis; Purpura
Hypogammaglobulinemia may be part of several different immunological or malignant conditions, and its origin is not always obvious. Furthermore, although autoimmune cytopenias are known to be associated with common variable immunodeficiency (CVID) and even may precede signs of immunodeficiency, this is not always recognized. Despite novel insight into the molecular immunology of common variable immunodeficiency, several areas of uncertainty remain. In addition, the full spectrum of immunological effects of the B cell depleting anti-CD20 antibody Rituximab has not been fully explored. To our knowledge this is the first report of development of CVID in a patient with normal immunoglobulin prior to Rituximab treatment.
Here we describe the highly unusual clinical presentation of a 34-year old Caucasian male with treatment refractory immune thrombocytopenic purpura and persistent lymphadenopathy, who was splenectomized and received multiple courses of high-dose corticosteroid before treatment with Rituximab resulted in a sustained response. However, in the setting of severe pneumococcal meningitis, hypogammaglobulinemia was diagnosed. An extensive immunological investigation was performed in order to characterize his immune status, and to distinguish between a primary immunodeficiency and a side effect of Rituximab treatment. We provide an extensive presentation and discussion of the literature on the basic immunology of CVID, the mechanism of action of Rituximab, and the immunopathogenesis of hypogammaglobulinemia observed in this patient.
We suggest that CVID should be ruled out in any patient with immune cytopenias in order to avoid diagnostic delay. Likewise, we stress the importance of monitoring immunoglobulin levels before, during, and after Rituximab therapy to identify patients with hypogammaglobulinemia to ensure initiation of immunoglobulin replacement therapy in order to avoid life-threatening invasive bacterial infections. Recent reports indicate that Rituximab is not contra-indicated for the treatment of CVID-associated thrombocytopenia, however concomitant immunoglobulin substitution therapy is of fundamental importance to minimize the risk of infections. Therefore, lessons can be learned from this case report by clinicians caring for patients with immunodeficiencies, haematological diseases or other autoimmune disorders, particularly, when Rituximab treatment may be considered.
Hypogammaglobulinemia; Common variable immunodeficiency; Immune thrombocytopenic purpura; Rituximab
We report a case of concurrent thrombotic thrombocytopenic purpura (TTP) and immune thrombocytopenic purpura (ITP) in a 63-year-old woman who had been receiving treatment with bevacizumab for metastatic neuroendocrine tumour (NET). At diagnosis, she had severe anaemia and thrombocytopenia with elevated lactate dehydrogenase and many schistocytes on the peripheral blood smear. She was treated with frequent fresh frozen plasma infusions and plasmapheresis with poor response. Later, she was found to have platelet surface glycoprotein antibodies in the serum and received four cycles of rituximab, vincristine, cyclophosphamide (rituximab-CVP) and steroids in addition to plasma therapy. The haemoglobin and platelet counts improved. To our knowledge, this is the first reported case of concurrent TTP and ITP in a patient with metastatic NET diagnosed while receiving bevacizumab therapy, who was successfully treated with the combination of rituximab, vincristine, cyclophosphamide and steroids.
Thrombotic thrombocytopenic purpura and idiopathic thrombocytopenic purpura are two well recognized syndromes that are characterized by low platelet counts. In contrast, essential thrombocythemia is a myeloproliferative disease characterized by abnormally high platelet numbers.
The coexistence of thrombotic thrombocytopenic purpura and idiopathic thrombocytopenic purpura in a single patient has been reported in the literature on a few occasions. However, having essential thrombocythemia complicating the picture has never been reported before.
We present a case where thrombotic thrombocytopenic purpura, essential thrombocythemia, and idiopathic thrombocytopenic purpura were diagnosed in a 42-year-old African-American woman in the space of a few years; we are reporting this case with the aim of drawing attention to this undocumented occurrence, which remains under investigation.
As the three conditions have different natural histories and require different treatment modalities, it is important to recognize that these diseases may be seen sequentially. This case emphasizes the importance of reviewing peripheral blood smears for evaluation of thrombocytopenia and bone marrow aspirations for diagnosis of thrombocythemia in order to reach an accurate diagnosis and tailor therapy accordingly. Moreover, this case demonstrates the variability and complexity of platelet disorders. This occurrence of three different types of platelet disorders in one patient remains a pure observation on our part; regardless, this does raise the possibility of a common underlying, as yet undiscovered, pathophysiology that could explain the phenomenon.
Immune thrombocytopenic purpura (ITP) is a relatively common autoimmune disorder in which antibodies are produced to circulating platelets. Symptoms can be mild, but for most patients the risk of severe bleeding is unacceptable and treatment is required. Glucocorticoids followed by splenectomy had been the mainstays of therapy. High dose intravenous immunoglobulin and anti-RhD therapy are available for patients with severe illness, but produce only temporary benefit. Rituximab may provide more durable responses, danazol may be underutilized, and immunosuppressants and cytotoxic agents are less often required. Recently the pathophysiology of ITP has been more clearly elucidated, particularly the importance of decreased production of platelets in most patients and the very blunted rise that occurs in serum thrombopoietin (TPO). The isolation of TPO and better understanding of its role in thrombopoiesis has led to the development of new highly effective treatments. TPO analogs had some successes in treating highly refractory ITP patients but were taken out of development due to TPO-antibody induction. Two second-generation TPO-mimetics, romiplostim and the orally available eltrombopag, have recently been licensed in some territories for the treatment of ITP. Approval of eltrombopag was based on results from Phase II and III placebo-controlled clinical trials and a long-term extension study. About 80% of patients achieve significant increases in platelet count (11% of placebo patients), with reduced bleeding and reduced use of concomitant medications; responses are often durable with no tachyphylaxis. The side effects of eltrombopag are generally mild and not worse than placebo, although there are concerns about hepatic dysfunction, and the potentials for thromboses, marrow reticulin fibrosis, rebound thrombocytopenia and cataracts. This is an important new option for highly refractory patients, and its niche in earlier treatment (and for other thrombocytopenic disorders) is yet to be defined.
eltrombopag; immune thrombocytopenic purpura; autoimmune disorder; serum thrombopoietin
The clinical course and response to therapy of patients with immune thrombocytopenic purpura (ITP) are not completely determined by the level of IgG present on the platelet surface. It is possible that antibodies of other immunoglobulin classes also play a role in platelet destruction in some of these patients. Therefore, we studied 175 patients with ITP for the presence of IgM anti-platelet antibodies using radiolabeled polyclonal or monoclonal anti-IgM. We observed that 57% of patients with clinical ITP had increased levels of IgM on their platelets, compared with normal controls and patients with thrombocytopenia who did not have ITP (less than 10%), (P less than 0.01). We obtained similar results using either radiolabeled polyclonal or monoclonal anti-IgM, reagents whose integrity was first characterized using erythrocytes coated with defined amounts of IgM antibody. Among patients with increased platelet-IgM there was a significant correlation both with the presence of increased platelet-C3 as well as the amount of platelet-C3 (P less than 0.01, r = 0.53). We demonstrated the presence of warm-reacting IgM anti-platelet antibodies in the plasma of two of these patients who were further studied. The isolated IgM fraction from these two plasmas was able to activate complement and place 3H-C3 on normal platelets. These studies demonstrate the presence of warm-reacting IgM anti-platelet antibodies in some patients with ITP. They suggest that the binding of complement to platelets by IgM antibodies may initiate platelet clearance as well as enhance the effect of IgG antibodies in ITP.
Secondary immune thrombocytopenic purpura (ITP) associated with extranodal B-cell non-Hodgkin’s lymphoma (NHL) is extremely rare. The optimal management is not established. We report a first case of ITP in association with extranodal B-cell NHL originating in the lower petroclival region, successfully managed by local tumor control using conventional radiotherapy.
A 75-year-old man presented with a two-month history of hearing loss, hoarseness, and dysphagia. Neuroimaging revealed a large enhanced lesion in the left lower petroclival bone near the jugular foramen. Isolated unilateral parotid lymphadenopathy was also noted. Preoperative laboratory findings were normal, except for elevation of serum soluble interleukin-2 receptor level. A suboccipital craniotomy was performed and a biopsy sample was taken. Histological and immunohistochemical examination confirmed small B-cell lymphoma with plasmacytic differentiation. After initiation of radiotherapy, thrombocytopenia (24,000/µl) rapidly developed. Serological and bone marrow examination confirmed ITP. Prednisone was given at 1 mg/kg/day and radiation therapy was continued. After more than 32Gy, platelet count rapidly normalized. Radiotherapy to the tumor site achieved local tumor control and ITP was resolved. No evidence of recurrence and normal platelet count were confirmed at the two-year follow-up examination.
Local control of the tumor was considered important in the resolution of secondary ITP in association with extranodal NHL of the skull base region.
B-cell lymphoma; immune thrombocytopenic purpura; radiotherapy; skull base
Background: Idiopathic thrombocytopenic purpura (ITP) is a disease that commonly affects women of reproductive age and is associated with maternal and fetal complications.
Objective: The aim of the present study was to report the perinatal outcome in pregnant women with ITP.
Materials and Methods: Twenty one pregnant women with ITP admitted in a teaching hospital in Tehran, from October 2008 to February 2010, were enrolled in this prospective historical cohort study; course and perinatal outcome of pregnancies were studied.
Results: Seven (33.3%) cases had been diagnosed before pregnancy, while the other fourteen (66.7%) were diagnosed during pregnancy. During hospitalization, thirteen (62%) patients required treatment, eight (61.5%) of them with steroids, two (15.3%) received intravenous immunoglobulin (IVIG), and three (23%) were treated with steroids and IVIG. Three babies were delivered vaginally (14.3%), seventeen (81%) through cesarean section and one patient aborted her fetus. Nine mothers (42.9%) had platelet counts <50000/ml at the time of delivery; but postpartum hemorrhage occurred in 4 (19%) women and one women received platelet transfusion during cesarean section. Six (28.6%) women developed gestational diabetes. Pregnancy was complicated by preeclampsia in one woman and by abruptio placenta in another. One pregnancy terminated in intrauterine fetal death. Seventeen infants (89.5%) had normal platelet counts, and two (10.5%) had moderate thrombocytopenia. No infant showed signs of hemorrhage, but 2 neonates (10.5%) were diagnosed with intrauterine growth restriction.
Conclusion: Rate of gestational diabetes in pregnant women with ITP is higher than the general population. Rate of gestinational diabetes is 3-5% and postpartum hemorrhage is 5-7% in general. Postpartum hemorrhage is common in these women. Severe thrombocytopenia and bleeding in the newborns are uncommon.
Pregnancy outcomes; Idiopathic thrombocytopenic purpura; Neonatal outcome
A variety of clinical manifestations are associated directly or indirectly with tuberculosis. Among them, haematological abnormalities can be found in both the pulmonary and extrapulmonary forms of the disease. We report a case of immune thrombocytopenic purpura (ITP) associated with intestinal tuberculosis in a liver transplant recipient. The initial management of thrombocytopenia, with steroids and intravenous immunoglobulin, was not successful, and the lack of tuberculosis symptoms hampered a proper diagnostic evaluation. After the diagnosis of intestinal tuberculosis and the initiation of specific treatment, a progressive increase in the platelet count was observed. The mechanism of ITP associated with tuberculosis has not yet been well elucidated, but this condition should be considered in cases of ITP that are unresponsive to steroids and intravenous immunoglobulin, especially in immunocompromised patients and those from endemic areas.
Immune thrombocytopenic purpura; Tuberculosis; Liver transplant; Thrombocytopenia; Intestinal tuberculosis
Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a low platelet count and normal bone marrow. Patients with ITP undergoing surgery are thought to have increased risk for postoperative complications because of their thrombocytopenia.
PRESENTATION OF CASE
we report the case of a 66-year-old woman with ITP who required an emergency operation for acute appendicitis associated with disseminated intravascular coagulation. Preoperative therapy consisted of platelet transfusions only, and intraoperative hemostasis was achieved. Postoperatively, high-dose intravenous immunoglobulin (IVIg) therapy led to an increased, stable, and adequate platelet count and good hemostasis.
The outcome of this case suggests that IVIg therapy is not always required for preoperative management of patients with.
IVIg therapy may be useful for postoperative management after emergency surgery.
ITP, idiopathic thrombocytopenic purpura; IVIg, intravenous immunoglobulin; WBC, white blood cell; CT, computed tomography; CRP, c-reactive protein; PT/INR, prothrombin time/international normalized ration; FDP, fibrin degradation products; DIC, disseminated intravascular coagulation; Disseminated intravascular coagulation; Platelet transfusion; Operation
Tuberculosis has a variety of hematological manifestations. Immune thrombocytopenic purpura is an uncommon manifestation of tuberculosis. We present a case of disseminated tuberculosis with isolated thrombocytopenia. While TB granulomas in the bone marrow can themselves cause hematological abnormalities, persistent thrombocytopenia refractory to anti-TB therapy may be ITP associated with TB.
Disseminated tuberculosis; immune thrombocytopenic purpura; intravenous immunoglobulin
Animal bites are typically harmless, but in rare cases infections introduced by such bites can be fatal. Capnocytophaga canimorsus, found in the normal oral flora of dogs, has the potential to cause conditions ranging from minor cellulitis to fatal sepsis. The tendency of C. canimorsus infections to present with varied symptoms, the organism’s fastidious nature, and difficulty of culturing make this a challenging diagnosis. Rarely, bacterial cytotoxins such as those produced by C. canimorsus may act as causative agents of TTP, further complicating the diagnosis. Early recognition is crucial for survival, and the variability of presentation must be appreciated. We present the first known case of C. canimorsus infection resulting in TTP that initially presented as splenic infarction.
72-year-old Caucasian male presented with a four-day history of abdominal pain, nausea, vomiting, diarrhea, and intermittent confusion. On presentation, vital signs were stable and the patient was afebrile. Physical examination was unremarkable apart from petechiae on the inner left thigh, and extreme diffuse abdominal pain to palpation and percussion along with positive rebound tenderness. Initial investigations revealed leukocytosis with left shift and thrombocytopenia, but normal liver enzymes, cardiac enzymes, lipase, INR and PTT. Abdominal CT demonstrated a non-enhancing spleen and hemoperitoneum, suggesting complete splenic infarction. Although the patient remained afebrile, he continued deteriorating over the next two days with worsening thrombocytopenia. After becoming febrile, he developed microangiopathic hemolytic anemia and hemodynamic instability, and soon after was intubated due to hypoxic respiratory failure and decreased consciousness. Plasma exchange was initiated but subsequently stopped when positive blood cultures grew a gram-negative organism. The patient progressively improved following therapy with piperacillin-tazobactam, which was switched to imipenem, then meropenem when Capnocytophaga was identified.
There is a common misconception amongst practitioners that the presence of systemic infection excludes the possibility of TTP and vice versa. This case emphasizes that TTP may occur secondary to a systemic infection, thereby allowing the two processes to coexist. It is important to maintain a wide differential when considering the diagnosis of either TTP or C. canimorsus infection since delays in treatment may have fatal consequences.
Capnocytophaga canimorsus; Thrombotic thrombocytopenic purpura; Splenic infarction; Dog bite
Thrombotic thrombocytopenic purpura (TTP) is an uncommon life-threatening disease characterized by microangiopathic hemolytic anemia and thrombocytopenia, commonly associated with infections, malignancy, drugs, and autoimmune diseases. We report a case of 19-year-old previously healthy female that presents with anemia and thrombocytopenia diagnosed with thrombotic thrombocytopenic purpura that was treated successfully with plasmapheresis and corticosteroids. Laboratory findings also revealed antinuclear antibodies and antibodies to double-stranded DNA. Two weeks after presentation developed inflammatory arthritis, fulfilling diagnostic criteria for systemic lupus erythematosus (SLE). Prompt diagnosis and treatment with plasma exchange and corticosteroids should be instituted as soon as the diagnosis of TTP is suspected, even if other diagnoses, including lupus, are possible. When present, the coexistence of these two etiologies can have a higher mortality than either disease alone. An underlying diagnosis of SLE should be considered in all patients presenting TTP and the study of this association may provide a better understanding of their immune-mediated pathophysiology.
Thrombopoietin mimetic agents are a novel therapeutic option for patients with chronic immune thrombocytopenic purpura (ITP). We report on the use of romiplostim, a thrombopoietin mimetic, throughout pregnancy.
A 28 year old primigravida with chronic ITP initiated a planned pregnancy on romiplostim. The second and third trimesters were marked by a cyclic pattern of thrombocytopenia requiring supplemental corticosteroids or intravenous immunoglobulin and resultant thrombocytosis. Increased romiplostim doses and daily corticosteroids stabilized the platelet count prior to induction of labor. The delivery was uneventful, though the newborn manifested anemia and intraventricular hemorrhage.
The decreased efficacy of romiplostim monotherapy is attributed to increased target-mediated drug disposition and the physiologic changes of pregnancy. Safety concerns still exist for the developmental effects of romiplostim on the fetus.
Although various hematologic abnormalities are seen in tuberculosis, immune thrombocytopenic purpura is a rare event.
We report a case of a 29 year-old male who was presented with immune thrombocytopenia-induced hemoptysis, macroscopic hematuria and generalized petechiae. The patient was found to have clinical, microbiological and radiological evidence of active pulmonary tuberculosis. The immune thrombocytopenic purpura was successfully treated with anti-tuberculous drugs combined with corticosteroids and high dose immune globulin therapy.
Immune thrombocytopenic purpura can be one of the hematological manifestations of tuberculosis which has a global prevalence with increasing incidence secondary to HIV infection.
Tuberculosis; immune thrombocytopenic purpura; immune thrombocytopenia
Severe bleeding in acute immune thrombocytopenic purpura (ITP) is rare but can cause significant complications to the patient. Here we report the case of a pediatric patient with acute ITP and hematuria refractory to anti-D immune globulin, high dose intravenous immunoglobulin G, and high dose steroids. Her hematuria was successfully treated with recombinant factor VIIa (rFVIIa). While further investigation on the use of rFVIIa in ITP is warranted, this case report contributes to the pediatric literature for its use during the course of an initial presentation of ITP with hemorrhagic complications.
immune thrombocytopenic purpura; pediatrics; recombinant factor VIIa; FX, factor X; HPF, high-power field; ITP, immune thrombocytopenic purpura; IVIG, intravenous immunoglobulin G; rFVIIa, recombinant factor VIIa
Over 100 extraintestinal manifestations are reported in ulcerative colitis (UC). A commonly reported hematological manifestation is autoimmune hemolytic anemia. On rare occasions, immune thrombocytopenic purpura (ITP) has been reported with UC. The presence of thrombocytopenia can complicate the clinical scenario as the number of bloody bowel movements is an important indicator of disease activity in UC. A proposed theory for this association is antigenic mimicry between a platelet surface antigen and bacterial glycoprotein. We are reporting a case of UC and associated ITP managed successfully with anti-TNF therapy. We also performed a systemic review of case reports and a case series reporting this association.
immune thrombocytopenic purpura; ulcerative colitis; anti-tumor necrosis factor antibodies; intravenous immunoglobulins; extraintestinal manifestation
Immune thrombocytopenic purpura (ITP) is an autoimmune disease that can cause bleeding disorders in patients, and presents in acute and chronic forms. The acute form is frequently seen in children, but the chronic form mainly inflicts adults. There are differences and similarities in clinical and laboratory findings of the disease between children and adults. We study these differences and similarities in these two groups of patients with ITP.
In this study, we retrospectively evaluated the clinical and laboratory data of 323 ITP cases within three years. None of our patients had a history of thrombocytopenia. Patients were classified into two groups of children (3 months to 16 years of age) and adults (≥ 16 years). Data analysis was conducted using SPSS software, and the analysis results were compared between the two age groups.
Overall, the disease prevalence was higher in women than men, but the prevalence of childhood ITP was higher in males than females. The prevalence of initial symptoms including petechiae, purpura and ecchymosis was 60.5% and 61%, respectively in all patients, but severe bleeding rarely occurred in patients (28.8%). 30.5% of patients had a history of infection before developing ITP, and the children had a higher frequency of infection (80.8%). Before treatment, the mean platelet count in adults and children was 33000/μL and 35000/μL, respectively.
Comparison of data in children and adults with ITP indicated similarities and differences in clinical and laboratory findings between the two groups with differences in prevalence, bleeding symptoms, initial platelet count and infection history.
Immune thrombocytopenic purpura; Autoimmune disease; Bleeding
Introduction. Sunitinib malate is an oral multitargeting tyrosine kinase inhibitor approved for the first line treatment of metastatic renal cell carcinoma. Sunitinib administration is associated with several adverse events including fatigue, diarrhea, skin toxicity, hypothyroidism, and cytopenia. Herein, we present a case of thrombotic thrombocytopenic purpura and clinical hypothyroidism presenting within 4 weeks of starting sunitinib therapy. Case Presentation. A 72-year-old woman with metastatic renal cell carcinoma presented with generalized fatigue 28 days after starting sunitinib 50 mg daily. She was found to have severe hypothyroidism, in addition to significant thrombocytopenia and anemia. The latter were explained by a clinical and laboratory diagnosis of thrombotic thrombocytopenic purpura. Sunitinib was stopped and she recovered completely after plasmapheresis. Conclusion. To our knowledge, this is the fourth case report of thrombotic thrombocytopenic purpura secondary to sunitinib. Oncologists should be aware of this rare but potentially fatal adverse event. We highly suggest to routinely test for platelet count and thyroid stimulating hormone level as early as two weeks after initiating sunitinib.
Two adult cases of thrombohaemolytic thrombocytopenic purpura are described. Both showed striking morphological changes in the red cells with increased saline osmotic fragility, in addition to thrombocytopenia and generalized hyaline thrombi affecting small blood vessels. These changes support the hypothesis that this is a triple auto-immune disorder affecting red cells, platelets, and small blood vessels.
Three cases of immune thrombocytopenic purpura after the first
dose of recombinant hepatitis B vaccine occurred in infants under 6 months of age. Other possible causes of this condition were excluded.
Antiplatelet antibodies were present. A defect in platelet production
was excluded in two children. Corticosteroid treatment was effective.
Subsequent administration of other vaccines (against polio, diphtheria,
and tetanus) did not cause relapse of thrombocytopenia.
Six patients had serious complications as consequences of treatment of idiopathic thrombocytopenic purpura. Five had splenectomy-related complications, one of them developed fatal intra-abdominal bleeding. Three patients acquired operation-related serious infection, two of them died. Serious neutropenia after vinblastine-loaded platelets occurred in one patient leading to pseudomonas septicaemia and panophthalmitis with permanent vision loss of left eye. Recurrence thrombocytopenia occurred in every case during serious complications. Early detection by awareness of the possibility of serious complications can reduce morbidity and mortality occurring after therapy of idiopathic thrombocytopenic purpura.
A case study involving a 55-year-old Caucasian male with end-stage glomerulosclerosis is presented here. Kidney biopsies showed no deposits on imunofluorescent microscopy. Relapsing massive haemoptysis and suspected bronchovascular malformation required lung lobectomy which revealed malformative and tortuous small blood vessels, with no vasculitis. Blood antinuclear antibodies, antineutrophil cytoplasmic antibodies and antiglomerular basement membrane antibodies were undetectable. Seric immunoglobulins and complement levels were normal. Three months later, arthralgia and joint oedema first appeared. Skin biopsy revealed vasculitis immune-reactive to immunoglobulin A. Systemic corticotherapy was then started. Two weeks later, the patient presented with abdominal pain melena and rectal bleeding (haematoquesia). Endoscopic study showed diffuse gastrointestinal haemorrhage. Angiographic study revealed diffuse lesions compatible with vasculitis and haemorrhage from multiple spots. Cyclophosphamide and then intravenous immunoglobulin were associated to treatment without response. Increasing blood loss occurred, with massive gastrointestinal haemorrhage and haemorrhagic ascitis. Death occurred due to uncontrolled diffuse bleeding. Necropsy findings showed generalised small vessels vasculitis compatible with Henoch–Schönlein purpura.
Henoch-Schönlein purpura (HSP) is a systemic vasculitis involving small vessels with deposition of immunoglobulin A (IgA) complexes, usually affecting children. Compared with children, HSP in adults is more severe and frequently associated with cancer. We report the case of a 49-year-old woman with medical history of kidney transplantation for segmental glomerular hyalinosis. Eight years after the transplantation, while taking combined immunosuppressive therapy with tacrolimus and azathioprine indicated for the prevention against transplant rejection, she developed a Henoch-Schönlein purpura. Vasculitis involves skin and sciatic peroneal nerve and she received systemic corticosteroid treatment. Because of four relapses and corticosteroid dependence, the patient was treated with rituximab (two intravenous infusions of 1000 mg given two weeks apart). Successful outcome was observed along two years of follow-up. This new case of successful use of rituximab in HSP promotes more investigations of this treatment in clinical trials.
We report two cases of immune thrombocytopenic purpura (ITP) associated with acute coronary artery syndrome highlighting the interventions done in every case along with the medications used during intervention and as outpatient. The first case is that of a woman with ITP exacerbation while on dual antiplatelet therapy and the second case is that of a male presenting with non-ST elevation myocardial infarction (NSTEMI) while in a thrombocytopenic crisis. In both cases antiplatelet therapy was held and thrombopoietic therapy was initiated before resuming full anticoagulation and coronary intervention. Given the paucity of data on ITP and antiplatelets treatment in the setting of acute coronary syndrome, no strict recommendations can be proposed, but antiplatelets appear to be safe acutely and in the long term in this category of patients as long as few measures are undertaken to minimize the risks of bleeding and thrombosis.