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| CASE REPORT |
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| Year : 2022 | Volume
: 17
| Issue : 3 | Page : 741-743 |
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Immune thrombocytopenic purpura in an elderly male
Mahesh Mahadeviah1, Nikhil Ramdas Shinde2, Mamatha Shivanagappa3, Madhumitha Mahesh4
1 Professor of Medicine, JSS Hospital and Medical College, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
2 Junior Resident in Medicine, JSS Hospital and Medical College, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
3 Associate Professor of Obstetrics and Gynecology, JSS Hospital and Medical College, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
4 MBBS Student, JSS Hospital and Medical College, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
| Date of Submission | 30-May-2020 |
| Date of Decision | 29-Nov-2020 |
| Date of Acceptance | 01-Dec-2020 |
| Date of Web Publication | 2-Nov-2022 |
Correspondence Address:
Dr. Nikhil Ramdas Shinde
Shinde Hospital, New Jalna Road, At Post Taluka Deulgaon Raja, Dist. Buldhana 443 204, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jdmimsu.jdmimsu_187_20
Idiopathic Thrombocytopenic Purpura (ITP) is an acquired disorder in which there is immune mediated destruction of platelets and also inhibition of platelet release from the megakaryocytes.[1] The features are by mucocutaneous bleeding and a low platelet count with an otherwise normal peripheral blood cells and smear. ITP is a heterogeneous disease with varying severity and clinical course. It is mainly a disorder of children. In adults the peak prevalence is between 20-50 years.[2] The clinical features in adults are different from those seen in children. ITP in persons above 60 years is being increasingly recognized in literature. ITP in elderly differs in its presentation, course and severity compared to its manifestations in younger adults. The response to treatment is different and the presence of co-morbid conditions such as diabetes, hypertension and ischemic heart disease needs to be kept in mind in the management algorithm.[3] A case of ITP in elderly is presented herewith with a brief review of literature.
Keywords: Idiopathic thrombocytopenic purpura, incidental thrombocytopenia, preoperative thrombocytopenia, thrombocytopenia, thrombocytopenia in elderly
How to cite this article:
Mahadeviah M, Shinde NR, Shivanagappa M, Mahesh M. Immune thrombocytopenic purpura in an elderly male. J Datta Meghe Inst Med Sci Univ 2022;17:741-3 |
| Introduction | |  |
Idiopathic thrombocytopenic purpura (ITP) is an acquired disorder in which there are immune-mediated destruction of platelets and also inhibition of platelet release from the megakaryocytes.[1] The features are by mucocutaneous bleeding and a low platelet count with an otherwise normal peripheral blood cells and smear. ITP is a heterogeneous disease with varying severity and clinical course. It is mainly a disorder of children. In adults, the peak prevalence is between 20 and 50 years.[2] The clinical features in adults are different from those seen in children. ITP in persons above 60 years is being increasingly recognized in the literature. ITP in the elderly differs in its presentation, course, and severity compared to its manifestations in younger adults. The response to treatment is different, and the presence of comorbid conditions such as diabetes, hypertension, and ischemic heart disease needs to be kept in mind in the management algorithm.[3] A case of ITP in the elderly is presented herewith with a brief review of the literature.
| Case Report | | |
A 78-year-old patient admitted under the urology department for benign prostatic hypertrophy and posted for transurethral resection of the prostate was referred to us for our opinion about low platelet levels. During routine preoperative investigations, the urologists had noted thrombocytopenia with a platelet count of 12,000/mcl.
The patient was diabetic on tablet metformin 500 mg once daily. There was no history of fever, myalgia suggestive of a viral infection. He was not on drugs such as aspirin, heparin, or nonsteroidal anti-inflammatory drugs. There was no history of hematemesis or melena.
On examination, there was no pallor, petechiae, or gum bleeding. The systemic examination was unremarkable. The platelet count was repeated, and it was 16,000/mcl. Other formed elements were within normal limits. Peripheral blood smear showed thrombocytopenia. Blood urea was 24 mg/dl, and serum creatinine was 0.7 mg/dl.
Antinuclear antibody was negative, LDH level was 150 U/l (normal 140–280 U/l), and HIV was negative.
Bone marrow examination revealed megakaryocytic hyperplasia [Figure 1]. | Figure 1: Bone marrow smear showing hyperplasia (H and E stain, ×40). Arrows indicating megakaryocytes
Click here to view |
The isolated thrombocytopenia without any leukopenia or anemia indicated increased platelet destruction as the possible cause of thrombocytopenia.
In view of the above, a diagnosis of ITP was made and he was advised 70 mg prednisolone/day. Repeat platelet count after 1 week was 167,000. There was no thrombocytopenia on repeat testing weekly over the next 3 weeks. He was advised to come for regular follow-up to our outpatient department.
| Discussion | | |
ITP is caused by autoantibodies to platelets. The antigenic target in most cases is the Gp II b/IIIa complex. The mechanism of origin of these antibodies is not known. These antibodies may be directed toward viral antigens and then cross-react with platelet antigens. These antibodies can also react with developing megakaryocytes in the marrow.[4]
The common drugs causing thrombocytopenia are heparin, sulfonamides, quinine, sulfonylureas, rifampicin, and hydrochlorothiazide.[5]
Diagnosis of ITP is by exclusion, and the same is applicable in the elderly also. The differential diagnoses are drug-induced thrombocytopenia and myelodysplasia. In our patient, there were no features of myelodysplasia such as Pelger-Huet anomaly, nucleated RBC, and immature granulocytes in the peripheral blood smear. Splenomegaly excludes the diagnosis of ITP.
Clinicians should have awareness of ITP in different age groups. Certain special features of importance of ITP in the elderly are to be remembered. Severe hemorrhagic manifestations are common. The drug response is variable. Splenectomy is beneficial.
Bizzoni et al.[6] retrospectively evaluated 178 ITP patients with a mean age of 72 years. They concluded that low-dose prednisone is an appropriate initial treatment for elderly persons. They stress that an adequate follow-up is advisable, given that isolated thrombocytopenia could, in some cases, be the first sign of another underlying pathology.
Andres et al.[7] reviewed 41 consecutive elderly ITP patients (≥65 years old) in two ITP centers in France. Analyzed were patient clinical characteristics, along with the therapies used and side effects and patient response rates. They concluded that age influences the hemorrhagic pattern of ITP expression as well as responses to and adverse effects of conventional ITP therapies.
Elderly patients with ITP with platelet count >50,000 without any bleeding manifestations need to be monitored for the same. Follow-up repeated counts are needed. If platelet count is <30,000, therapy is indicated. If platelet count is <50,000 and >30,000 with additional risk factors such as hypertension and peptic ulcer, potential for trauma in such patients requires treatment. Glucocorticoids act in this disease by preventing the sequestration of antibody-coated platelet by the spleen. Many elderly will be receiving antiplatelet drugs because of cerebrovascular and cardiovascular atherosclerotic diseases, and this has to be kept in mind while evaluating and treating thrombocytopenia of whatever cause.
The notable features in this case were age more than years, incidental detection, good response with steroid in dosage of 1 mg/kg, and lack of any adverse drug reactions of steroid.
| Conclusion | | |
Clinicians must be aware that ITP does occur in the elderly. The special characteristics, response, and complications related to treatment should be kept in mind in the management of the condition.
Acknowledgments
We thank Dr. Sapna Patel, MD (Pathology), Assistant Professor of Pathology Department of Pathology, JSS Hospital, for her help in bone marrow evaluation. We are grateful to Dr. Mahesh Rajashekariah, DM (Hematology), Consultant Hematologist, JSS Hospital, for his assistance.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Fogarty PF, Segal JB. The epidemiology of immune thrombocytopenic purpura. Curr Opin Hematol 2007;14:515-9.  |
| 2. | Sandler SG, Tutuncuoglu SO. Immune thrombocytopenic purpura - Current management practices. Expert Opin Pharmacother 2004;5:2515-27. |
| 3. | Neunert C, Lim W, Crowther M, Cohen A, Solberg L Jr, Crowther MA, et al. The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia. Blood 2011;117:4190-207. |
| 4. | Stasi R, Evangelista ML, Stipa E, Buccisano F, Venditti A, Amadori S. Idiopathic thrombocytopenic purpura: Current concepts in pathophysiology and management. Thromb Haemost 2008;99:4-13. |
| 5. | McMillan R. The pathogenesis of chronic immune thrombocytopenic purpura. Semin Hematol 2007;44:S3-S11. |
| 6. | Bizzoni L, Mazzucconi MG, Gentile M, Santoro C, Bernasconi S, Chiarotti F, et al. Idiopathic thrombocytopenic purpura (ITP) in the elderly: Clinical course in 178 patients. Eur J Haematol 2006;76:210-6. |
| 7. | Andres E, Zulfiqar AA, Serraj K, Zimmer J, Vogel T, Maloisel F. Idiopathic thrombocytopenic purpura in elderly patients: A two center retrospective study of 41 cases. J Blood Disord Transfus. 2015;6:2. |
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