Generally speaking a normal platelet count ranges from 150,000 and 450,000 per mm³. These limits, however, are determined by the 2.5th lower and upper percentile, and a deviation does not necessary imply any form of disease.

Signs and symptoms

Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count. Occasionally, there may be bruising, nosebleeds and/or bleeding gums.

It is vital that a full medical history is elicited, to ensure the low platelet count is not due to a secondary process. It is also important to ensure that the other blood cell types red blood cells, and white blood cells, are not also suppressed.

Diagnosis

Laboratory tests might include: full blood count, liver enzymes, renal function, vitamin B12 levels, folic acid levels, erythrocyte sedimentation rate.

If the cause for the low platelet count remains unclear, bone marrow biopsy is often undertaken, to differentiate whether the low platelet count is due to decreased production or peripheral destruction.

Causes

Decreased platelet counts can be due to a number of disease processes:

decreased production
- vitamin B12 or folic acid deficiency
- leukemia or myelodysplastic syndrome
peripheral destruction
- immune thrombocytopenic purpura (ITP)
- thrombotic thrombocytopenic purpura (TTP)
- hemolytic-uremic syndrome (HUS)
- disseminated intravascular coagulation (DIC)
- paroxysmal nocturnal hemoglobinuria
- antiphospholipid syndrome
- medication-induced:
  - Many of the commonly used drugs may cause thrombocytopenia or low platelet counts. Some drugs like anticancer drugs and valproic acid causes thrombocytopenia in a dose depended mechanism by causing myelosuppression. Some other groups of drugs cause thrombocytopenia by immunological mechanisms. Based up on the mechanism immunological drug induced can be caused by two types.
  - Example of the first mechanism is the quinidine group of drugs. This is caused by drug depended binding of Fab part of the pathological antibody with the platelets, causing the destruction of platelets.. Fc portion of the antibody molecule is not involved in the binding process.
  - Example of the second mechanism is heparin induced thrombocytopenia (HIT). In this type the Fab portion of the pathological antibody binds to platelet factor 4 (PF4).When complexed with heparin or other drugs, the Fc portion of the antibody molecule bind to platelet receptors causing platelet activation. Since Fc portion of the antibody is bound to the platelets, they are not available to the Fc receptors of the reticulo-endothelial cells. This may explain, why severe thrombocytopenia not commonly seen in patients with HIT.
  - A full list of known drugs causing thrombocytopenia is available at the linked website. Most of the elderly patients are on multiple medications and the intake of these drugs must always be considered in the differential diagnosis of thrombocytopenia.
  - heparin-induced thrombocytopenia (HIT or white clot syndrome): this is a rare but serious condition that may occur in a hospitalized population especially in the cardiac units where they are exposed to large quantities of heparin. HIT may occur with a delay of 4 to 14 days after exposure to heparin. As mentioned above the heparin-PF4 antibody complex will activate the platelets, and this will lead to clotting. A term known as paradoxical thrombosis (HITT, where the last T is for thrombosis) is often used to describe this condition.
  - abciximab-induced thrombocytopenia

In some tropical countries, dengue infection is a known rather common cause of thrombocytopenia associated with fever.

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Vinorelbine induced interstitial pneumonitis: a case report
From CHEST, 10/1/05 by Mayank Vats

INTRODUCTION: Vinorelbine (Navalbine), a newer Vinca alkaloid has been increasingly used in the chemotherapy of non-small-cell Bronchogenic carcinoma & metastatic breast carcinoma. Initially, it appeared to have a favorable side-effect profile with dose & duration limited myelo-suppression (Granulocytopenia, Thrombocytopenia) being the major toxicityl. With more frequent use of Vinorelbine, new side effects of this drug are being reported. We are reporting a case of Interstitial Pneumonitis developing after Vinorelbine therapy for Bronchoalveolar carcinoma.

CASE PRESENTATION: K.K. 46 year old farmer smoker presented to our OPD with complaints of dull diffuse chest pain on right side, cough with mucoid expectoration >200 ml/d & breathlessness. On physical examination breath sounds were diminished in intensity on right side, coarse crept was present in mid & lower chest. Chest X-Ray revealed diffuse heterogenous infiltrates with air-bronchogram in right lung. Patient was previously treated for bronchopneumonia with broad-spectrum antibiotics elsewhere but had no improvement. Considering the possibility of malignancy, Fibre-Optic Bronchoscopy revealed excessive mucoid secretions. Bronchial-brush and Bronchoscopic-lavage was negative for microbiology & cytology, so lung biopsy was done, it showed bronchoalveolar carcinoma. CT-scan chest revealed, focal area of apparent parenchymal consolidation with linear strands extending to the periphery. After complete evaluation & basic investigation {Complete Blood Count (CBC), Liver Function Test, Renal Function Test} we planned chemotherapy with Vinorelbine, hence Vinorelbine 50 mg (as the body surface area was 1.68m2) over 10 minutes was infused after proper hydration, patient tolerated the drug well & after observation for 1 day, he was discharged on request. After 3 days, patient returned with complaints of increasing dyspnoea, dry cough & severe distress. He was tachycardiac, accessory muscles of respiration was working, breath sounds were diminished and of bronchial nature on right side, Chest X-Ray revealed extensive consolidation on whole of right lung. His CBC was normal & sputum for Gram stain/culture was negative. However because of suspicion of community-acquired-pneumonia, broad-spectrum antibiotic & intravenous steroids were started, patient responded well with clearance of radiological-infiltrates. Next week, IInd cycle of Vinorelhine 50 mg over 10 minutes was given & on IInd day of IInd cycle patients again developed breathlessness & dry cough. CXR showed homogenous consolidation with air-bronchogram in right lung. This time considering the possibility of Vinorelbine induced pneumonitis, Trans-bronchial-lung-Biopsy was done revealing focal fibrosis, eosinophilic-proteinaceous exudate & reactive proliferation of type-II-pneumocytes, diffuse alveolar damage & hyaline-membrane. Patient was put only on intravenous methyl-prednisolone 5O0-mg 8-hourly & symptomatic treatment. After 3days of treatment he responded with some clearance of radiographic infiltrates, hence confirming the diagnosis of Vinorelbine induced Interstitial Pneumonitis.

DISCUSSIONS: This is probably the first case-report documenting Interstitial Pneumonitis after Vinorelbine administration. The clinical course, radiological & pathologic characteristics, rapid response to steroid & absence of other potential causes are suggestive of drug-induced pneumonitis. Many chemo-therapetic agents like bleomycin, busulfan have been implicated with development of interstitial pneumonitis, but this is probably the first case-report of Vinorelbine induced interstitial pneumonitis The mechanism is unknown, but is believed to be an allergic-immunological process as is shown by rapid & near-complete response after drug cessation & steroids.

CONCLUSION: Vinorelbine toxicity should be strongly considered in diagnosis of interstitial pneumonitis developing after short period of administration, urgent diagnostic workup is essential to exclude other etiology & to establish drug as a cause of interstitial pneumonitis & to enable early institution of steroid therapy which given prompt response.

REFERENCES:

(1) Roland T. Skeel. Anti-Neoplastic drugs & biologic response modifiers: classification use & toxicity of clinically useful agents. In Handbook of Cancer Chemotherapy. Ed. Roland T. Skeel. V ed. P.142, 1999. Lippincott, Williams & Wilkins.

DISCLOSURE: Mayank Vats, None.

Mayank Vats MD * Rakesh C. Gupta MD Deepa V. Khandelwal MBBS Neeraj Gupta MD Pramod Dadhich MD J.L.N. Medical College, Ajmer, Rajasthan, India

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