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Date of last update: 10/21/2017.
Forum Name: Lung Cancer
|mark83 - Mon Aug 02, 2010 2:20 am||
My father, 62 yrs old, non-smoker, and a retired bank employee, was diagnosed as either having TB or cancer -- his pulmonologist apparently isn't pretty sure.
Back in 2005, he was diagnosed to have Pulmonary TB through X-ray although negative in sputum test. He started taking anti-TB medicines given by the government's department of health but stopped after 3 months because of his severing arthritis which he had already been suffering since 1998 (he had been taking NSAIDs for this).
In March 2010, he was diagnosed to have Benign Prostatic Hyperplasia and was taking Finasteride for 1 month then followed by Terazosin. He was admitted to the hospital by this time, sharing a room with someone who apparently had a pulmonary disease. After being discharged, he began coughing and was losing weight and appetite. He was given Ciprofloxacin but the symptoms never improved. We thought this could just be a side-effect of Terazosin as indicated in the medicine's literature.
In the same month, he was again diagnosed with secondary Pulmonary TB through X-RAY by a radiologist in our community hospital.
To verify if it's really correct, a pulmonologist in a private hospital, again conducted another X-RAY and found a lung mass at the right lower lobe. He suggested a biopsy. This is the CT-scan guided biopsy result:
Preliminary CT Scan of the right lower lobe density shows a lobulated density (atelectatic) seen in the posterior segment of the right lower lobe encasing the right lower lobe bronchus. No calcification seen. There is also loculated minimal left pleural fluid. With introduction of G20 spinal needle with patient in prone position shows the tip is within the central aspect of the right lower lobe density.
Specimen: FNAB, Lung
Microscopic Examination: The smears show numerous red cells, moderate polymorphonuclear and mononuclear leukocytes enmeshed in mucin and a few clusters of benign columnas epithelial cells. There are no definite tumor cells seen.
Diagnosis: CYTOLOGY SUGGESTIVE OF INFLAMMATORY PROCESS
Specimen: CELL BLOCK, LUNG MASS
Microscopic Examination: shows amorphous eosinophilic materia in which embedded are abundant red blood cells moderate polymorphonuclear leukocytes and few lymphocytes. There are no tumor cells see.
Diagnosis: NO TUMOR CELLS SEEN
Given this result, the doctor is still suspicious and is considering Bronchoalveolar Carcinoma. His final diagnosis is: LUNG MASS RIGHT PULMONARY TB versus MALIGNANCY.
Now, he is suggesting open surgery biopsy. This suggestion is really impossible right now since my father is weak due to shortness of breath when doing any activity -- although his breathing is ok when at rest and he can even breathe without oxygen support. Only when coughing hard sometimes that usually appears at night or early in the morning that makes his breathing hard. He also experiences fever at night or early in the morning.
He had been given Cefixime for one week, and his fevers became infrequent and the phlegm became white from yellowish. However, after several days, fevers came back that caused shortness of breath and his phlegm turned yellowish again. Now the doctor has given him Levofloxacin (Levox 750mg tablet) and Sporanox ( Itraconazole) for 7 days. Again, fever was gone and his phlegm was turning into white. But a week after, he had fever again, night sweats, and his phlegm yellowish.
He has been taking anti-TB for one month and a week already and he has somehow felt some improvement in the symptoms -- though he is still having fever and sweating every now and then.
Could this really be TB or Cancer?
Are Levofloxacin and Itraconazole safe to continue despite the fact that he had already taken these more than a week ago? (he stopped taking them last July 21).
Can combination antibiotic therapy help aside from anti-TB?
Any advise or suggestion? What are the necessary steps to take given my father's condition -- this situation is so paradoxical for me since we cannot easily transport my father from the rural province to Manila where the sophisticated medical equipment and service are available -- we don't even have bronchoscopy in our place. So we have to make him, at least, feel better before transporting him -- the reason I'm asking about antibiotic therapy in the hope that this might improve his condition.
Thank you very much in advance.
|Dr.M.Aroon kamath - Sat Sep 04, 2010 9:39 am||
There are several lung pathologies that are very difficult to distinguish on clinical and radiological grounds from lung cancers.Modern imaging also may not be able to sort these out.
The most important clue from the history that you have provided is perhaps the presence of the "amorphous eosinophilic material" that was found on CT- guided lung biopsy.Therefore, let us take it from there.
I do not know if special stains were used to identify this material.I will discuss in brief a few important conditions in which this type of material may be seen.
- Nodular Parenchymal Amyloidosis,
- Pulmonary alveolar proteinosis (PAP),and
- pneumocystis jiroveci pneumonia.
Amyloidosis: The clinical syndromes pertaining to amyloidosis involving the respiratory tract are
(a) Tracheobronchial amyloidosis - this is usually localised and tend to recur.
(b) Diffuse alveolar septal amyloidosis(diffuse parenchymal) - this occurs in systemic amyloidosis or with underlying monoclonal lymphoplasmacytoid lymphoma.
(c) Nodular Parenchymal - presents as solitary or multiple nodules with a predilection for the lower lung zones, often attaining a size of upto 15 cm. Pulmonary nodular amyoidosis (PNA) may be detected incidentally on imaging, during bronchoscopy or may present with clinical symptoms(progressive dyspnea). These lesions are often called ‘Amyloidoma’s. They are not associated with systemic amyloidosis.
On light microscopy, amyloid appears as an amorphous, eosinophilic, PAS -ve or scantly positive, extracellular substance. Congo Red stained specimens with the characteristic apple-green birefringence in polarised light are invaluable in the identification of amyloid.
Apart from these forms of pulmonary amyloidosis, localized amyloid deposits have been seen to occur in
- Pulmonary marginal zone lymphoma (a type of low-grade non-Hodgkin's lymphoma) and
- Primary Sjogrens syndrome, which has been reported in association with solitary or multiple pulmonary amyloid nodules.
Pulmonary alveolar proteinosis (PAP): Young adults in the third or fourth decade of life are frequently affected. Male to female ratio is about 3:1. Nearly 70% of affected individuals have a history of cigarette smoking. A significant minority of patients may be immunocompromised. Most common presenting symptoms are dyspnea and dry cough. Low grade fever may also occur, but may indicate the possibility of a superimposed infection. Digital clubbing is seen in about a third of patients.
Diagnosis requires demonstration of the distinctive amorphous, granular eosinophilic exudates, very typical of PAP.These granular exudates are PAS-positive and are also immunoreactive for surfactant apoprotein.
Frothy eosinophilic material with "bubbles"(foamy) in an inflammatory-to-necrotic background is often seen in Pneumocystis jiroveci pneumonia.
Tuberculosis can masquerade in numerous ways and can be confirmed only by appearances on biopsy, a positive culture, or using the newer Polymerase Chain Reaction (PCR) testing.
In your father's case, nodular amyloidosis appears to be a strong contender.
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