notes by dr Claudio Italiano
The real clinical cases.
Why talk to you about lung cancer?
Because it's a subtle and insidious neoplasm, which stabs you behind when you least expect it. In fact I remember the case of a friend of mine, whom I followed at the dawn of my medical profession, when he started to accuse hemoptysis and dysphonia and had turned to the otolaryngologist. The otorine had prescribed a therapy with vit. B12 and insufflation (sic!). After some time the dysphonia had become overt and the patient revalued, from another otorino to which I had addressed, this time at the Policlinico di Messina, there was an evident compression of the recurrent laryngeal nerve, with paralysis of a vocal cord. In fact, the patient could not pronounce the letter "e", which, as is known, is made with the two vocal cords that vibrate tight and accolades between them. This patient had had cough, bronchitis and hemoptysis in the previous months, ie blood sputum. The cause of the cancer was smoking, he smoked just like a Turk, for reasons of work stress, in the waiting periods between one client and another.
Another case, unfortunately very close to me, has manifested itself in an even
more subtle way; the patient presented a showy and sudden pleural effusion,
which did not regress with the cortisone and diuretic therapy of the loop (lasix)
associated with the canrenoate or even with the repeated evacuative
thoracentesis: it reformed in an imposing and sudden manner, in the last months,
with the speed of 1-2 days, while initially the pleural effusion was formed
every six months.
Performed a thoracentesis, this time in the environment of Thoracic Surgery, still at the Policlinico di Messina, this documented a right lung with an atelectatic lobe, an inflamed pleura with fibrin synechiae and yellowish rats suspected of heteroplasia; during the thoracentesis, about 1,500 cc of pleural fluid, amber-colored, cloudy, came out and we talked about "1 st stage empyema". In the days to follow, however, the lung continued to drain dramatically 350, 400 cc of pleural fluid / day, for a total of 2500-3000 cc over 7 days. Contrast CT scan was negative and even the pleural biopsies that had been performed did not document mesotheliomas or other lesions. It was only the cytological examination of the pleural fluid, repeated over time, to document atypical cells, coming from a hypotetic, bronchogenic squamous carcinoma. The patient did not overcome the stress of drainage, given the already debilitated clinical conditions and the basic cardiological problems and it was not possible to go further with the treatments and the investigations of the case, that could have understood a BAL or a fibroscopy.
Other times, on the other hand, it is a "bad ilo" lung that conceals in its context a lymph node package that receives drainage from an associated carcinoma, as an image of "ilo globoso". The patient was the first to accuse Pancoast's syndrome, ie the tumor involved the costal pleura and the brachial plexus, causing a very intense chest pain in the right shoulder, which was first exchanged for a right scapolomer arthritis, given a previous trauma of the shoulder that he had suffered the patient for a fall and the demanding working activity that he had in his youth as a worker in the mines. The other signs had been a very intense dyspnoea, not even explainable by the hemogas (the respiratory gases were within the limits of the norm, both for the partial pressure of oxygen and carbon dioxide, which for the pH), insistent, tiring cough, with a lot of production of a frothy and purulent sputum, but never bloody, and epigastric pain that simulated a gastric ulcer, another sign was dysphagia and anorexia, with absolute rejection of food and inexplicable weight loss (cf. bronchitis and systemic disease). Lastly, the patient had recurrent exposure to exacerbations of chronic obstructive pulmonary disease, with fever, increasingly less sensitive to antibiotic treatment, and an explicable insomnia with probable brain metastases and with the nighttime dyspnea resulting from the decubitus and compression of the lung. Other times the paracaval lymph nodes are given which give compression on the superior vena cava and cause venous stasis and the so-called "mantle edema syndrome".
(ie from the Greek epì demòs logòs, study on the people).
Lung cancer is a continuously increasing cancer, if it is true that from 1950 to
1980 the cases of tumors have risen by 330% in women and 225% in men and growing
in men of color. In the US, where adenocarcinoma is the hit parade, they are the
leading cause of cancer death for both males (> 100,000 / year) and females (>
50,000 / year). Maximum incidence: 55-65 years. Even us and our hinterland, if
Rome does not intervene enforcing environmental laws and rehabilitation, has
contributed a lot to epidemiological cases! At diagnosis only 20% have a
localized form; usually, however, the prognosis is always bad. Survival at 5
years is only 30% for males and 50% for females (in women the most frequent form
is adenocarcinoma). Over the years, changes in frequency of histotype have been
observed (adenocarcinoma is currently the most common form in the USA).
This is related to changes in living customs, the use of cigarettes in women and the fact that they also work in industry like men. Lung tumors can be distinguished in "primitive" and "secondary", that is, in tumors that arise from the lung or that are manifested as distant metastases, called "repetitions" in medical jargon. Still the primitive ones, that is those of the lung, can be benign in 5% of cases or malignant and these are the most frequent with 95% of cases. Let's say immediately that the tumor of the lung is actually a tumor that derive from the bronchus and, more accurately, from the epithelial lining of the bronchus, especially the large bronchi, and especially the hilum, that is at the point where the bronchus enters the parenchyma. pulmonary, whereas the connective tissues, ie those of the filling tissue, are very rare and are mostly sarcomas. Another distinction "small" is in "small cell tumors" and "non-small cell tumors" and this distinction finds reason to be in the high degree of malignancy of the first forms, which more frequently than others produce metastases, especially in the brain.
Passive smoking is also risky for the
genesis of the tumor as the active one; in addition, smog and atmospheric
pollution (industrial chemical substances (nickel, chromium, arsenic and cadmium,
ionizing radiation) and permanence in closed environments such as mines where
radon exists, (cf. Risk of respiratory cancer and industrial pollution). We
still need to think of the multi-factorial genesis, that is, predisposing
environmental and genetic factors.The diet with fatty foods predisposes, while
preferring a diet based on fruits and vegetables, with deficiency of vit E and
beta-carotene prevents the onset of neoplasia Then the tumor, as my late
professor said, "is a song that stutters in the cradle": familiarity and
mutations of the RB gene (patients with retinoblastoma that reach adulthood) and
the p53 gene first degree have a risk of develop lung cancer or another neoplasm
of 2/3 higher).
Radon is an odorless and colorless gas, generated by the decay processes of the
radio, itself produced by the decay of uranium, present widely in the earth's
crust (granite and minerals used for the construction of houses). Radon
represents a volatile and radioactive element, capable of inducing DNA mutations
and therefore representing a concrete risk of neoplasia, in relation to absolute
mortality from lung cancer it has been estimated that from 5 to 20% of tumor
onset mortal is due to this exposure, especially in miners.
Asbestos fibers (needle-shaped body surrounded by brownish round inclusions) in
cytological aspirate developed for the diagnosis of lung cancer. Asbestos, in
addition to being implicated in the pathogenesis of asbestosis and pleural
mesothelioma, shows a synergistic role with tobacco smoke for the development of
lung carcinoma
Although definitive data are not yet present, exposure to smog and air pollution
(products of combustion of petroleum derivatives and processing products that
involve the use of particular metals such as nickel and chromium) is called into
question in the pathogenesis of deadly lung cancer.
The oncogenic capacity of viruses has been widely demonstrated in the animal
model, although recent evidence suggests the potential role of papillomavirus,
JC poliomavirus, simian virus 40 (SV40), BK virus and cytomegalovirus in the
pathogenesis of human lung carcinoma . These viruses can alter the cell cycle
and block the processes of apoptosis, promoting an abnormal control of cell
replication and the subsequent development of neoplasia.
The presence of hereditary abnormalities of p53 (such as Li-Fraumeni syndrome) and of Rb predispose to lung carcinoma. A further gene involved seems to be the gene coding for cytochrome CYP1A1, of the P450 enzyme system family, responsible for the metabolism of some drugs, of aromatic compounds and of benzopyrene. Polymorphisms of this gene involve an altered metabolism of the carcinogenic compounds present. in cigarette smoke, with greater susceptibility to cancer for those who have inherited the enzymatic variant of CYP1A1.
Pneumology index