#pleural disease symptoms

[mesolawcenter]

Why Is Mesothelioma Incurable in 2024? | Behind the Reason

Introduction Mesothelioma, a rare and aggressive form of cancer, remains challenging to cure despite advances in medical research. Its unique characteristics and the way it develops make it difficult to treat effectively. This article explores why mesothelioma is incurable and what options are available for patients.

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1. What Makes Mesothelioma Different from Other Cancers? Mesothelioma originates in the mesothelial cells that line organs like the lungs and abdomen.

Aggressive nature: It spreads quickly to nearby tissues.

Late diagnosis: Symptoms often appear decades after asbestos exposure.

2. Why Is Mesothelioma Difficult to Diagnose Early? The latency period of mesothelioma, combined with non-specific symptoms, leads to delayed detection.

Latency period: Can be 20-50 years from asbestos exposure to symptom onset.

Similar symptoms: Mimics conditions like pneumonia or bronchitis.

3. How Does Mesothelioma Spread in the Body? Mesothelioma tends to spread to nearby organs and tissues, complicating treatment.

Localized spread: Often extends to the lungs, diaphragm, or heart.

Metastasis: Advanced stages may spread to distant parts of the body.

4. What Treatment Options Are Available for Mesothelioma? While there is no cure, treatments can help manage symptoms and prolong life.

Surgery: Removes tumors but is not always possible due to spread.

Chemotherapy: Helps to shrink tumors and manage growth.

Radiation therapy: Used to target cancer cells and reduce pain.

5. Are There Any Emerging Treatments for Mesothelioma? New therapies aim to improve patient outcomes and quality of life.

Immunotherapy: Boosts the body's immune response to target cancer cells.

Gene therapy: Investigates altering cell behavior to combat the disease.

Clinical trials: Offer access to cutting-edge treatments.

6. What Is the Focus of Current Mesothelioma Research? Research continues to explore better detection methods and new treatments.

Early detection: Developing blood tests and biomarkers for earlier diagnosis.

Targeted therapy: Aims to attack specific cancer cells without harming healthy cells.

Conclusion The incurability of mesothelioma is largely due to its aggressive nature, late diagnosis, and the complexity of its spread. Despite these challenges, advancements in research provide hope for better management and improved quality of life for those affected.

FAQs

Why does mesothelioma take so long to develop? The asbestos fibers cause chronic irritation that eventually leads to cancer after many years.

Can mesothelioma be detected before symptoms appear? Currently, it is difficult, but researchers are working on early detection methods.

Is palliative care common for mesothelioma patients? Yes, palliative care is often used to manage pain and improve comfort.

Why can't surgery cure mesothelioma? Surgery cannot always remove all cancer cells due to their spread to surrounding tissues.

Are mesothelioma survival rates improving? New treatments have improved some outcomes, but survival rates remain low.

What is the most promising new treatment for mesothelioma? Immunotherapy has shown promise in extending survival in some patients.

[transgenderteensurvivalguide]

Can binding cause pleural effusion?

I've been feeling pressure in my rib and chest area for a while and recently it's gotten worse as well as my ability to breath, could it be from binding? I don't have any bruised or broken ribs

I do have an inflammatory disease but I don't think it's that

Lee says:

We are not medical professionals, which is why I would recommend that you speak to someone who is!

I can't tell you whether the symptoms that you are experiencing are caused by binding or worsened by binding because I'm not a medical professional who has taken your medical history and examined you, but I can tell you that it's important to get it checked out by someone who can diagnose the issue and recommend a plan to address it.

You should call your primary care provider/general practitioner/family doctor, and/or send a message to them through the patient portal if there is one.

If you don't have a doctor or other provider who you usually see for an annual check-up or sick visit, you could look to see if there are any urgent care clinics near you who accept your insurance.

And don't bind until you've been cleared to do so by a medical professional-- it sucks, but it's time to take a break from binding, just in case it could exacerbate the issue.

If you've been having unexplained issues breathing for a while, you should see a medical professional. That's always true. If you're worried about telling your parents about your concerns about binding because you're closeted or they don't approve of you binding, don't mention binding when you explain why you'd like to go to the doctor, just tell your parents about your symptoms.

If you think that your parents might not allow you to go to the doctor, start by going to the school nurse, explaining your symptoms, and see if they'd call your parents or write a note for your parents recommending that they take you to the doctor. That might make them more likely to take you if they tend to otherwise disregard your concerns.

But when you do go to the doctor, do mention your binding, as well as what symptoms you're experiencing and how long you've been experiencing them.

I've had two family members get pneumonia in the last year, and one had to be hospitalized and the other needed a CT scan to diagnose lung issues, and both needed antibiotics. There are a lot of illnesses and injuries that can cause issues with breathing (example one: COVID!) but some things don't always improve without treatment.

It seems like you've been having these issues for a while, so I'd encourage you to do whatever you have to be sure you get the care that you need instead of waiting it out and seeing if you get better.

I hope you feel better soon anon! And again, please do seek out medical attention IRL!

[lastlycoris]

Liver transplantation.

The one time you might actually want cancer.

Why? Because having a primary liver cancer bumps you up on the liver transplant list. But it can't just be any cancer - there's a criteria for acceptable cancer burden for adult liver transplant, which is known as Milan Criteria. Essentially one big tumor smaller than 5 cm or 3 small tumors less than 3 cm each. The tumor can't have left the liver either aka metastasis. However if it's too small (<2 cm ), you don't get priority listing for having that cancer. Kind of like Goldilocks - the tumor has to be just right.

Now first off, you almost never get a primary liver tumor aka hepatocellular carcinoma (HCC) without something wrong in the liver in the first place.

This is usually Cirrhosis aka fibrosis of the liver, which can be caused by Hepatitis C or more commonly drinking too much alcohol too often. The liver fails cause its cells are dead or dying, and the resulting scarring prevents blood from your GI tract from returning properly to your systemic blood. This pseudo-blockage results in fluid backing up in your body, resulting in ascites (fluid in the belly) and pleural effusion (fluid in the lung space) and generalized soft tissue swelling.

The body tries to compensate for this by making alternate paths. Problem is the liver is also a filter, and bypassing the filter through an alternate path affects the brain - a common symptom is confusion and sometimes coma in these patients. Official term is hepatic encephalopathy.

Cirrhosis patients can also literally turn yellow because bilirubin, which occurs from the normal breakdown of red blood cells, can't be processed well by a dysfunctional liver. Liver does a lot of other important stuff too, but I'd go on forever with that - so I'll end that here.

In any case, the only treatment for cirrhosis is getting a new liver - once cirrhosis occurs, it cannot reverse, only worsen. The liver transplant list uses its own criteria known as MELD which I also won't get into here, but generally the sicker you are, the higher you are on the transplant list.

Cirrhosis is essentially a breeding ground for primary liver cancer because cirrhosis is essentially repeated constant inflammation - and all it takes is one cell to heal in the absolutely worst way - and then you have a cancer. This is why cirrhosis patients get yearly liver imaging screening to detect that.

Milan Criteria was created because a good number of liver transplants in cancer patients turned out to have recurrent liver cancer in the new liver. After Milan was implemented, long-term recurrence-free survival improved from 30% to 75%. I believe the sizes used in Milan acts as a surrogate for the likelihood of microscopic metastasis, cancer that's left the liver but too small to be seen in imaging, but don't quote me on that.

Now why did I bring this up? One of the residents asked out loud about why we don't just cut out the cancer.

For one, cirrhosis ensures another one will pop up eventually, and for two, cutting a cancer out also means cutting out good tissue (or semi-okay in a cirrhotic's case) to create the disease-free margin. You don't have much good tissue left in a cirrhosis liver.

You could ablate the cancer by frying it with heat or freezing it, but you again have the issues of damaging normal tissue. Typically excision or ablation is done when there's no chance patient will get a donor liver.

There's also TACE (transarterial chemoembolization) which can be used to shrink tumors, usually back into the limits imposed by Milan criteria. Because if your cancer is too big for Milan, you don't get a liver. There are strict rules for that, and if you break them, your liver transplant service is not getting donor livers.

[mcatmemoranda]

Reviewing questions:

Blindness is a potentially devastating complication of sarcoidosis. Ocular sarcoid can develop in up to half of all cases and most commonly presents as anterior uveitis or keratoconjunctivitis. The most serious complication is optic neuritis.

A complete ophthalmologic examination at the time of diagnosis is recommended, as asymptomatic disease can result in permanent visual impairment. All patients with sarcoidosis should have a careful history and physical examination to identify other organ involvement before having further testing, including ECG, pulmonary-function testing, and baseline laboratory studies (calcium level, alkaline-phosphatase level, renal-function, and hepatic-function tests) to evaluate the extent of disease.

McConnell's sign is defined as right ventricular free wall akinesis with sparing of the apex. Typically this looks as if the apex of the RV is a trampoline. Echocardiogram shows right ventricular strain and a positive McConnell sign, which is indicative of pulmonary embolism (PE).

All patients who have known or suspected bronchiectasis and who are acutely ill with suspected lower respiratory tract infection should be empirically treated with an antipseudomonal antibiotic, such as cefepime until culture results are available to guide treatment decisions.

Heerfordt’s syndrome (uveoparotid fever) is another collection of clinical findings specific enough to diagnose sarcoidosis without a biopsy. These signs and symptoms include uveitis, parotid gland enlargement, and facial nerve palsy.

Lofgren’s syndrome is a form of acute sarcoidosis. Sarcoidosis is a multisystem disease characterized by the presence of noncaseating granulomas and although classically described in African Americans, it has one of its highest prevalences in the northern European population. Clinical variants exist with certain forms having diagnostic and prognostic value. Lofgren’s syndrome is the combination of erythema nodosum, bilateral hilar adenopathy, migratory polyarthralgias, and fever. This pattern is so consistent that it has 95% diagnostic specificity and allows diagnosis of sarcoidosis without a biopsy. Among European patients, the presence of Lofgren’s syndrome portends to a good prognosis. For mild disease symptomatic treatment with non-steroidal anti-inflammatory agents is reasonable or low dose prednisone may be added.

The optimal management of laryngotracheitis (croup) is determined by the severity of disease. There are numerous scoring systems for croup severity, with the Westley croup score being the most validated and most often used. The Westley croup severity scale includes evaluation for the presence of stridor at rest, retractions, and cyanosis as well as assessment of mental status and air entrance. Regardless of any official scoring system, most physicians would consider the presence of retractions and stridor at rest to be indications of moderate to severe disease that requires evaluation in the emergency department. The presence of cyanosis, confusion, depressed mentation, agitation, severe retractions, or absent breath sounds would indicate severe disease and/or the possibility of impending respiratory failure.

Mild cases of croup are treated on an outpatient basis with cool mist therapy and fluid replacement. Moderate cases may require supplemental oxygen, oral or intramuscular corticosteroids, or racemic epinephrine. Severe cases are best treated with hospitalization and racemic epinephrine.

Bottom Line: The most important step in initial management of laryngotracheitis includes nebulized epinephrine (racemic or L-epinephrine) and dexamethasone along with humidified oxygen, fever reduction, and hydration. Epinephrine acts almost immediately, while steroids have a delayed onset of action.

Pneumothorax is defined as a collection of air in the pleural space. The result is pleural separation of the visceral and parietal pleura. Spontaneous pneumothorax lacks an antecedent event (e.g. trauma). There are two types: primary and secondary. Primary spontaneous pneumothorax (PSP) occurs in patients without recognizable underlying lung disease. Secondary spontaneous pneumothorax (SSP) occurs in patients with visible underlying lung disease (e.g. COPD). The most common etiology of PSP is rupture of a subpleural bleb (which are usually not seen on imaging and are undiagnosed). Many cases initially diagnosed as PSP may eventually be diagnosed as SSP after further workup.

Management depends on the size of the pneumothorax. The spectrum of management includes watchful waiting, aspiration, chest tube insertion, and thoracoscopy with pleurodesis or lung resection.

Rhinosinusitis can be defined as either viral/bacterial and if bacterial, as complicated/uncomplicated. Complicated rhinosinusitis implies the extension of disease outside the nasal cavity/sinuses into adjacent structures, such as soft tissues, ophthalmologic tissues, and nervous system.

Current criteria for the presumptive (many of these cases may still be viral) diagnosis of acute bacterial rhinosinusitis (ABRS) include persistent symptoms lasting more than 10 days without any evidence of clinical improvement or a biphasic illness pattern which is also called double worsening, meaning the patient was sick, improved, and then became sicker a second time within a short time frame, usually within a 10 day period. The IDSA guidelines from 2012 also recommend the use of a high fever greater than 39C associated with severe symptoms for 3-4 days as being more consistent with bacterial rhinosinusitis. According to the guidelines by the American Academy of Otolaryngology-Head and Neck Surgery published in 2015, fever itself early in the course of illness is not sensitive or specific enough to warrant treatment based on this vital sign alone, and they do not recommend using this as criteria for the diagnosis of ABRS. They agree with the other criteria used by the IDSA and acknowledge that a "severe" presentation may warrant the use of antibiotics as recommended by the IDSA and the American Academy of Pediatrics which considers more than 3 days of high fever and purulent nasal discharge as a severe presentation of ABRS in children.

Summary Criteria for the Diagnosis of ABRS

Signs or symptoms of acute rhinosinusitis present for 10 days or more after symptom onset with no improvement

Acute worsening of improving rhinosinusitis within 4-6 days of symptom onset or "double-sickening."

Severe rhinosinusitis: onset of high fever greater than 39C and severe symptoms within 3-4 days of onset

Tx of ABRS: amoxicillin, amoxicillin-clavulanate, doxycycline if PCN allergic, or respiratory fluoroquinolone in kids who can't take doxycycline. I just had a pt in clinic who had bacterial rhinosinusitis and I gave him amoxicillin-clavulanate.

Bottom Line: In patients with ABRS who require antibiotic therapy, the initial therapy of choice is with amoxicillin with or without clavulanate.

One of the feared complications of acute bacterial rhinosinusitis (ABRS) is orbital cellulitis. This infection commonly develops in the setting of ABRS due to the direct extension of bacteria from the sinus cavity into the orbit. Commonly it can project through the roof of the maxillary sinus. Additionally, there can be extension through the adjacent soft tissues. The diagnosis of this condition is clinical and is confirmed with radiographic imaging (CT scan of the sinuses). The presence of pain/difficulty with eye movement, double vision, eye swelling, and erythema should be concerning for orbital infection. The initial imaging test of choice would be with a contrasted CT study of the face and orbits. An MRI could also be performed and has similar accuracy, but is generally slower and more expensive to obtain. Additionally, patients with suspected orbital cellulitis should be evaluated by ophthalmology in the emergency department and started on IV antibiotics with coverage for MRSA (vancomycin generally).

If the sinuses are the suspected source, ampicillin-sulbactam or piperacillin-tazobactam can be added to vancomycin as long as there is no concern for CNS involvement. If the CNS is involved, it should be noted that both ampicillin-sulbactam and piperacillin-tazobactam have relatively poor CNS penetration, and a 3rd generation cephalosporin (ceftriaxone) should be used with the addition of metronidazole for coverage of anaerobic organisms. General guidelines for sepsis and infection should be followed with the physician obtaining the regular laboratories including a complete blood count, metabolic profile, blood cultures, and lactate.

Symptoms of Complicated ABRS:

Proptosis or impaired extraocular movements Painful eye movements Diplopia or impaired vision Periorbital edema or erythema Cranial nerve palsies Altered mental status Neck stiffness/meningeal signs Papilledema

Complications of ABRS:

Meningitis Orbital cellulitis Cavernous sinus thrombosis/thrombophlebitis Preseptal cellulitis

Ruptured eardrum:

Tympanic membrane perforations are commonly caused by trauma or acute otitis media and are usually noted on otoscopic examination. Perforations with marked hearing loss or other concerning neurologic signs such as nystagmus, ataxia, or vomiting should receive a prompt evaluation by an otolaryngologist. Supportive care only is a perfectly reasonable treatment plan for patients with simple perforations with minimal hearing loss and no neurologic signs. Many perforations will heal spontaneously within 4 weeks and require no intervention.

[txhospitals1234]

Pneumonia Specialists in Hyderabad: Expert Care for Your Respiratory Health

Pneumonia is a serious respiratory condition that affects millions of people each year. It occurs when the air sacs in the lungs become inflamed, often due to an infection. Pneumonia can cause severe breathing difficulties, fever, and fatigue, and in some cases, it can be life-threatening. Early diagnosis and treatment are crucial for managing pneumonia effectively and preventing complications.

If you or a loved one is suffering from pneumonia or showing symptoms such as persistent cough, chest pain, shortness of breath, or fever, seeking the help of a qualified pneumonia specialist is essential. Hyderabad is home to several top pulmonologists and pneumonia specialists who provide expert care and ensure that patients receive the best treatment options.

At TX Hospitals, we have a team of experienced specialists who are highly skilled in diagnosing and treating pneumonia. Our pulmonologists use advanced diagnostic tools and treatment protocols to offer personalized care for every patient.

1. Dr. Sathish Pogula – Experienced Pneumonia Specialist

Dr. Sathish Pogula is a highly respected chest and pneumonia specialist in Hyderabad. With an MBBS, MD, and IDCCM qualification, Dr. Pogula has extensive experience in treating respiratory conditions, including pneumonia. His expertise in critical care medicine allows him to handle even the most severe cases of pneumonia, ensuring that patients receive timely and effective treatment.

Dr. Pogula uses advanced diagnostic methods such as chest X-rays, CT scans, and blood tests to determine the exact cause of pneumonia and create a tailored treatment plan. Whether it's bacterial, viral, or fungal pneumonia, Dr. Pogula ensures that every patient receives the right medication and support to recover swiftly.

2. Dr. Naresh Dude – Renowned Pulmonologist and Pneumonia Expert

Dr. Naresh Dude, with his MBBS, DNB, and FCCM certifications, is one of the leading pulmonologists in Hyderabad. Specializing in pulmonary medicine and critical care, Dr. Dude has vast experience in diagnosing and treating pneumonia, especially in severe or complicated cases. His thorough approach to patient care and his use of the latest medical technology ensure that patients receive the best possible outcomes.

Dr. Dude’s expertise in managing pneumonia in high-risk patients, such as the elderly, immunocompromised individuals, and those with chronic conditions, makes him one of the top choices for pneumonia treatment in Hyderabad. His compassionate care and dedication to improving his patients' quality of life have earned him a stellar reputation.

3. Dr. Rohith Reddy – Pulmonary Medicine Specialist

Dr. Rohith Reddy, an MBBS graduate with an MD in Pulmonary Medicine, is known for his expertise in treating various respiratory conditions, including pneumonia. Dr. Reddy takes a holistic approach to patient care, addressing not only the pneumonia itself but also the underlying conditions that may contribute to its development, such as asthma, COPD, or heart disease.

His patient-centered approach ensures that treatment plans are customized to each patient’s unique needs, helping them recover quickly and prevent future respiratory infections. Dr. Reddy's vast experience and knowledge make him one of the top pneumonia specialists in Hyderabad.

4. Dr. M.V. Sree Keerthi – Specialist in Pulmonary and Respiratory Care

Dr. M.V. Sree Keerthi is a highly skilled pulmonologist specializing in treating pneumonia and other respiratory conditions. With an MBBS, DNB, and DTCD in Pulmonary Medicine, Dr. Keerthi has extensive training in managing both uncomplicated and complex pneumonia cases.

Dr. Keerthi uses a combination of medical interventions, including antibiotics, antivirals, and antifungals, as well as respiratory therapies, to treat pneumonia. She is also skilled in managing pneumonia-related complications such as respiratory failure or pleural effusion, ensuring comprehensive care for her patients.

Why Choose TX Hospitals for Pneumonia Treatment?

TX Hospitals is equipped with state-of-the-art facilities and a team of highly skilled pneumonia specialists who offer advanced care for patients suffering from respiratory conditions. Our hospital offers a wide range of diagnostic tools, including digital X-rays, CT scans, and pulmonary function tests, to accurately diagnose pneumonia and determine its cause.

Services at TX Hospitals:

Comprehensive Pneumonia Diagnosis: We offer advanced diagnostic tests, such as blood tests, chest X-rays, and sputum cultures, to identify the type and cause of pneumonia.

Personalized Treatment Plans: Based on the diagnosis, our specialists create customized treatment plans, including antibiotics, antivirals, and antifungals, along with respiratory support if necessary.

Critical Care: For severe cases of pneumonia, we offer intensive care services, including mechanical ventilation and monitoring, to support respiratory function.

Pulmonary Rehabilitation: We provide rehabilitation programs to help patients recover and regain their lung function after an illness like pneumonia.

Book an Appointment Today

If you or a loved one is suffering from pneumonia, don't wait for symptoms to worsen. Book an appointment with one of our expert pneumonia specialists at TX Hospitals today. Our team is committed to providing timely, effective, and compassionate care to help you recover quickly.

For appointments, call 9089 48 9089. Our team at TX Hospitals is here to help you breathe easier and get back to a healthy, active life.

At TX Hospitals, we are committed to providing the highest quality care for all respiratory conditions, including pneumonia. With our experienced specialists and advanced treatment options, we ensure that every patient receives the care they need for a full recovery.

[myrawjcsmicasereports]

 Diversity of Radiological Imaging and Clinical Course in Pulmonary MALT Lymphoma  by Aras G1, Zirek Mandal T1, Kanmaz D1, Pehlivan S1, Fener N2, Özbek in Journal of Clinical Case Reports Medical Images and Health SciencesM3.

Abstract :

A 59-year-old male patient was admitted to the emergency department with a three-month history of worsening dyspnea, fatigue, and cough. His vital signs were recorded as follows: blood pressure 138/88 mmHg, heart rate 98 beats/min, respiratory rate 25 breaths/min, temperature 37.8°C, and oxygen saturation 91%. During the lung auscultation, breath sounds were absent in the lower left lung, while crepitant rales were audible in the upper zone and the right lung. CT scan of the chest showed 1 cm lymph nodes, pleural effusion, fibrotic changes, varicose-cystic bronchiectasis, as well as consolidations and atelectasis with air bronchograms in both lungs. Furthermore, thoracic ultrasonography revealed a large effusion in the left hemithorax, measuring 11 cm. He was hospitalized after the placement of a pleural catheter. Radiological diversity and the clinical course of the patient posed challenges for establishing a differential diagnosis. TL; DR: In this paper; we aimed to present a case of MALT lymphoma that manifested in the lung and caused diagnostic confusion with radiological and clinical symptoms.

 Introduction:

     MALT (Mucosa-Associated Lymphoid Tissue) is the lymphoid tissue that plays a role in mucosal defense. It includes functional memory B lymphocytes, which are essential for the immune response. They are not physiologically present in the lungs, but they become active there in response to infections and chronic antigenic stimulation. Marginal zone B-cell non-Hodgkin lymphoma (MALT Lymphoma) accounts for 8% of adult lymphomas. Although it is most commonly seen in the stomach, it can also be seen in the salivary glands, thyroid and lungs (1). It is the most common type of lymphoma in the lung. It presents common radiological, pathological, and clinical findings with infection and other granulomatous diseases, making differential diagnosis quite difficult for the clinician.In this paper, we aimed to present our case, which we had difficulty in diagnosing in the clinic. 

  Case Presentation:

 A 59-year-old male patient was admitted to the emergency department with worsening dyspnea, fatigue, and cough over the past three months. The chest X-ray of the patient showed a consolidation extending from the center to the periphery in the left upper zone near the aortic arch, an increased density indicative of pleural effusion with sinus obliteration on the left, and a consolidation extending from the hilum to the lower zone near the heart edge During the lung auscultation, breath sounds were absent in the lower left lung, while crepitant rales were detected in the upper zone and on the right side. Blood pressure was 138/88 mmHg, pulse was 98 beats /min, respiratory rate was 34 breaths/min, and oxygen saturation was 91%. At the time of admission, the patient's biochemical analysis results were as follows: Glucose 77 mg/dL (normal range: 70-115), urea 31 mg/dL (normal range: 17-43), creatinine 0.77 mg/dL, protein 65.8 g/L (normal range: 66- 83), albumin 39.3 g/dL (normal range: 35-53), LDH 423 U/L (normal range: <247), CRP 21.6 mg/L, procalcitonin <0.01ng/mL, and pro-BNP 8 pg/mL. The hemogram evaluation results were as follows: Leukocyte count 8.27 x 10³/µL, Erythrocyte count 5.16 x 10⁶/uL, Hemoglobin 15.6 g/ dL, Hematocrit (Hct) 48.3%, Platelet count 240,000/uL, Lymphocyte count 2.05 x 10³/uL, Eosinophils 3.4%, and Neutrophil/Lymphocyte ratio 2.47 x 10e3/uL. 

    The patient’s chest CT scan showed 1 cm lymph nodes in the mediastinum, fibrotic changes extending to the pleura, varicose-cystic bronchiectasis, and consolidations and atelectasis with air bronchograms in both lungs. There was also a massive fluid of 11 cm in the left hemithorax. (Figure 2). A thoracentesis was conducted on the patient’s left side following the detection of 13 cm of pleural fluid on thoracic ultrasonography. Lymphocytes, polymorphonuclear leukocytes, and mesothelial cells were observed in the cytological examination of the pleural fluid, but no atypical cells were detected. There was 98% lymphocyte dominance in the cell count. In the biochemical analysis, the pH was 7.440, lactate dehydrogenase (LDH) was 206 U/L, total protein was 39.40 g/dL, albumin was 25 g/dL, glucose was 60 mg/dL, and adenosine deaminase (ADA) was 34.4 U/L. Gram staining of the fluid, bacterial, fungal, and acid-fast bacilli growth were all negative. The patient's fluid was drained by aspiration. An intrapleural catheter was placed due to the high amount of fluid and increased dyspnea. The patient was admitted to the ward and initiated on oxygen therapy, bronchodilators, and antibiotics. The pleural fluid sent for cytological analysis two more times during the patient's hospitalization was found to be serohemorrhagic. Upon reevaluating his microbiological results, no growth was observed. Although many lymphoid cells were seen in the cytopathological examination of the patient's second pleural fluid, no atypical features were monitored. The patient's condition stabilized during clinical follow-up, and the pleural catheter was removed. However, after a while, the patient's dyspnea complaint recurred and the catheter was placed again because of the increase in fluid on the radiograph (Figure 3). There was no change in the infection markers of the patient, who also had fever from time to time, and CRP ranged between 20 and 16 mg/dL during follow-up. There was no growth in his small amount of sputum and blood cultures taken during the fever. The patient underwent fiberoptic bronchoscopy and no endobronchial lesions were detected. Wang fine needle aspiration and bronchial lavage were applied to mediastinal lymphadenomegaly Wang IA revealed lymphoid cells, but a definitive diagnosis could not be obtained. No findings were found in the lavage other than bronchial epithelial cells and polymorphonuclear leukocytes

    No FDG uptake was detected in the pleural fluid during the patient's whole-body positron emission tomography (PET-CT) scan, though minimal FDG uptake was observed in certain pleural areas. Consolidated/ground glass foci with the focal lepidic appearance in places were detected with left lung lingular, lower lobe central SUVmax 9.14, and right lung lower lobe SUVmax 6.55 and were evaluated to be in favor of malignant processes. Abdominal ultrasonography was unremarkable. No extrapulmonary findings were monitored in PET-CT scan either.

    When Wang IA did not yield any results, endoscopic ultrasonographic bronchoscopy (EBUS) was performed. The pathological interpretation was in favor of granulomatous inflammation, as mature transformed lymphocytes, polymorphonuclear leukocytes, epithelioid histiocytes, and loose granuloma-like structures formed by epithelioid histiocyte clusters and multinucleated giant cells were observed in the materials obtained. Alveolar sarcoidosis was taken into account, but the serum angiotensin converting enzyme level was also found to be normal at 39.1 U/L (8- 52.0).

    The patient was discharged due to the clinical stability of the patient with CRP 3.2 and procalcitonin <0.01 and was called for a follow-up at a later date. In the meantime, the patient was discussed at the surgical council. A decision was made to perform video-assisted thoracoscopy due to the fluid not regressing, increased dyspnea, and malignant involvement in PET-CT.

    During the procedure conducted under general anesthesia, 400 cc of fluid was aspirated. Biopsies were obtained from two distinct areas of the pleura and from a nodular region on the diaphragm, followed by talc pleurodesis. Samples were sent to microbiology and pathology. The patient, having experienced no complications, was discharged following the procedure . Pathology: Samples taken from the parietal pleura and the nodule on the diaphragm were evaluated as low-grade non-Hodgkin Lymphoma and interpreted as extra-nodal marginal zone lymphoma (MALT) by the pathologist .

Discussion 

    Clinical: The patient, who had been admitted to the emergency room with symptoms of dyspnea, hypoxia, and fever, was hospitalized after pleural fluid was exudate and consolidation was detected. Although the patient's clinical symptoms were severe, CRP was moderately high, and the occasional fever despite antibiotic therapy during hospitalization suggested diagnoses such as malignancy and tuberculosis, in addition to non-specific infection. Lymphomatous proliferation can involve the lung in various ways. Non-Hodgkin or Hodgkin lymphoma can present in the lung through hematogenous spread or by invading from adjacent mediastinal lymph nodes. However, primary involvement of the lung is also possible. Primary lymphomas should not have extra-pulmonary organ involvement for at least 3 months after diagnosis. The most common are MALT and effusion lymphomas (2). Effusion lymphomas may involve the pericardial and peritoneal cavities, with the most common primary involvement being the pleura, without solid organ involvement. Human-Herpes-8 infection and EBV may be accompanied by fever and lymphocytic-exudative fluid. HHV-8 negative cases have a better prognosis (3). In this case, there was also an exudative pleural effusion. However, although pleural involvement was not detected in the fluid cytological examination, pleural involvement was detected in biopsies. However, it is not possible to say that the patient only has effusion lymphoma (PEL). MALT (Mucosa-associated Lymphoid Tissue) lymphoma is the type of lymphoma that most commonly involves pulmonary tissue, is often asymptomatic, and shows radiological alveolar opacities. Although it is more commonly affected in people aged 50-60, it can rarely be seen under the age of 30. It constitutes 60% of pulmonary lymphomas. Weight loss and fever are especially prominent during the aggressive phase, though the condition may initially be asymptomatic. Autoimmune disease may be the basis in 16% of cases (1,4). The prognosis of MALT lymphomas is good; 5–10-year survival is more than 80% (5).

   Radiological: 

MALT lymphoma exhibits radiological variability, appearing as single or multiple bilateral lesions on both chest radiography and thoracic tomography. Chronic alveolar localized opacities smaller than 5 cm on radiography are accompanied by consolidation in 50% of cases. Diffuse reticulonodular opacity, atelectasis, and pleural effusion are detected in less than 10% of cases (1). In our case, there was also pleural fluid along with similar findings. Findings such as consolidation (60-77%) with air bronchogram and increased vascularity or multiple mass nodules, ground glass, halo sign, galaxy sign specific to tuberculosis and sarcoidosis have been reported in case series and reports. In addition, varicose cystic bronchiectasis secondary to consolidation can be detected. However, it is not possible to state that these findings are specific to MALT lymphoma. These radiological images are also observed in adenocarcinoma, pneumonia, metastases, sarcoidosis, and tuberculosis (6,7). In this case, chest X-ray revealed bilateral multifocal consolidation and densities indicative of pleural effusion. Consolidation, pleural effusion, varicose cystic bronchiectasis changes and mediastinal lymphadenomegaly were detected on thoracic tomography. None of these radiological findings were specific to lymphoma and diagnosis could not have been made without pathological examination. The partial alleviation of the patient's clinical symptoms compared to the beginning and the patient's relief with the drainage of the pleural fluid suggested possibilities such as infection, alveolar sarcoidosis, or adenocarcinoma when we did not have pathological data. Nevertheless, when intermittent fevers began to occur during the clinical course, it was obvious that lymphoma could not be excluded from the diagnosis. No endobronchial lesion was detected in the bronchoscopy performed on the patient; Wang fine needle aspiration and then endobronchial ultrasonographic biopsy were performed for mediastinal lymphadenomegaly. The sensitivity and specificity of positron emission tomography (PET-CT) in lymphoma varies according to organ involvement. It has been reported as 80-100% in lung involvement (8, 9). In our case, high SUVmax FDG uptake in consolidated foci in lepidic structure was monitored in PET-CT, and pleural uptake was minimal. The presence of clinical symptoms and high FDG uptake necessitated a video-assisted-thoracoscopic (VATS) procedure.

Pathological: 

    In the pleural fluid sample examined at the start of the treatment, abundant lymphoid cells were detected, but no atypical structures were observed. There were findings of granulomatous inflammation in the samples obtained from the mediastinal lymph nodes of the patient. In fact, in the biopsy samples taken by video-assisted thoracoscopy, lowgrade B-cell non-Hodgkin Lymphoma (CD20 positive (diffuse cells), anti-BCL-2 positive, anti Ki-67 low positive) and extranodal marginal zone lymphoma were detected in the parietal pleura. Pathologically, the lymphomatous infiltrate in MALT lymphoma exhibits heterogeneous features and consists of small lymphocytes, centrocyte-like cells, monocytoid B cells, rarely large transformed cells and plasma cells (10). Necrosis is rare. Neoplastic cells are expressed in CD 20 and CD 79. Ki67 index is lower than 20%. Lymphoma and sarcoidosis are similar in terms of clinical and radiological phenotype. Distinguishing lowgrade lymphomas from sarcoid lesions can be challenging; sarcoid granulomatous lesions may be accompanied by lymphoid cell infiltration. In addition, sarcoid-like reactions are frequently seen in malignant lymphomas. Moreover, sarcoidosis-lymphoma syndrome was first described in the study by Brincker et al. They reported that lymphoma was 5.5 times more common in sarcoidosis patients than in the general population, indicating the presence of sarcoidosis years before lymphoma (11, 12). Kokuho N et al reported MALT lymphoma in the lung for the first time in a ten-year-old sarcoidosis case with ocular, gastric and lung involvement (13). In this case, granulomatous inflammation was detected in mediastinal LAMs, but no findings of sarcoidosis were found in ocular, cardiac, renal examinations, angiotensinconverting enzyme, calcium, alkaline phosphatase, and 24- hour urine calcium analyses. There was also no abnormality in abdominal ultrasonography. We believe that the granulomatous inflammation in our case was reactive to immune deficiency.

    Conclusion The patient was started on Rituximab treatment by the hematology department. Clinical and radiological improvement was observed following treatment. In the follow-up PET-CT examination, regression in consolidated areas, decrease in FDG uptake, and metabolic partial regression were detected compared to the initial examination (Figure 6). Lymphomas, which do not have specific radiological and symptomatic features, can mimic most diseases of the respiratory system and do not present with a noisy picture, requiring the clinician to be persistent in making the diagnosis.

References:

1. Borie R, Wislez M, Antoine M, Cadranel J (2017), Lymphoproliferative Disorders of the Lung. Respiration 94:157-175 2. Cadranel J, Wislez M, Antoine M (2002), Primary pulmonary lymphoma. Eur Respir J 20:750-62 3. Kattih Z, Mahajan A, Vojnic M, et al. (2022), Rapidly Accumulating Effusion in an Immunocompetent Woman, Chest 161: e377-e382 4. Wislez M, Thabut G, Antoine M et al. (2009); Clinical characteristics and prognostic factors of pulmonary MALT lymphoma. European Respiratory Journal 234: 1408-1416 5. Koss MN (2004) Malignant and benign lymphoid lesions of the lung. Ann Diagn Pathol 8:167-87 6. Song Y, Sung YE, Beck KS, et al. (2023) Radiological and pathological analysis of the galaxy sign in patients with pulmonary mucosaassociated lymphoid tissue (MALT) lymphoma. Thorac Cancer 14:2459-2466 7. Deng W, Wan Y, Yu JQ (2019) Pulmonary MALT Lymphoma has variable features on CT. Scientific Reports 9:8657 8. Albano D, Borghesi A, Bosio G, et al (2017) Pulmonary mucosaassociated lymphoid tissue lymphoma: 18F-FDG PET/CT and CT findings in 28 patients. Br J Radiol 90:20170311 9. Enomoto K, Hamada K, Inohara H, et al (2008) Mucosa-associated lymphoid tissue lymphoma studied with FDG-PET: a comparison with CT and endoscopic findings. Ann Nucl Med 22:261-267 10. Pina-Oviedo S, Roggli VL, Sporn TA, et al (2023) Diagnostic Approach to Pulmonary B-Cell Lymphomas in Small Biopsies, with Practical Recommendations to Avoid Misinterpretation. Diagnostics (Basel) 13:3321 11. Brincker H (1986) The sarcoidosis-lymphoma syndrome. Br J Cancer 54:467–73 12. El Jammal T, Pavic M, Gerfaud-Valentin M, et al. Sarcoidosis and Cancer: A Complex Relationship. Front Med (Lausanne) (2020) 24:594118 13. Kokuho N, Terasaki Y, Urushiyama H, et al. (2016) Pulmonary mucosa-associated lymphoid tissue lymphoma associated with pulmonary sarcoidosis: a case report and literature review. Hum Pathol 51:57-63 

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What is Pneumothorax?

Pneumothorax is a medical condition where air accumulates in the pleural space, the area between the lung and the chest wall. This can cause the lung to collapse, leading to difficulty breathing and chest pain. Pneumothorax can occur spontaneously, often in tall, thin individuals or as a result of injury, lung disease, or medical procedures. Symptoms may include sudden sharp chest pain and shortness of breath. Treatment options vary depending on the severity and cause, ranging from observation to procedures that remove the air from the pleural space.